CHRDL2 activates the PI3K/AKT pathway to ameliorate glucocorticoid-induced damages to bone microvascular endothelial cells (BMECs).

ABSTRACT: Steroid-induced avascular necrosis of the femoral head (ANFH) is characterized by the death of bone tissues, leading to the impairment of normal reparative processes within micro-fractures in the femoral head. Glucocorticoid (GCs)-induced bone microvascular endothelial cell (BMEC) damage has been reported to contribute to ANFH development. In this study, differentially expressed genes (DEGs) between necrosis of the femoral head (NFH) and normal samples were analyzed based on two sets of online expression profiles, GSE74089 and GSE26316. Chordin-like 2 (CHRDL2) was found to be dramatically downregulated in NFH samples. In GCs-stimulated BMECs, cellular damages were observed alongside CHRDL2 down-regulation. GCs-caused cell viability suppression, cell apoptosis promotion, tubule formation su

SUBMITTER: Huang X 

PROVIDER: S-EPMC11268171 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature