Persistent fibroblast activation in wound repair is believed to be the key 
reason for fibrosis and transforming growth factor (TGF)β is considered as one 
of the key mediators for the fibrogenic response, with the detailed mechanism 
largely unknown. Here we found that TGFβ1 treatment could induce a significant 
increase of endogenous TGFβ1 expression by enhancing the mRNA stability in 
cardiac fibroblasts. Further study revealed that TGFβ1 treatment translocated 
the nuclear HuR into cytoplasm, which in turn bound the ARE in the 3'UTR of 
TGFβ1 and increased the mRNA stability as seen from the RNA-IP and reporter 
assay. Knockdown of HuR decreased the endogenous expression of TGFβ1 under 
exogenous TGFβ1 treatment, simultaneously with the decrease of Col1a, Col3a and 
fibronectin expression. Our study here established a TGFβ1/HuR feedback circuit 
regulating the fibrogenic response in fibroblasts, and targeting this feedback 
loop is of great potential to control fibrosis.