期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1852, 期 7, 页码 1278-1287出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbadis.2015.02.013
关键词
Apelin; Renal I/R injury; Histone methylation; TGF-beta 1
资金
- National Basic Research Program of China [2012CB524901]
- Natural Science Foundation of China [81202557, 31271370, 81172971, 81222043, 31471208]
- Central University Basic Research Funds
- Municipal Key Technology Program of Wuhan (Wuhan Bureau of Science Technology) [201260523174]
- Health Bureau of Wuhan [WX12B06]
- Natural Science Foundation of Hubei Province [2013CFB359, 2014CF021]
Renal ischemia/reperfusion (I/R) injury is the most common cause of acute kidney injury, having a high rate of mortality and no effective therapy currently available. Apelin-13, a bioactive peptide, has been shown to inhibit the early lesions of diabetic nephropathy in several mouse models by us and others. To test whether apelin-13 protects against renal I/R induced injury, male rats were exposed to renal I/R injury with or without apelin-13 treatment for 3 days. Apelin-13 treatment markedly reduced the injury-induced tubular lesions, renal cell apoptosis, and normalized the injury induced renal dysfunction. Apelin-13 treatment inhibited the injury-induced elevation of inflammatory factors and Tgf-beta 1, as well as apoptosis. Apelin-13 treatment also inhibited the injury-induced elevation of histone methylation and Kmt2d, a histone methyltransferase of H3K4me2, following renal I/R injury. Furthermore, in cultured renal mesangial and tubular cells, apelin-13 suppressed the injury-induced elevation of Tgf-beta 1, apoptosis, H3K4me2 and Kmt2d under the in vitro hypoxia/reperfusion (H/R) conditions. Consistently, over-expression of apelin significantly inhibited H/R-induced elevation of TGF-beta 1, apoptosis, H3K4me2 and Kmt2d. The present study therefore suggests apelin-13 may be a therapeutic candidate for treating acute kidney injury. (C) 2015 Elsevier B.V. All rights reserved.
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