Background Renin-angiotensin-aldosterone system activation is the critical factor in renal remodeling and dysfunction. Our previous study suggested that miR-29b might attenuate angiotensin II-induced renal intestinal fibrosis in vitro. In the present study, we aim to determine that recombinant adeno-associated virus mediated miR-29b delivery can protect AngII-induced renal fibrosis and dysfunction.
Method Mice were treated with AngII via osmotic mini-pumps or PBS. Recombinant adeno-associated virus serotype 9 vectors were produced with the rBac-based system in SF9 cells. rAAV9-miR-29b or rAAV9-control-miR were injected into the kidney of a mouse model of AngII infusion. Role of miR-29b in renal fibrosis were assessed by Q-PCR, Western blot and histological examination.
Results In AngII-induced fibrotic kidney, miR-29b expression was down-regulated. rAAV9-miR-29b delivery significantly reversed renal dysfunction as indicated by decreased blood serum creatinine in AngII-infused mice. As far to organ remodeling, tubulointerstitial fibrosis and deposition of extracellular matrix deposition such as Collagen type I and type III were significantly decreased in kidney tissue of rAAV9-miR-29b delivered mouse.
Conclusion Our results show the great potential of rAAV9 as an applicable vector for miR-29b delivery for antifibrogenic factors in the treatment of renal dysfunction caused by tubulointerstitial fibrosis.