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2018 ; 2018
(ä): 1031367
Nephropedia Template TP
gab.com Text
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English Wikipedia
Metformin Improves Epithelial-to-Mesenchymal Transition Induced by TGF-?1 in
Renal Tubular Epithelial NRK-52E Cells via Inhibiting Egr-1
#MMPMID30050950
Guan M
; Li W
; Xu L
; Zeng Y
; Wang D
; Zheng Z
; Lyv F
; Xue Y
J Diabetes Res
2018[]; 2018
(ä): 1031367
PMID30050950
show ga
The early growth response- (Egr-) 1 has been found to play a key role in organ
fibrosis. Metformin has been shown to be effective in attenuating renal tubular
epithelial-to-mesenchymal transition (EMT), which is involved in renal fibrosis.
However, it is unknown whether metformin improves EMT via inhibiting Egr-1. In
this study, rat renal tubular epithelial (NRK-52 E) cells, treated by
transforming growth factor- (TGF-) ?1 of 10?ng/ml with or without metformin of
1?mmol/l, were transfected by siEgr-1 or M61-Egr-1 plasmids to knock down or
overexpress Egr-1, respectively. The gene and protein expressions of E-cadherin,
?-SMA, fibronectin (FN), and Egr-1 were determined by real-time quantitative PCR
and Western blotting, respectively. We observed that TGF-?1 significantly reduced
E-cadherin expression and upregulated the expressions of FN, ?-SMA, and Egr-1,
which can be reversed by metformin. M61-Egr-1 transfection could exacerbate EMT,
which can be reversed by metformin. Taken together, our data show that Egr-1
plays an important role in TGF-?1-induced EMT of renal tubular epithelial cells
and metformin improves EMT while inhibiting Egr-1, which provides a potential
novel target to combat renal fibrosis.
|*Epithelial-Mesenchymal Transition
[MESH]
|Animals
[MESH]
|Cell Line
[MESH]
|Early Growth Response Protein 1/genetics/*metabolism
[MESH]