Apelin inhibits the development of diabetic nephropathy by regulating histone acetylation in Akita mouse

Hong Chen, Jianshuang Li, Lihua Jiao, Robert B. Petersen, Jiong Li, Anlin Peng, Ling Zheng, Kun Huang

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

Diabetic nephropathy is the primary cause of end-stage renal disease. Increasing numbers of patients are suffering from this disease and therefore novel medications and therapeutic approaches are urgently needed. Here, we investigated whether apelin-13, the most active member of the adipokine apelin group, could effectively suppress the development of nephropathy in Akita mouse, a spontaneous type 1 diabetic model. Apelin-13 treatment decreased diabetes-induced glomerular filtration rate, proteinuria, glomerular hypertrophy, mesangial expansion and renal inflammation. The inflammatory factors, activation of NF-κB, histone acetylation and the enzymes involved in histone acetylation were further examined in diabetic kidneys and high glucose- or sodium butyrate-treated mesangial cells in the presence or absence of apelin-13. Apelin-13 treatment inhibited diabetes-, high glucose- and NaB-induced elevation of inflammatory factors, and histone hyperacetylation by upregulation of histone deacetylase 1. Furthermore, overexpression of apelin in mesangial cells induced histone deacetylation under high glucose condition. Thus, apelin-13 may be a novel therapeutic candidate for treatment of diabetic nephropathy via regulation of histone acetylation.

Original languageEnglish
Pages (from-to)505-521
Number of pages17
JournalJournal of Physiology
Volume592
Issue number3
DOIs
StatePublished - Feb 2014

Fingerprint

Dive into the research topics of 'Apelin inhibits the development of diabetic nephropathy by regulating histone acetylation in Akita mouse'. Together they form a unique fingerprint.

Cite this