| First Author | Chen H | Year | 2014 |
| Journal | J Physiol | Volume | 592 |
| Issue | 3 | Pages | 505-21 |
| PubMed ID | 24247978 | Mgi Jnum | J:217958 |
| Mgi Id | MGI:5616281 | Doi | 10.1113/jphysiol.2013.266411 |
| Citation | Chen H, et al. (2014) Apelin inhibits the development of diabetic nephropathy by regulating histone acetylation in Akita mouse. J Physiol 592(Pt 3):505-21 |
| abstractText | 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-kappaB, 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. |
