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2015 ; 8
(9
): 15214-21
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Follistatin-like 3 suppresses cell proliferation and fibronectin expression via
p38MAPK pathway in rat mesangial cells cultured under high glucose
#MMPMID26629006
Wang X
; Shi L
; Han Z
; Liu B
Int J Clin Exp Med
2015[]; 8
(9
): 15214-21
PMID26629006
show ga
Mesangial cells (MCs) proliferation and extracellular matrix (ECM) accumulation
are early features of diabetic nephropathy. Follistatin-like 3 (FSTL3), a member
of follistatin family, has been shown to regulate insulin and glucagon
sensitivities in diet-induced obesity and insulin resistance. However, the role
of FSTL3 in diabetic nephropathy is still unclear. Therefore, in this study, we
investigated the effects of FSTL3 on cell proliferation and ECM accumulation
expression in rat MCs cultured under high glucose, and elucidated the underlying
mechanism. We found that the expression of FSTL3 was decreased significantly in
MCs cultured high glucose condition. Overexpression of FSTL3 inhibited high
glucose-induced MC proliferation and blocked the G1/S phase transition under high
glucose condition. And, FSTL3 overexpression also reduced the expression of
?-smooth muscle actin (?-SMA) and fibronectin (FN) induced by high glucose.
Furthermore, overexpression of FSTL3 suppressed high-glucose-induced p38
phosphorylation in MCs. Taken together, our present study demonstrated that FSTL3
suppressed high glucose-induced MC proliferation and ECM accumulation via
inhibiting the p38MAPK signaling pathway, and that FSTL3 may be a potential
therapeutic target for the treatment of diabetic nephropathy.