Promotion of Inflammation, Apoptosis, and Inhibition of Autophagy by Overexpression of lncRNA SNHG12 in Acute Kidney Injury

There is a dispute regarding the roles of newly discovered lncRNAs in acute kidney injury (AKI). Therefore, this study discussed long non-coding RNA (lncRNA) small nuclear host gene 12 (SNHG12) in AKI and its molecular mechanism.

Lipopolysaccharide (LPS) induction was treated into renal tubular epithelial cells (HK-2 cells) to induce septic AKI in vitro. In the cell model, SNHG12, miR-1270, and tubulin beta class I (TUBB) expression patterns, along with p-p65, cleaved caspase-3, Beclin-1, p62, and autophagy related 7 (ATG7) protein expressions, were determined by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot. Cell viability was evaluated by cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) cytotoxicity assay, while apoptosis and inflammation were assessed by flow cytometry and enzymelinked immunosorbent assay (ELISA), respectively. At last, the mechanistic interaction between SNHG12, miR-1270, and TUBB was identified.

SNHG12 was highly expressed in LPS-induced HK-2 cells. Functionally, knocking down SNHG12 increased cell viability and autophagy, while inhibited LDH release, inflammation, and apoptosis. Mechanically, SNHG12 absorbed miR-1270 to upregulate TUBB expression, thereby aggravating inflammation, apoptosis, and inhibiting autophagy in AKI.

SNHG12 promotes inflammation, apoptosis, and autophagy by targeting the miR-1270/TUBB axis in AKI.