IndraLab
Statements
UCHL1 inhibits cell population proliferation. 37 / 40
|
34
3
reach
"In the present study, there are several novel findings regarding UCH-L1 as a negative regulator of maladaptive cardiac remodeling and dysfunction as follows : (i) UCH-L1 expression is enhanced in cardiac myocytes and fibroblasts during the earlier stage of cardiac adaptive hypertrophy and declined in the process of maladaptive responses to the sustained hemodynamic stress; (ii) UCH-L1 inhibits cardiac fibroblast proliferation via suppressing PDGF and PDGFRbeta signaling; (iii) UCH-L1 preferentially enhances PDGF-BB-induced suppression autophagic clearance of p21 WAF1 and Cip1 proteins in cardiac fibroblasts."
reach
"Of interest, overexpression of UCH-L1 enhanced the PDGF-BB-induced posttranscriptional upregulation of p21 WAF1 and Cip1 protein in cardiac fibroblasts (XREF_FIG), suggesting that UCH-L1 inhibits cardiac fibroblast proliferation via posttranscriptional enhancing the expression of p21 WAF1 and Cip1 to suppress the transition of G1 to S phase."
reach
"These results suggest that UCH-L1 facilitates autophagic degradation of p21 WAF1 and Cip1 to suppress proliferation of cardiac fibroblasts in chronically pressure overloaded heart, potentially acting as a novel feedback mechanism in the regulation of maladaptive cardiac remodeling and dysfunction."
reach
"To determine the molecular mechanism by which UCH-L1 suppresses cardiac fibroblast proliferation, we examined the effect of adenoviral overexpression of UCH-L1 on PDGF-BB-induced activation of MAPKs including extracellular signal regulated kinase (ERK), c-Jun N-terminal kinases (JNK) and p38, phosphoinositide 3-kinase (PI3K), and signal transducers and activators of transcription 3 (STAT3), that are linked to cardiac fibroblast growth XREF_BIBR."