CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension

Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate th...
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Autor*in:	M. Florencia Iulita [verfasserIn] Sonia Duchemin [verfasserIn] Diane Vallerand [verfasserIn] Tlili Barhoumi [verfasserIn] Fernando Alvarez [verfasserIn] Roman Istomine [verfasserIn] Cyril Laurent [verfasserIn] Jessica Youwakim [verfasserIn] Pierre Paradis [verfasserIn] Nathalie Arbour [verfasserIn] Ciriaco A. Piccirillo [verfasserIn] Ernesto L. Schiffrin [verfasserIn] Hélène Girouard [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte

Übergeordnetes Werk:	In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease - Wiley, 2012, 8(2019), 1
Übergeordnetes Werk:	volume:8 ; year:2019 ; number:1

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1161/JAHA.118.009372

Katalog-ID:	DOAJ064532992

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520			\|a Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery.
650		4	\|a angiotensin
650		4	\|a cerebral blood flow
650		4	\|a inflammation
650		4	\|a interleukin‐10
650		4	\|a lymphocyte
653		0	\|a Diseases of the circulatory (Cardiovascular) system
700	0		\|a Sonia Duchemin \|e verfasserin \|4 aut
700	0		\|a Diane Vallerand \|e verfasserin \|4 aut
700	0		\|a Tlili Barhoumi \|e verfasserin \|4 aut
700	0		\|a Fernando Alvarez \|e verfasserin \|4 aut
700	0		\|a Roman Istomine \|e verfasserin \|4 aut
700	0		\|a Cyril Laurent \|e verfasserin \|4 aut
700	0		\|a Jessica Youwakim \|e verfasserin \|4 aut
700	0		\|a Pierre Paradis \|e verfasserin \|4 aut
700	0		\|a Nathalie Arbour \|e verfasserin \|4 aut
700	0		\|a Ciriaco A. Piccirillo \|e verfasserin \|4 aut
700	0		\|a Ernesto L. Schiffrin \|e verfasserin \|4 aut
700	0		\|a Hélène Girouard \|e verfasserin \|4 aut
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Indexfelder

author_variant	m f i mfi s d sd d v dv t b tb f a fa r i ri c l cl j y jy p p pp n a na c a p cap e l s els h g hg
matchkey_str	article:20479980:2019----::drgltrtypoyepeetmardeerllofoiagoe
hierarchy_sort_str	2019
callnumber-subject-code	RC
publishDate	2019
allfields	10.1161/JAHA.118.009372 doi (DE-627)DOAJ064532992 (DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8 DE-627 ger DE-627 rakwb eng RC666-701 M. Florencia Iulita verfasserin aut CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery. angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte Diseases of the circulatory (Cardiovascular) system Sonia Duchemin verfasserin aut Diane Vallerand verfasserin aut Tlili Barhoumi verfasserin aut Fernando Alvarez verfasserin aut Roman Istomine verfasserin aut Cyril Laurent verfasserin aut Jessica Youwakim verfasserin aut Pierre Paradis verfasserin aut Nathalie Arbour verfasserin aut Ciriaco A. Piccirillo verfasserin aut Ernesto L. Schiffrin verfasserin aut Hélène Girouard verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 1 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:1 https://doi.org/10.1161/JAHA.118.009372 kostenfrei https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 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 1
spelling	10.1161/JAHA.118.009372 doi (DE-627)DOAJ064532992 (DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8 DE-627 ger DE-627 rakwb eng RC666-701 M. Florencia Iulita verfasserin aut CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery. angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte Diseases of the circulatory (Cardiovascular) system Sonia Duchemin verfasserin aut Diane Vallerand verfasserin aut Tlili Barhoumi verfasserin aut Fernando Alvarez verfasserin aut Roman Istomine verfasserin aut Cyril Laurent verfasserin aut Jessica Youwakim verfasserin aut Pierre Paradis verfasserin aut Nathalie Arbour verfasserin aut Ciriaco A. Piccirillo verfasserin aut Ernesto L. Schiffrin verfasserin aut Hélène Girouard verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 1 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:1 https://doi.org/10.1161/JAHA.118.009372 kostenfrei https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 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 1
allfields_unstemmed	10.1161/JAHA.118.009372 doi (DE-627)DOAJ064532992 (DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8 DE-627 ger DE-627 rakwb eng RC666-701 M. Florencia Iulita verfasserin aut CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery. angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte Diseases of the circulatory (Cardiovascular) system Sonia Duchemin verfasserin aut Diane Vallerand verfasserin aut Tlili Barhoumi verfasserin aut Fernando Alvarez verfasserin aut Roman Istomine verfasserin aut Cyril Laurent verfasserin aut Jessica Youwakim verfasserin aut Pierre Paradis verfasserin aut Nathalie Arbour verfasserin aut Ciriaco A. Piccirillo verfasserin aut Ernesto L. Schiffrin verfasserin aut Hélène Girouard verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 1 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:1 https://doi.org/10.1161/JAHA.118.009372 kostenfrei https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 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 1
allfieldsGer	10.1161/JAHA.118.009372 doi (DE-627)DOAJ064532992 (DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8 DE-627 ger DE-627 rakwb eng RC666-701 M. Florencia Iulita verfasserin aut CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery. angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte Diseases of the circulatory (Cardiovascular) system Sonia Duchemin verfasserin aut Diane Vallerand verfasserin aut Tlili Barhoumi verfasserin aut Fernando Alvarez verfasserin aut Roman Istomine verfasserin aut Cyril Laurent verfasserin aut Jessica Youwakim verfasserin aut Pierre Paradis verfasserin aut Nathalie Arbour verfasserin aut Ciriaco A. Piccirillo verfasserin aut Ernesto L. Schiffrin verfasserin aut Hélène Girouard verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 1 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:1 https://doi.org/10.1161/JAHA.118.009372 kostenfrei https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 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 1
allfieldsSound	10.1161/JAHA.118.009372 doi (DE-627)DOAJ064532992 (DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8 DE-627 ger DE-627 rakwb eng RC666-701 M. Florencia Iulita verfasserin aut CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery. angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte Diseases of the circulatory (Cardiovascular) system Sonia Duchemin verfasserin aut Diane Vallerand verfasserin aut Tlili Barhoumi verfasserin aut Fernando Alvarez verfasserin aut Roman Istomine verfasserin aut Cyril Laurent verfasserin aut Jessica Youwakim verfasserin aut Pierre Paradis verfasserin aut Nathalie Arbour verfasserin aut Ciriaco A. Piccirillo verfasserin aut Ernesto L. Schiffrin verfasserin aut Hélène Girouard verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 8(2019), 1 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:8 year:2019 number:1 https://doi.org/10.1161/JAHA.118.009372 kostenfrei https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 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 1
language	English
source	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 8(2019), 1 volume:8 year:2019 number:1
sourceStr	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 8(2019), 1 volume:8 year:2019 number:1
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topic_facet	angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte 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	M. Florencia Iulita @@aut@@ Sonia Duchemin @@aut@@ Diane Vallerand @@aut@@ Tlili Barhoumi @@aut@@ Fernando Alvarez @@aut@@ Roman Istomine @@aut@@ Cyril Laurent @@aut@@ Jessica Youwakim @@aut@@ Pierre Paradis @@aut@@ Nathalie Arbour @@aut@@ Ciriaco A. Piccirillo @@aut@@ Ernesto L. Schiffrin @@aut@@ Hélène Girouard @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
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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">DOAJ064532992</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309040510.0</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.118.009372</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ064532992</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ7491ecb9dfeb40cabf315a1958cae5e8</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">M. Florencia Iulita</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension</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 Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. 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callnumber-first	R - Medicine
author	M. Florencia Iulita
spellingShingle	M. Florencia Iulita misc RC666-701 misc angiotensin misc cerebral blood flow misc inflammation misc interleukin‐10 misc lymphocyte misc Diseases of the circulatory (Cardiovascular) system CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension
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topic_title	RC666-701 CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension angiotensin cerebral blood flow inflammation interleukin‐10 lymphocyte
topic	misc RC666-701 misc angiotensin misc cerebral blood flow misc inflammation misc interleukin‐10 misc lymphocyte misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc angiotensin misc cerebral blood flow misc inflammation misc interleukin‐10 misc lymphocyte misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc angiotensin misc cerebral blood flow misc inflammation misc interleukin‐10 misc lymphocyte misc Diseases of the circulatory (Cardiovascular) system
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title	CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension
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title_full	CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension
author_sort	M. Florencia Iulita
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	M. Florencia Iulita Sonia Duchemin Diane Vallerand Tlili Barhoumi Fernando Alvarez Roman Istomine Cyril Laurent Jessica Youwakim Pierre Paradis Nathalie Arbour Ciriaco A. Piccirillo Ernesto L. Schiffrin Hélène Girouard
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author-letter	M. Florencia Iulita
doi_str_mv	10.1161/JAHA.118.009372
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title_sort	cd4+ regulatory t lymphocytes prevent impaired cerebral blood flow in angiotensin ii‐induced hypertension
callnumber	RC666-701
title_auth	CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension
abstract	Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery.
abstractGer	Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery.
abstract_unstemmed	Background Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang II (P<0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba‐1+ cells in the brain cortex (P<0.05) and hippocampus (P<0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen. Conclusions Treg prevent impaired cerebrovascular responses in Ang II‐induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery.
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title_short	CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension
url	https://doi.org/10.1161/JAHA.118.009372 https://doaj.org/article/7491ecb9dfeb40cabf315a1958cae5e8 https://www.ahajournals.org/doi/10.1161/JAHA.118.009372 https://doaj.org/toc/2047-9980
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author2	Sonia Duchemin Diane Vallerand Tlili Barhoumi Fernando Alvarez Roman Istomine Cyril Laurent Jessica Youwakim Pierre Paradis Nathalie Arbour Ciriaco A. Piccirillo Ernesto L. Schiffrin Hélène Girouard
author2Str	Sonia Duchemin Diane Vallerand Tlili Barhoumi Fernando Alvarez Roman Istomine Cyril Laurent Jessica Youwakim Pierre Paradis Nathalie Arbour Ciriaco A. Piccirillo Ernesto L. Schiffrin Hélène Girouard
ppnlink	688605427
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doi_str	10.1161/JAHA.118.009372
callnumber-a	RC666-701
up_date	2024-07-03T23:19:45.142Z
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Florencia Iulita</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CD4+ Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II‐Induced Hypertension</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 Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg, CD4+CD25+) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown. Methods and Results C57BL/6 mice were perfused with angiotensin II (Ang II; 1000 ng/kg per minute) for 14 days and adoptive transfer of 3×105 CD4+CD25+ T cells was performed via 2 intravenous injections. Control mice received a sham surgery and PBS. Treg prevented Ang II‐induced neurovascular uncoupling (P<0.05) and endothelial impairment (P<0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin‐10. Administration of interleukin‐10 (60 ng/d) to hypertensive mice prevented Ang II‐induced neurovascular uncoupling (P<0.05). 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Nicht das Richtige dabei?