LncRNA TUG1 mitigates renal interstitial fibrosis through miR-542-3p / HIF-1α/VEGF axis

Chronic kidney disease (CKD) has been discovered to be closely associated with both long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), while the precise molecular processes behind this relationship are still unclear. This study evaluated the impact of miR-542-3p and lncRNA-TUG1 on renal fibrosis, along with the regulatory mechanisms that underlie them. Through tube formation assays, in vitro research showed that TUG1 knockdown might both improve angiogenesis and heal damaged endothelial cell-cell connections. We used Western blot and q-PCR methods in the UUO model to identify tissue hypoxia and fibrotic lesions. Additionally, we employed a cutting-edge method known as fluorescence microangiography (FMA) to find damage to the peritubular capillaries (PTCs), and MATLAB software was utilized to evaluate the data. Furthermore, by looking at the coexpression of CD31 and a-SMA, we were able to identify cells in the obstructed kidney that were transitioning from endothelium tomyofibroblasts.Moreover, the reduction of tissue hypoxia brought on by lncRNA TUG1 knockdown was dramatically reversed by inhibition of miR-542-3p, which also decreased the expression levels of fibrotic indicators. To sum up, our findings offer fresh perspectives on how TUG1 and the miR-542-3p / HIF-1α / VEGF axis are regulated as renal fibrosis advances.