E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta.

ABSTRACT:

Objective

Increased deposition of extracellular matrix (ECM) within the kidney is driven by profibrotic mediators including transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF). We investigated whether some of their effects may be mediated through changes in expression of certain microRNAs (miRNAs).

Research design and methods

Proximal tubular cells, primary rat mesangial cells, and human podocytes were analyzed for changes in the expression of key genes, ECM proteins, and miRNA after exposure to TGF-beta (1-10 ng/microl). Tubular cells were also infected with CTGF-adenovirus. Kidneys from diabetic apoE mice were also analyzed for changes in gene expression and miRNA levels.

Results

TGF-beta treatment was associated with morphologic an

SUBMITTER: Wang B 

PROVIDER: S-EPMC2889781 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature