Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is a protein involved in the regulation of RNA processing, cell metabolism, migration, proliferation, and apoptosis. However, the effect of hnRNPA2/B1 on injured endothelial cells (ECs) remains unclear. We investigated the effect of hnRNPA2/B1 on lipopolysaccharide- (LPS-) induced vascular endothelial injury in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. LPS was used to induce EC injury, and the roles of hnRNPA2/B1 in EC barrier dysfunction and inflammatory responses were measured by testing endothelial permeability and the expression of inflammatory factors after the suppression and overexpression of hnRNPA2/B1. To explore the underlying mechanism by which hnRNPA2/B1 regulates endothelial injury, we studied the VE-cadherin/β-catenin pathway and NF-κB activation in HUVECs. The results showed that hnRNPA2/B1 was elevated in LPS-stimulated HUVECs. Moreover, knockdown of hnRNPA2/B1 aggravated endothelial injury by increasing EC permeability and promoting the secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Overexpression of hnRNPA2/B1 can reduce the permeability and inflammatory response of HUVEC stimulated by LPS in vitro, while increasing the expression of VE-Cadherin and β-catenin. Furthermore, the suppression of hnRNPA2/B1 increased the LPS-induced NF-κB activation and reduced the VE-cadherin/β-catenin pathway. Taken together, these results suggest that hnRNPA2/B1 can regulate LPS-induced EC damage through regulating the NF-κB and VE-cadherin/β-catenin pathways.

中文翻译：

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hnRNPA2 / B1通过NF-κB途径和VE-钙粘蛋白/β-连环蛋白信号转导调节体外减轻LPS诱导的内皮损伤。

异构核糖核蛋白A2 / B1（hnRNPA2 / B1）是一种蛋白质，参与RNA加工，细胞代谢，迁移，增殖和凋亡的调控。但是，hnRNPA2 / B1对受损的内皮细胞（EC）的影响仍不清楚。我们调查了hnRNPA2 / B1对脂多糖-（LPS-）诱导的人脐静脉内皮细胞（HUVECs）的血管内皮损伤的作用及其潜在机制。LPS诱导EC损伤，并通过检测hnRNPA2 / B1抑制和过表达后检测内皮通透性和炎症因子的表达来测定hnRNPA2 / B1在EC屏障功能障碍和炎症反应中的作用。为了探讨hnRNPA2 / B1调节内皮损伤的潜在机制，我们研究了VE-钙粘蛋白/ β联蛋白途径和NF- κ的活化在HUVEC中。结果表明，在LPS刺激的HUVEC中hnRNPA2 / B1升高。此外，敲低hnRNPA2 / B1可以通过增加EC渗透性和促进炎性细胞因子TNF - α，IL- 1β和IL-6的分泌来加剧内皮损伤。hnRNPA2 / B1的过表达可降低LPS刺激的HUVEC的通透性和炎症反应，同时增加VE-钙黏着蛋白和β -catenin的表达。此外，hnRNPA2 / B1的抑制增加了LPS诱导的NF- κ的活化并降低了VE-钙粘蛋白/ β-连环蛋白途径。两者合计，这些结果表明，hnRNPA2 / B1可调节LPS诱导的EC损伤通过调节NF- κ B和VE-钙粘着蛋白/ β连环蛋白通路。