A major role of TWEAK/Fn14 axis as a therapeutic target for post-angioplasty restenosis.

ABSTRACT:

Background

Tumor necrosis factor-like weak inducer of apoptosis (Tnfsf12; TWEAK) and its receptor Fibroblast growth factor-inducible 14 (Tnfrsf12a; Fn14) participate in the inflammatory response associated with vascular remodeling. However, the functional effect of TWEAK on vascular smooth muscle cells (VSMCs) is not completely elucidated.

Methods

Next generation sequencing-based methods were performed to identify genes and pathways regulated by TWEAK in VSMCs. Flow-citometry, wound-healing scratch experiments and transwell migration assays were used to analyze VSMCs proliferation and migration. Mouse wire injury model was done to evaluate the role of TWEAK/Fn14 during neointimal hyperplasia.

Findings

TWEAK up-regulated 1611 and down-regulated 1091 genes in VSMCs. Usi

SUBMITTER: Mendez-Barbero N 

PROVIDER: S-EPMC6712059 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature