Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits

Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% hig...
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Autor*in:	Qingqing Yu [verfasserIn] Panpan Wei [verfasserIn] Liran Xu [verfasserIn] Congcong Xia [verfasserIn] Yafeng Li [verfasserIn] Haole Liu [verfasserIn] Xiaojie Song [verfasserIn] Kangli Tian [verfasserIn] Weilai Fu [verfasserIn] Rong Wang [verfasserIn] Weirong Wang [verfasserIn] Liang Bai [verfasserIn] Jianglin Fan [verfasserIn] Enqi Liu [verfasserIn] Sihai Zhao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 24(2023), 4, p 3819
Übergeordnetes Werk:	volume:24 ; year:2023 ; number:4, p 3819

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms24043819

Katalog-ID:	DOAJ080257682

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allfields	10.3390/ijms24043819 doi (DE-627)DOAJ080257682 (DE-599)DOAJe7c7ed188ad14ba392688830272a8f1e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qingqing Yu verfasserin aut Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry Panpan Wei verfasserin aut Liran Xu verfasserin aut Congcong Xia verfasserin aut Yafeng Li verfasserin aut Haole Liu verfasserin aut Xiaojie Song verfasserin aut Kangli Tian verfasserin aut Weilai Fu verfasserin aut Rong Wang verfasserin aut Weirong Wang verfasserin aut Liang Bai verfasserin aut Jianglin Fan verfasserin aut Enqi Liu verfasserin aut Sihai Zhao verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 4, p 3819 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:4, p 3819 https://doi.org/10.3390/ijms24043819 kostenfrei https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e kostenfrei https://www.mdpi.com/1422-0067/24/4/3819 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 4, p 3819
spelling	10.3390/ijms24043819 doi (DE-627)DOAJ080257682 (DE-599)DOAJe7c7ed188ad14ba392688830272a8f1e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qingqing Yu verfasserin aut Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry Panpan Wei verfasserin aut Liran Xu verfasserin aut Congcong Xia verfasserin aut Yafeng Li verfasserin aut Haole Liu verfasserin aut Xiaojie Song verfasserin aut Kangli Tian verfasserin aut Weilai Fu verfasserin aut Rong Wang verfasserin aut Weirong Wang verfasserin aut Liang Bai verfasserin aut Jianglin Fan verfasserin aut Enqi Liu verfasserin aut Sihai Zhao verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 4, p 3819 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:4, p 3819 https://doi.org/10.3390/ijms24043819 kostenfrei https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e kostenfrei https://www.mdpi.com/1422-0067/24/4/3819 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 4, p 3819
allfields_unstemmed	10.3390/ijms24043819 doi (DE-627)DOAJ080257682 (DE-599)DOAJe7c7ed188ad14ba392688830272a8f1e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qingqing Yu verfasserin aut Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry Panpan Wei verfasserin aut Liran Xu verfasserin aut Congcong Xia verfasserin aut Yafeng Li verfasserin aut Haole Liu verfasserin aut Xiaojie Song verfasserin aut Kangli Tian verfasserin aut Weilai Fu verfasserin aut Rong Wang verfasserin aut Weirong Wang verfasserin aut Liang Bai verfasserin aut Jianglin Fan verfasserin aut Enqi Liu verfasserin aut Sihai Zhao verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 4, p 3819 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:4, p 3819 https://doi.org/10.3390/ijms24043819 kostenfrei https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e kostenfrei https://www.mdpi.com/1422-0067/24/4/3819 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 4, p 3819
allfieldsGer	10.3390/ijms24043819 doi (DE-627)DOAJ080257682 (DE-599)DOAJe7c7ed188ad14ba392688830272a8f1e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qingqing Yu verfasserin aut Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry Panpan Wei verfasserin aut Liran Xu verfasserin aut Congcong Xia verfasserin aut Yafeng Li verfasserin aut Haole Liu verfasserin aut Xiaojie Song verfasserin aut Kangli Tian verfasserin aut Weilai Fu verfasserin aut Rong Wang verfasserin aut Weirong Wang verfasserin aut Liang Bai verfasserin aut Jianglin Fan verfasserin aut Enqi Liu verfasserin aut Sihai Zhao verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 4, p 3819 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:4, p 3819 https://doi.org/10.3390/ijms24043819 kostenfrei https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e kostenfrei https://www.mdpi.com/1422-0067/24/4/3819 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 4, p 3819
allfieldsSound	10.3390/ijms24043819 doi (DE-627)DOAJ080257682 (DE-599)DOAJe7c7ed188ad14ba392688830272a8f1e DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qingqing Yu verfasserin aut Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry Panpan Wei verfasserin aut Liran Xu verfasserin aut Congcong Xia verfasserin aut Yafeng Li verfasserin aut Haole Liu verfasserin aut Xiaojie Song verfasserin aut Kangli Tian verfasserin aut Weilai Fu verfasserin aut Rong Wang verfasserin aut Weirong Wang verfasserin aut Liang Bai verfasserin aut Jianglin Fan verfasserin aut Enqi Liu verfasserin aut Sihai Zhao verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 4, p 3819 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:4, p 3819 https://doi.org/10.3390/ijms24043819 kostenfrei https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e kostenfrei https://www.mdpi.com/1422-0067/24/4/3819 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 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_70 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_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 4, p 3819
language	English
source	In International Journal of Molecular Sciences 24(2023), 4, p 3819 volume:24 year:2023 number:4, p 3819
sourceStr	In International Journal of Molecular Sciences 24(2023), 4, p 3819 volume:24 year:2023 number:4, p 3819
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Qingqing Yu @@aut@@ Panpan Wei @@aut@@ Liran Xu @@aut@@ Congcong Xia @@aut@@ Yafeng Li @@aut@@ Haole Liu @@aut@@ Xiaojie Song @@aut@@ Kangli Tian @@aut@@ Weilai Fu @@aut@@ Rong Wang @@aut@@ Weirong Wang @@aut@@ Liang Bai @@aut@@ Jianglin Fan @@aut@@ Enqi Liu @@aut@@ Sihai Zhao @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ080257682
language_de	englisch
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callnumber-first	Q - Science
author	Qingqing Yu
spellingShingle	Qingqing Yu misc QH301-705.5 misc QD1-999 misc urotensin II misc atherosclerosis misc vulnerable plaque misc angiogenesis misc coronary plaque misc Biology (General) misc Chemistry Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits
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topic_title	QH301-705.5 QD1-999 Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits urotensin II atherosclerosis vulnerable plaque angiogenesis coronary plaque
topic	misc QH301-705.5 misc QD1-999 misc urotensin II misc atherosclerosis misc vulnerable plaque misc angiogenesis misc coronary plaque misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc urotensin II misc atherosclerosis misc vulnerable plaque misc angiogenesis misc coronary plaque misc Biology (General) misc Chemistry
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title	Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits
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title_full	Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits
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author_browse	Qingqing Yu Panpan Wei Liran Xu Congcong Xia Yafeng Li Haole Liu Xiaojie Song Kangli Tian Weilai Fu Rong Wang Weirong Wang Liang Bai Jianglin Fan Enqi Liu Sihai Zhao
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title_sort	urotensin ii enhances advanced aortic atherosclerosis formation and delays plaque regression in hyperlipidemic rabbits
callnumber	QH301-705.5
title_auth	Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits
abstract	Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development.
abstractGer	Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development.
abstract_unstemmed	Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development.
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title_short	Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits
url	https://doi.org/10.3390/ijms24043819 https://doaj.org/article/e7c7ed188ad14ba392688830272a8f1e https://www.mdpi.com/1422-0067/24/4/3819 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits

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