MiR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction

Ryuji Morizane; Shizuka Fujii; Toshiaki Monkawa; Ken Hiratsuka; Shintaro Yamaguchi; Koichiro Homma; Hiroshi Itoh

doi:10.1038/srep04578

MiR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction

Ryuji Morizane, Shizuka Fujii, Toshiaki Monkawa, Ken Hiratsuka, Shintaro Yamaguchi, Koichiro Homma, Hiroshi Itoh

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Abstract

micro RNAs (miRNAs) are small non-coding RNAs that act as posttranscriptional repressors by binding to the 3′-UTR of target mRNAs. On the other hand, mesenchymal-epithelial transition (EMT) and kidney fibrosis is a pathological process of chronic kidney disease (CKD), and its relationship to miRNAs is becoming recognized as a potential target for CKD therapies. To find new miRNAs involved in EMT, we examined miRNA expression in experimental models of EMT and renal epithelialization using microarray, and found that miR-34c attenuates EMT induced by TGF-β in a mouse tubular cell line. To confirm the effects of miR-34c in vivo, we administered the precursor of miR-34c to mice with unilateral ureteral obstruction, and miR-34c decreased kidney fibrosis area and the expression of connective tissue growth factor, α-SMA, collagen type 1, collagen type 3 and fibronectin. In conclusion, our study showed miR-34c attenuates EMT and kidney fibrosis of mice with ureteral obstruction.

Original language	English
Article number	4578
Journal	Scientific reports
Volume	4
DOIs	https://doi.org/10.1038/srep04578
Publication status	Published - 2014 Apr 3

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title = "MiR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction",

abstract = "micro RNAs (miRNAs) are small non-coding RNAs that act as posttranscriptional repressors by binding to the 3′-UTR of target mRNAs. On the other hand, mesenchymal-epithelial transition (EMT) and kidney fibrosis is a pathological process of chronic kidney disease (CKD), and its relationship to miRNAs is becoming recognized as a potential target for CKD therapies. To find new miRNAs involved in EMT, we examined miRNA expression in experimental models of EMT and renal epithelialization using microarray, and found that miR-34c attenuates EMT induced by TGF-β in a mouse tubular cell line. To confirm the effects of miR-34c in vivo, we administered the precursor of miR-34c to mice with unilateral ureteral obstruction, and miR-34c decreased kidney fibrosis area and the expression of connective tissue growth factor, α-SMA, collagen type 1, collagen type 3 and fibronectin. In conclusion, our study showed miR-34c attenuates EMT and kidney fibrosis of mice with ureteral obstruction.",

author = "Ryuji Morizane and Shizuka Fujii and Toshiaki Monkawa and Ken Hiratsuka and Shintaro Yamaguchi and Koichiro Homma and Hiroshi Itoh",

note = "Funding Information: We thank Mari Fujiwara for technical assistance at the Core Instrumentation Facility, Keio University School of Medicine. This work was supported in part by Grant-in-Aid for Scientific Research (KAKENHI, 23890203, 21591038, 24591211) and grant from Daiwa Securities Health Foundation.",

year = "2014",

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day = "3",

doi = "10.1038/srep04578",

language = "English",

volume = "4",

journal = "Scientific Reports",

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T1 - MiR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction

AU - Morizane, Ryuji

AU - Fujii, Shizuka

AU - Monkawa, Toshiaki

AU - Hiratsuka, Ken

AU - Yamaguchi, Shintaro

AU - Homma, Koichiro

AU - Itoh, Hiroshi

N1 - Funding Information: We thank Mari Fujiwara for technical assistance at the Core Instrumentation Facility, Keio University School of Medicine. This work was supported in part by Grant-in-Aid for Scientific Research (KAKENHI, 23890203, 21591038, 24591211) and grant from Daiwa Securities Health Foundation.

PY - 2014/4/3

Y1 - 2014/4/3

N2 - micro RNAs (miRNAs) are small non-coding RNAs that act as posttranscriptional repressors by binding to the 3′-UTR of target mRNAs. On the other hand, mesenchymal-epithelial transition (EMT) and kidney fibrosis is a pathological process of chronic kidney disease (CKD), and its relationship to miRNAs is becoming recognized as a potential target for CKD therapies. To find new miRNAs involved in EMT, we examined miRNA expression in experimental models of EMT and renal epithelialization using microarray, and found that miR-34c attenuates EMT induced by TGF-β in a mouse tubular cell line. To confirm the effects of miR-34c in vivo, we administered the precursor of miR-34c to mice with unilateral ureteral obstruction, and miR-34c decreased kidney fibrosis area and the expression of connective tissue growth factor, α-SMA, collagen type 1, collagen type 3 and fibronectin. In conclusion, our study showed miR-34c attenuates EMT and kidney fibrosis of mice with ureteral obstruction.

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MiR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction

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