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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Biomed+Res+Int
2014 ; 2014
(ä): 376191
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Follistatin, an activin antagonist, ameliorates renal interstitial fibrosis in a
rat model of unilateral ureteral obstruction
#MMPMID24883308
Maeshima A
; Mishima K
; Yamashita S
; Nakasatomi M
; Miya M
; Sakurai N
; Sakairi T
; Ikeuchi H
; Hiromura K
; Hasegawa Y
; Kojima I
; Nojima Y
Biomed Res Int
2014[]; 2014
(ä): 376191
PMID24883308
show ga
Activin, a member of the TGF-? superfamily, regulates cell growth and
differentiation in various cell types. Activin A acts as a negative regulator of
renal development as well as tubular regeneration after renal injury. However, it
remains unknown whether activin A is involved in renal fibrosis. To clarify this
issue, we utilized a rat model of unilateral ureteral obstruction (UUO). The
expression of activin A was significantly increased in the UUO kidneys compared
to that in contralateral kidneys. Activin A was detected in glomerular mesangial
cells and interstitial fibroblasts in normal kidneys. In UUO kidneys, activin A
was abundantly expressed by interstitial ?-SMA-positive myofibroblasts.
Administration of recombinant follistatin, an activin antagonist, reduced the
fibrotic area in the UUO kidneys. The number of proliferating cells in the
interstitium, but not in the tubules, was significantly lower in the
follistatin-treated kidneys. Expression of ?-SMA, deposition of type I collagen
and fibronectin, and CD68-positive macrophage infiltration were significantly
suppressed in the follistatin-treated kidneys. These data suggest that activin A
produced by interstitial fibroblasts acts as a potent profibrotic factor during
renal fibrosis. Blockade of activin A action may be a novel approach for the
prevention of renal fibrosis progression.