open access

Vol 83, No 1 (2024): Folia Morphologica
Original article
Submitted: 2023-02-10
Accepted: 2023-03-21
Published online: 2023-04-20
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TLN1 synergizes with ITGA5 to ameliorate cardiac microvascular endothelial cell dysfunction

Xianfeng Wang1, Wenkai Mao2, Xiaofeng Ma3
·
Pubmed: 37144848
·
Folia Morphol 2024;83(1):92-101.
Affiliations
  1. Emergency Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai, P.R. China
  2. Medical Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai, P.R. China
  3. Personnel Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai, P.R. China

open access

Vol 83, No 1 (2024): Folia Morphologica
ORIGINAL ARTICLES
Submitted: 2023-02-10
Accepted: 2023-03-21
Published online: 2023-04-20

Abstract

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.

Abstract

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.

Get Citation

Keywords

Talin-1, integrin, coronary artery disease, cardiac microvascular endothelial cells, atherosclerosis

About this article
Title

TLN1 synergizes with ITGA5 to ameliorate cardiac microvascular endothelial cell dysfunction

Journal

Folia Morphologica

Issue

Vol 83, No 1 (2024): Folia Morphologica

Article type

Original article

Pages

92-101

Published online

2023-04-20

Page views

645

Article views/downloads

440

DOI

10.5603/FM.a2023.0031

Pubmed

37144848

Bibliographic record

Folia Morphol 2024;83(1):92-101.

Keywords

Talin-1
integrin
coronary artery disease
cardiac microvascular endothelial cells
atherosclerosis

Authors

Xianfeng Wang
Wenkai Mao
Xiaofeng Ma

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