絞り込み

16404

広告

目標上積みの「タラノア対話」合意 (毎日新聞)

[PR] 温室ガス削減 「パリ協定」控え18年の1年間かけ実施へ 【ボン五十嵐和大】ドイツのボンで開催中の国連気候変動枠組み条約第23回締約国会議(COP23)...

  1. ドイツの温暖化会議で決議採択 - 福井新...
  2. 国内初の種類 恐竜の卵の化石を展示 山口...
  3. 温暖化、COP23大筋合意 先進国の削減...
  4. 本人望めば蘇生中止 消防庁委託研究班提言...

ニュース一覧

PRMT1 mediates podocyte injury and glomerular fibrosis through phosphorylation of ERK pathway.

著者 Yu Z
Biochem Biophys Res Commun.2017 Nov 09 ; ():.
この記事をPubMed上で見るPubMedで表示
この記事をGoogle翻訳上で見る Google翻訳で開く

スターを付ける スターを付ける     (2view , 0users)

Full Text Sources

Miscellaneous

Diabetic nephropathy (DN) is characterized by a change of glomerular structure and dysfunction of filtration barrier, which significantly accompanied by podocytes apoptosis and glomerular fibrosis. Angiotensin Ⅱ(Ang Ⅱ) induced activation of ERK1/2 signaling plays important roles in causing apoptosis of podocytes in DN kidneys. Previous studies have shown that PRMT1 have a pro-inflammatory function through activating ERK1/2 signaling pathway during development of chronic pulmonary disease, However, its role in DN development has not been investigated. Here, we detected a higher expression of PRMT1 in podocytes of kidneys from DN patients compared with normal kidneys. High glucose administration induced elevation of PRMT1 expression in podocytes in vitro, accompanied with higher phosphorylation of ERK and cleaved caspase-3. AMI-1, a selective inhibitor for PRMT1, could block these effects caused by glucose treatment. In vivo administration of AMI-1 also attenuated apoptosis of podocytes during DN development of high-fatty diet-induced diabetic mice. Epithelial to mesenchymal transition during DN development, which characterized by extracellular matrix deposition in podocytes, was also restrained by AMI-1 treatment. Collectively, this study firstly demonstrated that PRMT1 exert podocyte-injury effects in mouse glomerulus through Ang Ⅱ/ERK pathway, which reveals a potential therapeutic target for DN.
PMID: 29129692 [PubMed - as supplied by publisher]
印刷用ページを開く Endnote用テキストダウンロード