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.
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.
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.
摘要：
动脉粥样硬化的复杂过程被认为始于内皮细胞功能障碍,晚期动脉粥样硬化是冠状动脉疾病（CAD）的根本原因。揭示CAD相关内皮细胞损伤的潜在机制可能有助于治疗。用氧化低密度脂蛋白（ox-LDL）处理心脏微血管内皮细胞（CMVEC）以模拟损伤模型。Talin-1(TLN1)和整合素α5(ITGA5)参与增殖,凋亡，血管生成,炎症反应，并对CMVECs中的氧化应激进行了评估。TLN1过表达辅助CMVECs抵抗ox-LDL刺激，减少细胞增殖和血管生成，减少细胞凋亡，炎症反应，和氧化应激。TLN1过表达引发增加的ITGA5,并且ITGA5敲低逆转了TLN1过表达对上述方面的影响。一起,TLN1与ITGA5协同改善CMVECs功能障碍。这一发现表明他们可能参与CAD，提高他们的水平有利于疾病的缓解。
