Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis

Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascular...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Pu, Xiangyuan [verfasserIn] Chan, Kenneth [verfasserIn] Yang, Wei [verfasserIn] Xiao, Qingzhong [verfasserIn] Zhang, Li [verfasserIn] Moore, Andrew D. [verfasserIn] Liu, Chuanju [verfasserIn] Webb, Tom R. [verfasserIn] Caulfield, Mark J. [verfasserIn] Samani, Nilesh J. [verfasserIn] Zhu, Jianhua [verfasserIn] Ye, Shu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell

Übergeordnetes Werk:	Enthalten in: Atherosclerosis - Amsterdam [u.a.] : Elsevier Science, 1970, 296, Seite 11-17
Übergeordnetes Werk:	volume:296 ; pages:11-17

DOI / URN:	10.1016/j.atherosclerosis.2020.01.015

Katalog-ID:	ELV003744280

Internformat


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024	7		\|a 10.1016/j.atherosclerosis.2020.01.015 \|2 doi
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100	1		\|a Pu, Xiangyuan \|e verfasserin \|4 aut
245	1	0	\|a Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
264		1	\|c 2020
336			\|a nicht spezifiziert \|b zzz \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation.
650		4	\|a ADAMTS7
650		4	\|a Angiogenesis
650		4	\|a Atherosclerosis
650		4	\|a Endothelial cell
700	1		\|a Chan, Kenneth \|e verfasserin \|0 (orcid)0000-0002-5571-7549 \|4 aut
700	1		\|a Yang, Wei \|e verfasserin \|4 aut
700	1		\|a Xiao, Qingzhong \|e verfasserin \|4 aut
700	1		\|a Zhang, Li \|e verfasserin \|4 aut
700	1		\|a Moore, Andrew D. \|e verfasserin \|4 aut
700	1		\|a Liu, Chuanju \|e verfasserin \|4 aut
700	1		\|a Webb, Tom R. \|e verfasserin \|4 aut
700	1		\|a Caulfield, Mark J. \|e verfasserin \|4 aut
700	1		\|a Samani, Nilesh J. \|e verfasserin \|4 aut
700	1		\|a Zhu, Jianhua \|e verfasserin \|4 aut
700	1		\|a Ye, Shu \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Atherosclerosis \|d Amsterdam [u.a.] : Elsevier Science, 1970 \|g 296, Seite 11-17 \|h Online-Ressource \|w (DE-627)306654091 \|w (DE-600)1499887-7 \|w (DE-576)081984545 \|x 1879-1484 \|7 nnns
773	1	8	\|g volume:296 \|g pages:11-17
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912			\|a GBV_ILN_2034
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912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4326
912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
936	b	k	\|a 44.85 \|j Kardiologie \|j Angiologie
951			\|a AR
952			\|d 296 \|h 11-17

Indexfelder

author_variant	x p xp k c kc w y wy q x qx l z lz a d m ad adm c l cl t r w tr trw m j c mj mjc n j s nj njs j z jz s y sy
matchkey_str	article:18791484:2020----::fetfcrnrhatiesascaevratfdmsoedt
hierarchy_sort_str	2020
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publishDate	2020
allfields	10.1016/j.atherosclerosis.2020.01.015 doi (DE-627)ELV003744280 (ELSEVIER)S0021-9150(20)30031-9 DE-627 ger DE-627 rda eng 610 DE-600 44.85 bkl Pu, Xiangyuan verfasserin aut Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation. ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell Chan, Kenneth verfasserin (orcid)0000-0002-5571-7549 aut Yang, Wei verfasserin aut Xiao, Qingzhong verfasserin aut Zhang, Li verfasserin aut Moore, Andrew D. verfasserin aut Liu, Chuanju verfasserin aut Webb, Tom R. verfasserin aut Caulfield, Mark J. verfasserin aut Samani, Nilesh J. verfasserin aut Zhu, Jianhua verfasserin aut Ye, Shu verfasserin aut Enthalten in Atherosclerosis Amsterdam [u.a.] : Elsevier Science, 1970 296, Seite 11-17 Online-Ressource (DE-627)306654091 (DE-600)1499887-7 (DE-576)081984545 1879-1484 nnns volume:296 pages:11-17 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.85 Kardiologie Angiologie AR 296 11-17
spelling	10.1016/j.atherosclerosis.2020.01.015 doi (DE-627)ELV003744280 (ELSEVIER)S0021-9150(20)30031-9 DE-627 ger DE-627 rda eng 610 DE-600 44.85 bkl Pu, Xiangyuan verfasserin aut Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation. ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell Chan, Kenneth verfasserin (orcid)0000-0002-5571-7549 aut Yang, Wei verfasserin aut Xiao, Qingzhong verfasserin aut Zhang, Li verfasserin aut Moore, Andrew D. verfasserin aut Liu, Chuanju verfasserin aut Webb, Tom R. verfasserin aut Caulfield, Mark J. verfasserin aut Samani, Nilesh J. verfasserin aut Zhu, Jianhua verfasserin aut Ye, Shu verfasserin aut Enthalten in Atherosclerosis Amsterdam [u.a.] : Elsevier Science, 1970 296, Seite 11-17 Online-Ressource (DE-627)306654091 (DE-600)1499887-7 (DE-576)081984545 1879-1484 nnns volume:296 pages:11-17 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.85 Kardiologie Angiologie AR 296 11-17
allfields_unstemmed	10.1016/j.atherosclerosis.2020.01.015 doi (DE-627)ELV003744280 (ELSEVIER)S0021-9150(20)30031-9 DE-627 ger DE-627 rda eng 610 DE-600 44.85 bkl Pu, Xiangyuan verfasserin aut Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation. ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell Chan, Kenneth verfasserin (orcid)0000-0002-5571-7549 aut Yang, Wei verfasserin aut Xiao, Qingzhong verfasserin aut Zhang, Li verfasserin aut Moore, Andrew D. verfasserin aut Liu, Chuanju verfasserin aut Webb, Tom R. verfasserin aut Caulfield, Mark J. verfasserin aut Samani, Nilesh J. verfasserin aut Zhu, Jianhua verfasserin aut Ye, Shu verfasserin aut Enthalten in Atherosclerosis Amsterdam [u.a.] : Elsevier Science, 1970 296, Seite 11-17 Online-Ressource (DE-627)306654091 (DE-600)1499887-7 (DE-576)081984545 1879-1484 nnns volume:296 pages:11-17 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.85 Kardiologie Angiologie AR 296 11-17
allfieldsGer	10.1016/j.atherosclerosis.2020.01.015 doi (DE-627)ELV003744280 (ELSEVIER)S0021-9150(20)30031-9 DE-627 ger DE-627 rda eng 610 DE-600 44.85 bkl Pu, Xiangyuan verfasserin aut Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation. ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell Chan, Kenneth verfasserin (orcid)0000-0002-5571-7549 aut Yang, Wei verfasserin aut Xiao, Qingzhong verfasserin aut Zhang, Li verfasserin aut Moore, Andrew D. verfasserin aut Liu, Chuanju verfasserin aut Webb, Tom R. verfasserin aut Caulfield, Mark J. verfasserin aut Samani, Nilesh J. verfasserin aut Zhu, Jianhua verfasserin aut Ye, Shu verfasserin aut Enthalten in Atherosclerosis Amsterdam [u.a.] : Elsevier Science, 1970 296, Seite 11-17 Online-Ressource (DE-627)306654091 (DE-600)1499887-7 (DE-576)081984545 1879-1484 nnns volume:296 pages:11-17 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.85 Kardiologie Angiologie AR 296 11-17
allfieldsSound	10.1016/j.atherosclerosis.2020.01.015 doi (DE-627)ELV003744280 (ELSEVIER)S0021-9150(20)30031-9 DE-627 ger DE-627 rda eng 610 DE-600 44.85 bkl Pu, Xiangyuan verfasserin aut Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation. ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell Chan, Kenneth verfasserin (orcid)0000-0002-5571-7549 aut Yang, Wei verfasserin aut Xiao, Qingzhong verfasserin aut Zhang, Li verfasserin aut Moore, Andrew D. verfasserin aut Liu, Chuanju verfasserin aut Webb, Tom R. verfasserin aut Caulfield, Mark J. verfasserin aut Samani, Nilesh J. verfasserin aut Zhu, Jianhua verfasserin aut Ye, Shu verfasserin aut Enthalten in Atherosclerosis Amsterdam [u.a.] : Elsevier Science, 1970 296, Seite 11-17 Online-Ressource (DE-627)306654091 (DE-600)1499887-7 (DE-576)081984545 1879-1484 nnns volume:296 pages:11-17 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.85 Kardiologie Angiologie AR 296 11-17
language	English
source	Enthalten in Atherosclerosis 296, Seite 11-17 volume:296 pages:11-17
sourceStr	Enthalten in Atherosclerosis 296, Seite 11-17 volume:296 pages:11-17
format_phy_str_mv	Article
bklname	Kardiologie Angiologie
institution	findex.gbv.de
topic_facet	ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell
dewey-raw	610
isfreeaccess_bool	false
container_title	Atherosclerosis
authorswithroles_txt_mv	Pu, Xiangyuan @@aut@@ Chan, Kenneth @@aut@@ Yang, Wei @@aut@@ Xiao, Qingzhong @@aut@@ Zhang, Li @@aut@@ Moore, Andrew D. @@aut@@ Liu, Chuanju @@aut@@ Webb, Tom R. @@aut@@ Caulfield, Mark J. @@aut@@ Samani, Nilesh J. @@aut@@ Zhu, Jianhua @@aut@@ Ye, Shu @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	306654091
dewey-sort	3610
id	ELV003744280
language_de	englisch
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The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ADAMTS7</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Angiogenesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Atherosclerosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Endothelial cell</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chan, Kenneth</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-5571-7549</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield 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author	Pu, Xiangyuan
spellingShingle	Pu, Xiangyuan ddc 610 bkl 44.85 misc ADAMTS7 misc Angiogenesis misc Atherosclerosis misc Endothelial cell Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
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topic_title	610 DE-600 44.85 bkl Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis ADAMTS7 Angiogenesis Atherosclerosis Endothelial cell
topic	ddc 610 bkl 44.85 misc ADAMTS7 misc Angiogenesis misc Atherosclerosis misc Endothelial cell
topic_unstemmed	ddc 610 bkl 44.85 misc ADAMTS7 misc Angiogenesis misc Atherosclerosis misc Endothelial cell
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title	Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
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title_full	Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
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author_browse	Pu, Xiangyuan Chan, Kenneth Yang, Wei Xiao, Qingzhong Zhang, Li Moore, Andrew D. Liu, Chuanju Webb, Tom R. Caulfield, Mark J. Samani, Nilesh J. Zhu, Jianhua Ye, Shu
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title_sort	effect of a coronary-heart-disease-associated variant of adamts7 on endothelial cell angiogenesis
title_auth	Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
abstract	Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation.
abstractGer	Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation.
abstract_unstemmed	Background and aims: Recent studies have unveiled an association between ADAMTS7 gene variation and coronary artery disease (CAD) caused by atherosclerosis. We investigated if the ADAMTS7 Serine214-to-Proline substitution arising from a CAD-associated variant affected angiogenesis, since neovascularization plays an important role in atherosclerosis.Methods and results: ADAMTS7 knockdown in vascular endothelial cells (ECs) attenuated their angiogenesis potential, whereas augmented ADAMTS7-Ser214 expression had the opposite effect, leading to increased ECs migratory and tube formation ability. Proteomics analysis showed an increase in thrombospondin-1, a reported angiogenesis inhibitor, in culture media conditioned by ECs with ADAMTS7 knockdown and a decrease of thrombospondin-1 in media conditioned by ECs with ADAMTS7-Ser214 overexpression. Cleavage assay indicated that ADAMTS7 possessed thrombospondin-1 degrading activity, which was reduced by the Ser214-to-Pro substitution. The pro-angiogenic effect of ADAMTS7-Ser214 diminished in the presence of a thrombospondin-1 blocking antibody.Conclusions: The ADAMTS7 Ser217-to-Pro substitution as a result of ADAMTS7 polymorphism affects thrombospondin-1 degradation, thereby promoting atherogenesis through increased EC migration and tube formation.
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title_short	Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis
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author2	Chan, Kenneth Yang, Wei Xiao, Qingzhong Zhang, Li Moore, Andrew D. Liu, Chuanju Webb, Tom R. Caulfield, Mark J. Samani, Nilesh J. Zhu, Jianhua Ye, Shu
author2Str	Chan, Kenneth Yang, Wei Xiao, Qingzhong Zhang, Li Moore, Andrew D. Liu, Chuanju Webb, Tom R. Caulfield, Mark J. Samani, Nilesh J. Zhu, Jianhua Ye, Shu
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doi_str	10.1016/j.atherosclerosis.2020.01.015
up_date	2024-07-06T20:39:24.017Z
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Effect of a coronary-heart-disease-associated variant of ADAMTS7 on endothelial cell angiogenesis

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