Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression

Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazol...
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Autor*in:	Yukihiko Aoyagi [verfasserIn] Tadashi Furuyama [verfasserIn] Kentaro Inoue [verfasserIn] Daisuke Matsuda [verfasserIn] Yutaka Matsubara [verfasserIn] Arihide Okahara [verfasserIn] Tetsuro Ago [verfasserIn] Yutaka Nakashima [verfasserIn] Masaki Mori [verfasserIn] Takuya Matsumoto [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell

Übergeordnetes Werk:	In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease - Wiley, 2012, 8(2019), 23
Übergeordnetes Werk:	volume:8 ; year:2019 ; number:23

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1161/JAHA.118.011911

Katalog-ID:	DOAJ064527611

Internformat


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100	0		\|a Yukihiko Aoyagi \|e verfasserin \|4 aut
245	1	0	\|a Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
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520			\|a Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.
650		4	\|a angiotensin II type 1 receptor
650		4	\|a budding uninhibited by benzimidazole‐related 1
650		4	\|a hypertension
650		4	\|a nicotinamide adenine dinucleotide phosphate oxidase‐4
650		4	\|a renal proximal tubule cell
653		0	\|a Diseases of the circulatory (Cardiovascular) system
700	0		\|a Tadashi Furuyama \|e verfasserin \|4 aut
700	0		\|a Kentaro Inoue \|e verfasserin \|4 aut
700	0		\|a Daisuke Matsuda \|e verfasserin \|4 aut
700	0		\|a Yutaka Matsubara \|e verfasserin \|4 aut
700	0		\|a Arihide Okahara \|e verfasserin \|4 aut
700	0		\|a Tetsuro Ago \|e verfasserin \|4 aut
700	0		\|a Yutaka Nakashima \|e verfasserin \|4 aut
700	0		\|a Masaki Mori \|e verfasserin \|4 aut
700	0		\|a Takuya Matsumoto \|e verfasserin \|4 aut
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912			\|a GBV_ILN_171
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_224
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_636
912			\|a GBV_ILN_2004
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2007
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
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912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2108
912			\|a GBV_ILN_2110
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2118
912			\|a GBV_ILN_2122
912			\|a GBV_ILN_2143
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912			\|a GBV_ILN_2152
912			\|a GBV_ILN_2153
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912			\|a GBV_ILN_2336
912			\|a GBV_ILN_2470
912			\|a GBV_ILN_2507
912			\|a GBV_ILN_2522
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4035
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4046
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
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912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4336
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
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Indexfelder

author_variant	y a ya t f tf k i ki d m dm y m ym a o ao t a ta y n yn m m mm t m tm
matchkey_str	article:20479980:2019----::teutooagoesninuehpresoibb1oepesomcvaersinfnit
hierarchy_sort_str	2019
callnumber-subject-code	RC
publishDate	2019
allfields	10.1161/JAHA.118.011911 doi (DE-627)DOAJ064527611 (DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918 DE-627 ger DE-627 rakwb eng RC666-701 Yukihiko Aoyagi verfasserin aut Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4. angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system Tadashi Furuyama verfasserin aut Kentaro Inoue verfasserin aut Daisuke Matsuda verfasserin aut Yutaka Matsubara verfasserin aut Arihide Okahara verfasserin aut Tetsuro Ago verfasserin aut Yutaka Nakashima verfasserin aut Masaki Mori verfasserin aut Takuya Matsumoto verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 23 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:23 https://doi.org/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2019 23
spelling	10.1161/JAHA.118.011911 doi (DE-627)DOAJ064527611 (DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918 DE-627 ger DE-627 rakwb eng RC666-701 Yukihiko Aoyagi verfasserin aut Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4. angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system Tadashi Furuyama verfasserin aut Kentaro Inoue verfasserin aut Daisuke Matsuda verfasserin aut Yutaka Matsubara verfasserin aut Arihide Okahara verfasserin aut Tetsuro Ago verfasserin aut Yutaka Nakashima verfasserin aut Masaki Mori verfasserin aut Takuya Matsumoto verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 23 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:23 https://doi.org/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2019 23
allfields_unstemmed	10.1161/JAHA.118.011911 doi (DE-627)DOAJ064527611 (DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918 DE-627 ger DE-627 rakwb eng RC666-701 Yukihiko Aoyagi verfasserin aut Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4. angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system Tadashi Furuyama verfasserin aut Kentaro Inoue verfasserin aut Daisuke Matsuda verfasserin aut Yutaka Matsubara verfasserin aut Arihide Okahara verfasserin aut Tetsuro Ago verfasserin aut Yutaka Nakashima verfasserin aut Masaki Mori verfasserin aut Takuya Matsumoto verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 23 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:23 https://doi.org/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2019 23
allfieldsGer	10.1161/JAHA.118.011911 doi (DE-627)DOAJ064527611 (DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918 DE-627 ger DE-627 rakwb eng RC666-701 Yukihiko Aoyagi verfasserin aut Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4. angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system Tadashi Furuyama verfasserin aut Kentaro Inoue verfasserin aut Daisuke Matsuda verfasserin aut Yutaka Matsubara verfasserin aut Arihide Okahara verfasserin aut Tetsuro Ago verfasserin aut Yutaka Nakashima verfasserin aut Masaki Mori verfasserin aut Takuya Matsumoto verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 23 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:23 https://doi.org/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2019 23
allfieldsSound	10.1161/JAHA.118.011911 doi (DE-627)DOAJ064527611 (DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918 DE-627 ger DE-627 rakwb eng RC666-701 Yukihiko Aoyagi verfasserin aut Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4. angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system Tadashi Furuyama verfasserin aut Kentaro Inoue verfasserin aut Daisuke Matsuda verfasserin aut Yutaka Matsubara verfasserin aut Arihide Okahara verfasserin aut Tetsuro Ago verfasserin aut Yutaka Nakashima verfasserin aut Masaki Mori verfasserin aut Takuya Matsumoto verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 23 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:23 https://doi.org/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2019 23
language	English
source	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 8(2019), 23 volume:8 year:2019 number:23
sourceStr	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 8(2019), 23 volume:8 year:2019 number:23
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell Diseases of the circulatory (Cardiovascular) system
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container_title	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
authorswithroles_txt_mv	Yukihiko Aoyagi @@aut@@ Tadashi Furuyama @@aut@@ Kentaro Inoue @@aut@@ Daisuke Matsuda @@aut@@ Yutaka Matsubara @@aut@@ Arihide Okahara @@aut@@ Tetsuro Ago @@aut@@ Yutaka Nakashima @@aut@@ Masaki Mori @@aut@@ Takuya Matsumoto @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	688605427
id	DOAJ064527611
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ064527611</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309040451.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2019 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1161/JAHA.118.011911</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ064527611</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJe719c45cd6ae47ba933172b2c92c7918</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Yukihiko Aoyagi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">angiotensin II type 1 receptor</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">budding uninhibited by benzimidazole‐related 1</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hypertension</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">nicotinamide adenine dinucleotide phosphate oxidase‐4</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">renal proximal tubule cell</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Tadashi Furuyama</subfield><subfield code="e">verfasserin</subfield><subfield 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callnumber-first	R - Medicine
author	Yukihiko Aoyagi
spellingShingle	Yukihiko Aoyagi misc RC666-701 misc angiotensin II type 1 receptor misc budding uninhibited by benzimidazole‐related 1 misc hypertension misc nicotinamide adenine dinucleotide phosphate oxidase‐4 misc renal proximal tubule cell misc Diseases of the circulatory (Cardiovascular) system Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
authorStr	Yukihiko Aoyagi
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topic_title	RC666-701 Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression angiotensin II type 1 receptor budding uninhibited by benzimidazole‐related 1 hypertension nicotinamide adenine dinucleotide phosphate oxidase‐4 renal proximal tubule cell
topic	misc RC666-701 misc angiotensin II type 1 receptor misc budding uninhibited by benzimidazole‐related 1 misc hypertension misc nicotinamide adenine dinucleotide phosphate oxidase‐4 misc renal proximal tubule cell misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc angiotensin II type 1 receptor misc budding uninhibited by benzimidazole‐related 1 misc hypertension misc nicotinamide adenine dinucleotide phosphate oxidase‐4 misc renal proximal tubule cell misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc angiotensin II type 1 receptor misc budding uninhibited by benzimidazole‐related 1 misc hypertension misc nicotinamide adenine dinucleotide phosphate oxidase‐4 misc renal proximal tubule cell misc Diseases of the circulatory (Cardiovascular) system
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hierarchy_parent_title	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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title	Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
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title_full	Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
author_sort	Yukihiko Aoyagi
journal	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
journalStr	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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author_browse	Yukihiko Aoyagi Tadashi Furuyama Kentaro Inoue Daisuke Matsuda Yutaka Matsubara Arihide Okahara Tetsuro Ago Yutaka Nakashima Masaki Mori Takuya Matsumoto
container_volume	8
class	RC666-701
format_se	Elektronische Aufsätze
author-letter	Yukihiko Aoyagi
doi_str_mv	10.1161/JAHA.118.011911
author2-role	verfasserin
title_sort	attenuation of angiotensin ii–induced hypertension in bubr1 low‐expression mice via repression of angiotensin ii receptor 1 overexpression
callnumber	RC666-701
title_auth	Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
abstract	Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.
abstractGer	Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.
abstract_unstemmed	Background Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.
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container_issue	23
title_short	Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression
url	https://doi.org/10.1161/JAHA.118.011911 https://doaj.org/article/e719c45cd6ae47ba933172b2c92c7918 https://www.ahajournals.org/doi/10.1161/JAHA.118.011911 https://doaj.org/toc/2047-9980
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author2	Tadashi Furuyama Kentaro Inoue Daisuke Matsuda Yutaka Matsubara Arihide Okahara Tetsuro Ago Yutaka Nakashima Masaki Mori Takuya Matsumoto
author2Str	Tadashi Furuyama Kentaro Inoue Daisuke Matsuda Yutaka Matsubara Arihide Okahara Tetsuro Ago Yutaka Nakashima Masaki Mori Takuya Matsumoto
ppnlink	688605427
callnumber-subject	RC - Internal Medicine
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doi_str	10.1161/JAHA.118.011911
callnumber-a	RC666-701
up_date	2024-07-03T23:18:10.768Z
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BubR1 (budding uninhibited by benzimidazole‐related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results Twenty 24‐week‐old male BubR1 low‐expression mice (BubR1L/L mice) and age‐matched BubR1+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1+/+ mice was significantly attenuated in BubR1L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1L/L mice. We evaluated AGTR1 and Nox‐4 (nicotinamide adenine dinucleotide phosphate oxidase‐4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II‐induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N‐terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. 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Attenuation of Angiotensin II–Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression

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