Long non-coding RNA NKILA weakens TNF-α-induced inflammation of MRC-5 cells by miR-21 up-regulation

Abstract

Background: Infantile pneumonia (IP) seriously affects the health of children. This article mainly discussed the protective effect of long non-coding RNA NKILA (lnc NKILA) on IP by detecting cell viability, apoptosis and inflammatory response of MRC5 cells. Methods: Cell counting kit-8 (CCK-8) was used to detect cell viability, while flow cytometry was used to detect cell apoptosis. The expression of apoptosis-associated factors (Bcl-2, Bax, PARP and Cleaved-PARP) and NF-jB and JNK pathway-related factors (t-IjBa, p-IjBa, t-p65, p-p65, b-actin, t-JNK and p-JNK) were tested by western blot. Otherwise, productions of inflammatory factors interleukin (IL)-1b and IL-6 were tested by enzyme-linked immunosorbent assay (ELISA) and western blot. Furthermore, RNA levels were respectively tested and changed by RT-qPCR and cell transfection. Results: Tumour necrosis factor-a (TNF-a) treatment reduced cell viability, induced cell apoptosis and promoted inflammatory factors expression. NKILA overexpression remitted TNF-a-induced injury. Moreover, NKILA positively regulated miR-21. miR-21 inhibition could weaken the functions of NKILA overexpression on TNF-a-induced injury. At last, NKILA and miR-21 were involved in the regulation of JNK and NF-jB pathways. Conclusions: NKILA overexpression remitted TNF-a-induced MRC5 cell injury by up-regulation of miR-21 and via inactivation of JNK and NF-jB signaling pathways. ARTICLE HISTORY

Tamsulosin attenuates high glucose- induced injury in glomerular endothelial cells

“…High glucose induces an inflammatory cascade and enhances the expressions of adhesion molecules in GECs. TNF-α is an important pro-inflammatory cytokine involved in various inflammatory responses [23][24][25]. Previous studies have reported that the TNF-α level in patients with DN is higher than in healthy people [26].…”

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

“…Additionally, lnc‐ANRIL/miR‐125a axis shows more efficient in the prediction of the sepsis risk, correlation with the organ damage and a series of inflammatory factors of sepsis 32 . Overexpression of lnc NKILA leads to the upregulation of miR‐21, inhibition of JNK/NF‐κB pathway, and reduces immune response and lung fibroblast apoptosis and cell viability in pediatric pneumonia 33 . lncRNA and miRNA are active regulator of both pro‐inflammatory and anti‐inflammatory responses, participating in the maintaince of a balance between pathogen clearance and normal morphology in the pulmonary system.…”

Senescent response in inner annulus fibrosus cells in response to TNFα, H2O2, and TNFα-induced nucleus pulposus senescent secretome

“…Specifically, two studies have indicated that AF and NP cells may decrease their expression of GPX and GSH when exposed to ROS stress or in menopause mediated IVD degeneration (59,60). Alternatively, other studies have identified noncoding RNAs such as NKILA/miR-21 (61,62), and cellular proteins such as Sirt6 (63), or prolonged NF-κB activation can increase resistance to the cytotoxic effects of TNFα (64). This suggests that other mechanisms of TNFα signaling regulation may play a role in the iAF cells resistance to TNFα mediated senescence.…”