Renal miR-214-3p plays a functional and potentially genetic role in the development of hypertension, which might be mediated in part by targeting eNOS.

Oxidative stress and inflammation have been demonstrated to be involved in the onset and promotion of diabetic nephropathy (DN).Tanshinone IIA (Tan) possesses both antioxidant and anti-inflammatory properties. Here, the aim of the present study was to explore whether Tan could attenuate renal damage in the rats with streptozotocin (STZ)-induced diabetes and its potential mechanisms. Tan was gavaged to STZ-induced diabetic rats at the dose of 10mg/kg once a day for 12 weeks. Tan treatment significantly attenuated albuminuria and renal histopathology in diabetic rats. Besides, Tan treatment also effectively inhibited oxidative stress and inflammatory reaction in the kidneys of diabetic rats. Our study provided evidence that the protective effect of Tan on diabetes-induced renal injury is associated with inhibition of oxidative stress and inflammation. Tan may be a potential candidate for the treatment of DN.

MicroRNA miR-192-5p is one of the most abundant microRNAs in the kidney and targets the mRNA for ATP1B1 (β1 subunit of Na + /K +-ATPase). Na + /K +-ATPase drives renal tubular reabsorption. We hypothesized that miR-192-5p in the kidney would protect against the development of hypertension. We found miR-192-5p levels were significantly lower in kidney biopsy specimens from patients with hypertension (n=8) or hypertensive nephrosclerosis (n=32) compared to levels in controls (n=10). Similarly, Dahl salt-sensitive rats showed less miR-192-5p in the renal cortex compared with congenic SS.13 BN26 rats that had reduced salt sensitivity (n=9, p<0.05). Treatment with anti-miR-192-5p delivered through renal artery injection in uninephrectomized SS.13 BN26 rats exacerbated hypertension significantly. Mean arterial pressure on a 4% NaCl high-salt diet at day 14 post anti-miR-192-5p treatment was 16 mmHg higher than in rats treated with scrambled anti-miR (n=8 and 6, p<0.05). Similarly, Mir192 knockout mice on the high-salt diet treated with angiotensin II for 14 days exhibited a mean arterial pressure 22 mmHg higher than wild-type mice (n=9 and 5, p<0.05). Furthermore, protein levels of ATP1B1 were higher in Dahl rats than in SS.13 BN26 rats. Na + /K +-ATPase activity increased in the renal cortex of SS.13 BN26 rats nine days post-treatment with anti-miR-192-5p compared to that of control anti-miR treated rats. Intra-renal knockdown of ATP1B1 attenuated hypertension in SS. 13 BN26 rats with intra-renal knockdown of miR-192-5p. In conclusion, miR-192-5p in the kidney protects against the development of hypertension, which is mediated, at least in part, by targeting Atp1b1.