The mechanism of RACK1 regulating LPS-induced functional damage of rat pulmonary microvascular endothelial cells
10.19405/j.cnki.issn1000-1492.2025.09.018
- VernacularTitle:RACK1 调控 LPS 致大鼠肺微血管内皮细胞损伤的机制研究
- Author:
Qiqi Li
1
;
Xianghui Wu
1
;
Qinghai You
1
Author Information
1. Dept of Respiratory and Critical Care Medicine，The First Affiliated Hospital of Anhui Medical University，Hefei 230022
- Publication Type:Journal Article
- Keywords:
receptor of activated protein kinase C 1;
sonic hedgehog signaling pathway;
pulmonary microvascular endothelial cells;
permeability;
caveolin-1
- From:
Acta Universitatis Medicinalis Anhui
2025;60(9):1704-1711
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of receptor of activated protein kinase C 1 ( RACK1) on lipopo- lysaccharide ( LPS) -induced barrier function in rat pulmonary microvascular endothelial cells ( RPMVEC) and its interplay with the Sonic hedgehog ( SHH) signaling pathway．
Methods:RPMVEC were cultured in vitro and ran- domly divided into si-NC，si-NC + LPS，si-RACK1，si-RACK1 + LPS，si-RACK1 + LPS + Vismodegib and Vis- modegib + SAG groups．The RACK1 of RPMVEC was silenced by small interfering RNA ( siRNA) technology and the cells were treated with LPS ( 10 mg / L) ，SHH signaling pathway inhibitor ( Vismodegib) ( 20 μmol / L) and SHH signaling pathway agonist ( SAG) ( 1 μmol / L) ．Following the intervention，the expressions of RACK1 and caveolin-1 in RPMVEC were detected by immunofluorescence ，while the transendothelial electrical resistance ( TEER) was evaluated using the method of Transwell，and the expression levels of RACK1，glioma-associated on- cogene homolog 1 ( Gli-1) and caveolin-1 were detected by Western blot．
Results:Silencing RACK1 increased the TEER value of RPMVEC induced by LPS ( P＜0. 05) ．The expression of caveolin-1 decreased ( P＜0. 05) ，and the expression of Gli-1 increased ( P ＜0. 05) ．Inhibiting the SHH signaling pathway could reverse the increased TEER value of LPS-induced RPMVEC caused by silencing RACK1 ( P ＜0. 05) ，and the expressions of RACK1 and caveolin-1 increased ( P＜0. 05) ．Activation of the SHH signaling pathway increased the TEER value of LPS- induced RPMVEC caused by silencing RACK1 ( P ＜0. 05) ，and the expressions of RACK1 and caveolin-1 de- creased ( P＜0. 05) ．
Conclusion :RACK1 plays a role in LPS-induced hyperpermeability of RPMVEC，and its effect may be achieved by modulating the SHH signaling pathway and caveolin-1．
- Full text:2026032813342000476RACK1调控LPS致大鼠肺微血管内皮细胞损伤的机制研究_李琪琪.pdf
