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2016 ; 11
(9
): e0162186
Nephropedia Template TP
Cho JH
; Ryu HM
; Oh EJ
; Yook JM
; Ahn JS
; Jung HY
; Choi JY
; Park SH
; Kim YL
; Kwak IS
; Kim CD
PLoS One
2016[]; 11
(9
): e0162186
PMID27607429
show ga
Alpha1-antitrypsin (AAT) exerts its anti-inflammatory effect through regulating
the activity of serine proteinases. This study evaluated the inhibitory effects
of AAT against the transforming growth factor (TGF)-?1 induced
epithelial-to-mesenchymal transition (EMT) in unilateral ureter obstruction (UUO)
mice and Madin-Darby canine kidney (MDCK) cells. C57BL/6 mice with induced UUO
were injected intraperitoneally with AAT (80 mg/Kg) or vehicle for 7 days. MDCK
cells were treated with TGF-?1 (2 ng/mL) for 48 hours to induce EMT, and
co-treated with AAT (10 mg/mL) to inhibit the EMT. Masson's trichrome and Sirius
red staining was used to estimate the extent of renal fibrosis in UUO mice. The
expression of alpha-smooth muscle actin (?-SMA), vimentin, fibronectin, collagen
I, and E-cadherin in MDCK cells and kidney tissue were evaluated. Masson's and
Sirius red staining revealed that the area of renal fibrosis was significantly
smaller in AAT treated UUO group compared with that of UUO and vehicle treated
UUO groups. AAT treatment attenuated upregulation of Smad2/3 phosphorylation in
UUO mouse model. Co-treatment of MDCK cells with TGF-?1 and AAT significantly
attenuated the changes in the expression of ?-SMA, vimentin, fibronectin,
collagen I, and E-cadherin. AAT also decreased the phosphorylated Smad3
expression and the phosphorylated Smad3/Smad3 ratio in MDCK cells. AAT treatment
inhibited EMT induced by TGF-?1 in MDCK cells and attenuated renal fibrosis in
the UUO mouse model. The results of this work suggest that AAT could inhibit the
process of EMT through the suppression of TGF-?/Smad3 signaling.
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