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2015 ; 8
(9
): 15262-8
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Overexpression of RACK1 inhibits collagen synthesis in keloid fibroblasts via
inhibition of transforming growth factor-?1/Smad signaling pathway
#MMPMID26629012
Zhou P
; Shi L
; Li Q
; Lu D
Int J Clin Exp Med
2015[]; 8
(9
): 15262-8
PMID26629012
show ga
Keloids are benign skin tumors characterized by collagen accumulation and
hyperproliferation of fibroblasts. The receptor for activated C-kinase 1 (RACK1)
was involved in liver fibrosis. However, the role of RACK1 in dermal fibrosis
keloids is still unclear. Therefore, in this study, we investigated the effects
of RACK1 on keloid fibroblasts (KFs) and transforming growth factor-?1
(TGF-?1)-induced collagen expression and explored the underlying mechanism. We
found that RACK1 was decreased in KFs, overexpression of RACK1 significantly
inhibited TGF-?1-induced KFs proliferation. RACK1 also obviously inhibited the
expression of TGF-?1-induced TGF-? receptor I, II, type I collagen and ?-smooth
muscle actin (?-SMA) in human KFs. In addition, RACK1 suppressed the expression
of TGF-?1-induced Smad2 and Smad3 phosphorylation in human KFs. Taken together,
our study suggested that RACK1 inhibits collagen synthesis in KFs via inhibition
the TGF-?1/Smad signaling pathway, and RACK1 is a potential target for treatment
of the keloid disease.