In vitro evaluation of Verteporfin and exploration of TEAD palmitoylation inhibition in Piezo1-YAP/TAZ signaling and ECM remodeling.

ABSTRACT: Fibrosis is characterized by excessive extracellular matrix (ECM) deposition driven by mechanical stress, yet the underlying molecular mechanisms remain incompletely understood. To investigate whether mechanical stress-induced ECM remodeling is mediated by YAP/TAZ-TEAD signaling and whether pharmacological modulation can mimic or reverse these effects. Nucleus pulposus (NP) cells were exposed to mechanical stress and treated with the MST1/2 inhibitor XMU-MP-1 or the YAP/TAZ-TEAD inhibitor Verteporfin (VP). Nuclear localization of YAP/TAZ-TEAD, expression of canonical TEAD target genes (CTGF, CYR61, ANKRD1), and ECM markers (Col1, Col2, α-SMA, FN, CTGF) were analyzed by Western blot, qPCR, and immunofluorescence. Mechanical stress induced nuclear accumulation of YAP/TAZ-TEAD, upregulated TE

SUBMITTER: Xiaojun Z 

PROVIDER: S-EPMC12715214 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature