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Integrin ανβ3 modulates lipopolysaccharide-induced hyperpermeability in cardiac microvascular endothelial cells.
Bioscience, Biotechnology, and Biochemistry ( IF 1.6 ) Pub Date : 2020-04-30 , DOI: 10.1080/09168451.2020.1759399
Li Li 1 , Zhou Rongfang 1 , Zhen Junhai 1 , Chen Changqin 1 , Yan Jing 1
Affiliation  

Previous studies suggest an association of cardiac microvascular endothelial cells (CMECs) hyperpermeability with sepsis-related cardiac injury. Our results showed that CMECs permeability was dependent upon concentration and time of lipopolysaccharides (LPS) stimulation. Integrin ανβ3 expression decreased after LPS stimulation. Pretreatment with anti-integrin ανβ3 antibody enhanced LPS-induced hyperpermeability. Upregulation of integrin ανβ3 decreased LPS-induced hyperpermeability. F-actin remodeling was enhanced after LPS stimulation and was inhibited by up-regulation of integrin ανβ3. Inhibition of Src or Rac1 reduced CMECs permeability after LPS stimulation, but there were no differences in the phosphorylation of Src and Rac1 when over-expressing or blocking integrin β3. After pretreatment with Src or Rac1 inhibitor, no significant difference was found in the expression of integrin ανβ3 in LPS-induced CMECs. These finding suggested that integrin ανβ3 overexpression decreased LPS-stimulated CMECS permeability by inhibition of cytoskeletal remodeling, but the mechanism might not be mediated via Src/Rac1 signaling.



中文翻译:

整联蛋白ανβ3调节脂多糖诱导的心脏微血管内皮细胞的通透性。

先前的研究表明,心脏微血管内皮细胞(CMEC)的高通透性与败血症相关的心脏损伤相关。我们的结果表明,CMECs的渗透性取决于脂多糖(LPS)刺激的浓度和时间。LPS刺激后整合素ανβ3表达降低。用抗整合素ανβ3抗体预处理可增强LPS诱导的通透性。整联蛋白ανβ3的上调降低了LPS诱导的通透性。LPS刺激后,F-肌动蛋白重塑得到增强,并被整联蛋白ανβ3的上调抑制。Src或Rac1的抑制作用降低了LPS刺激后CMEC的通透性,但是当过表达或阻断整联蛋白β3时,Src和Rac1的磷酸化没有差异。用Src或Rac1抑制剂预处理后,LPS诱导的CMECs中整合素ανβ3的表达没有明显差异。这些发现表明整联蛋白ανβ3的过表达通过抑制细胞骨架重塑而降低了LPS刺激的CMECS通透性,但该机制可能不是通过Src / Rac1信号传导介导的。

更新日期:2020-04-30
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