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

08:00 EDT 9th September 2019 | BioPortfolio

Summary of "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-α) 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-α 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-α. However, Mirt2 overexpression moderated TNF-α-caused apoptosis associated with inflammation and oxidative stress. Mirt2 suppressed TNF-α-induced accumulation of miR-101, and based on this Mirt2 exhibited anti-inflammatory roles. Additionally, TNF-α-triggered phosphorylation of regulators was blocked by Mirt2 while restored by miR-101 mimic. In short Mirt2 overexpression exhibited anti-inflammatory properties through miR-101 suppression. Through down-regulating miR-101, Mirt2 blocked TNF-α-triggered NF-κB/p38MAPK pathway.


Journal Details

This article was published in the following journal.

Name: International immunopharmacology
ISSN: 1878-1705
Pages: 105878


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Medical and Biotech [MESH] Definitions

An inflammation of the NASAL MUCOSA triggered by ALLERGENS.

The turning off of GENETIC TRANSCRIPTION in certain regions of CHROMATIN without changes in the DNA sequence. Typically epigenetic repression is a way that developmental changes are programmed at the cellular level.

Process by which micro-organisms adapt quickly to a preferred rapidly-metabolizable intermediate through the inhibition or repression of genes related to CATABOLISM of less preferred source(s).

Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.

Defense mechanisms involving approach and avoidance responses to threatening stimuli. The sensitizing process involves intellectualization in approaching or controlling the stimulus whereas repression involves unconscious denial in avoiding the stimulus.

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