βklotho is essential for the anti-endothelial mesenchymal transition effects of N-acetyl-seryl-aspartyl-lysyl-proline.

ABSTRACT: Endothelial-mesenchymal transition (EndMT) has emerged as an essential bioprocess responsible for the development of organ fibrosis. We have previously reported that fibroblast growth factor receptor 1 (FGFR1) is involved in the anti-EndMT effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). FGFR1 is expressed on the cell membrane and performs its biological function through interaction with co-receptors, including βklotho (KLB). However, it remains unknown whether KLB is involved in the anti-EndMT effects of AcSDKP. Here, we demonstrated that AcSDKP increased KLB expression in an FGFR1-dependent manner and that KLB deficiency induced AcSDKP-resistant EndMT via the induction of the mitogen-activated protein kinase (MAPK) pathway. In cultured endothelial cells, AcSDKP increased KLB pro

SUBMITTER: Gao R 

PROVIDER: S-EPMC6487725 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature