Long non-coding RNA Mirt2 prevents TNF-α-triggered inflammation via the repression of microRNA-101

Parkinson's disease is normally accompanied by excessive inflammation. Myocardial infraction associated transcript 2 (Mirt2) has an activity to relieve inflammation in numerous cell types. Here, we aimed to investigate whether Mirt2 could elevate the resistance of SH-Sy5y cells to inflammation. Tumor necrosis factor alpha (TNF-alpha) was used to induce inflammation in SH-Sy5y cells. Mirt2 overexpressed or silenced cells were established. MicroRNA-101 (miR-101) mimic was used to up-regulate miR-101. Viable and apoptotic cells as well as reactive oxidative species (ROS) were detected after staining. Proteins associated with apoptosis, interleukin (IL) and signaling regulators were evaluated by Western blot. IL secretion was assessed by ELISA. Mirt2 and miR-101 were determined by qRT-PCR. We discovered that TNF-alpha weakened viability of SH-Sy5y cells and resulted in sensitivity to apoptosis with cleavage of PARP and caspase-3. Expression and secretion of IL-6 as well as generation of ROS were facilitated by TNF-alpha. However, Mirt2 overexpression moderated TNF-alpha-caused apoptosis associated with inflammation and oxidative stress. Mirt2 suppressed TNF-alpha-induced accumulation of miR-101, and based on this Mirt2 exhibited anti-inflammatory roles. Additionally, TNF-alpha-triggered phosphorylation of regulators was blocked by Mirt2 while restored by miR-101 mimic. In short Mirt2 overexpression exhibited antiinflammatory properties through miR-101 suppression. Through down-regulating miR-101, Mirt2 blocked TNF-alpha-triggered NF-kappa B/p38MAPK pathway.