{"title":"TLN1 与 ITGA5 协同改善心脏微血管内皮细胞功能障碍。","authors":"Xianfeng Wang, Wenkai Mao, Xiaofeng Ma","doi":"10.5603/FM.a2023.0031","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The complex process of atherosclerosis is thought to begin with endothelial cell dysfunction, and advanced atherosclerosis is the underlying cause of coronary artery disease (CAD). Uncovering the underlying mechanisms of CAD-related endothelial cell injury may contribute to the treatment.</p><p><strong>Materials and methods: </strong>Cardiac microvascular endothelial cells (CMVECs) were treated with oxidised low-density lipoprotein (ox-LDL) to mimic an injury model. The involvement of Talin-1 (TLN1) and integrin alpha 5 (ITGA5) in the proliferation, apoptosis, angiogenesis, inflammatory response, and oxidative stress in CMVECs were assessed.</p><p><strong>Results: </strong>TLN1 overexpression assisted CMVECs in resistance to ox-LDL stimulation, with alleviated cell proliferation and angiogenesis, reduced apoptosis, inflammatory response, and oxidative stress. TLN1 overexpression triggered increased ITGA5, and ITGA5 knockdown reversed the effects of TLN1 overexpression on the abovementioned aspects. Together, TLN1 synergized with ITGA5 to ameliorate the dysfunction in CMVECs.</p><p><strong>Conclusions: </strong>This finding suggests their probable involvement in CAD, and increasing their levels is beneficial to disease relief.</p>","PeriodicalId":12251,"journal":{"name":"Folia morphologica","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"TLN1 synergizes with ITGA5 to ameliorate cardiac microvascular endothelial cell dysfunction.\",\"authors\":\"Xianfeng Wang, Wenkai Mao, Xiaofeng Ma\",\"doi\":\"10.5603/FM.a2023.0031\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The complex process of atherosclerosis is thought to begin with endothelial cell dysfunction, and advanced atherosclerosis is the underlying cause of coronary artery disease (CAD). Uncovering the underlying mechanisms of CAD-related endothelial cell injury may contribute to the treatment.</p><p><strong>Materials and methods: </strong>Cardiac microvascular endothelial cells (CMVECs) were treated with oxidised low-density lipoprotein (ox-LDL) to mimic an injury model. The involvement of Talin-1 (TLN1) and integrin alpha 5 (ITGA5) in the proliferation, apoptosis, angiogenesis, inflammatory response, and oxidative stress in CMVECs were assessed.</p><p><strong>Results: </strong>TLN1 overexpression assisted CMVECs in resistance to ox-LDL stimulation, with alleviated cell proliferation and angiogenesis, reduced apoptosis, inflammatory response, and oxidative stress. TLN1 overexpression triggered increased ITGA5, and ITGA5 knockdown reversed the effects of TLN1 overexpression on the abovementioned aspects. Together, TLN1 synergized with ITGA5 to ameliorate the dysfunction in CMVECs.</p><p><strong>Conclusions: </strong>This finding suggests their probable involvement in CAD, and increasing their levels is beneficial to disease relief.</p>\",\"PeriodicalId\":12251,\"journal\":{\"name\":\"Folia morphologica\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Folia morphologica\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5603/FM.a2023.0031\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/5/5 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"ANATOMY & MORPHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Folia morphologica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5603/FM.a2023.0031","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/5/5 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
TLN1 synergizes with ITGA5 to ameliorate cardiac microvascular endothelial cell dysfunction.
Background: The complex process of atherosclerosis is thought to begin with endothelial cell dysfunction, and advanced atherosclerosis is the underlying cause of coronary artery disease (CAD). Uncovering the underlying mechanisms of CAD-related endothelial cell injury may contribute to the treatment.
Materials and methods: Cardiac microvascular endothelial cells (CMVECs) were treated with oxidised low-density lipoprotein (ox-LDL) to mimic an injury model. The involvement of Talin-1 (TLN1) and integrin alpha 5 (ITGA5) in the proliferation, apoptosis, angiogenesis, inflammatory response, and oxidative stress in CMVECs were assessed.
Results: TLN1 overexpression assisted CMVECs in resistance to ox-LDL stimulation, with alleviated cell proliferation and angiogenesis, reduced apoptosis, inflammatory response, and oxidative stress. TLN1 overexpression triggered increased ITGA5, and ITGA5 knockdown reversed the effects of TLN1 overexpression on the abovementioned aspects. Together, TLN1 synergized with ITGA5 to ameliorate the dysfunction in CMVECs.
Conclusions: This finding suggests their probable involvement in CAD, and increasing their levels is beneficial to disease relief.
期刊介绍:
"Folia Morphologica" is an official journal of the Polish Anatomical Society (a Constituent Member of European Federation for Experimental Morphology - EFEM). It contains original articles and reviews on morphology in the broadest sense (descriptive, experimental, and methodological). Papers dealing with practical application of morphological research to clinical problems may also be considered. Full-length papers as well as short research notes can be submitted. Descriptive papers dealing with non-mammals, cannot be accepted for publication with some exception.