Downregulating LncRNA XIST attenuated contrast-induced nephropathy injury via regulating miR-133a-3p/NLRP3 axis

AbstractLong non-coding RNA X-inactive specific transcript (LncRNA XIST) is involved in several diseases. However, the molecular mechanism of XIST and its relation with miR-133a-3p in contrast-induced nephropathy (CIN) remained vague. Sprague –Dawley (SD) rats were assigned to Control, Sham, and CIN groups at random (n = 15 for each group). Histological examination on the kidney tissues was performed using hematoxylin and eosin (HE) and periodic acid-Schiff (PAS) staining. Mean serum creatinine (SCr) and blood urea nitrogen (BUN) c ontents was measured by colorimetric microplate method. Levels of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). The cells viability and apoptosis were respectively detected by MTT assay and flow cytometry. Target gene and potential binding sites between XIST, miR -133a-3p and NLR Family Pyrin Domain Containing 3 (NLRP3) were predicted using online databases and confirmed by dual-luciferase reporter assay. Relative mRNA and protein expressions of XIST, miR-133a-3p, NLRP3, apoptosis-associated speck-like protein (ASC) and Cleaved caspase-1 were measured with q uantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. In the rat CIN model, Ioversol induced kidney morphology changes, with increase on SCr and BUN contents, elevated levels of inflammatory cytokines and upregulated expressions of XIST, NLRP3, ASC and Cleaved caspase -1. Silencing XIST reversed the effects of Ioversol o...
Source: Journal of Thrombosis and Thrombolysis - Category: Hematology Source Type: research