Mechanistically, S100A12 inhibited miR-30a expression, which was controlled by HDAC, and miR-30a downregulated NLRP3 expression by directly targeting its 3'-UTR.<b>Conclusions</b>: S100A12 plays an important role in the pathogenesis of DR by activating retinal microglia via a miR-30a-dependent mechanism.
In conclusion, increased activation of macroglia (GFAP), microglia (Iba-1 and OX-42) and perivascular macrophages (F4/80 and CD14) together with pro-inflammatory (IL-1β and IL-6) and pro-angiogenic markers (PECAM-1, ICAM-1, VEGF, Flt-1, and Flk-1), suggested a critical role for NLRP3 inflammasome in the Akimba mouse model depicting advanced stages of DR pathogenesis.
Furthermore, the elevated expressions of NLRP3 and ASC were observed in the fibrovascular membranes from 21 adults with proliferative DR when compared with the 22 controls.
Resolvin D1 inhibits inflammatory response in STZ-induced diabetic retinopathy rats: Possible involvement of NLRP3 inflammasome and NF-κB signaling pathway.