Pro-inflammatory and pro-fibrotic role of long non-coding RNA RMRP in pediatric asthma through targeting microRNA-206/CCL2 axis

Abstract

Asthma is an inflammatory pulmonary illness that plagues infants and young children. We carried out this investigation to examine the role of long noncoding RNA (lncRNA) RNA component of mitochondrial RNA processing endoribonuclease (RMRP) in an asthmatic mouse model induced by ovalbumin (OVA) and human airway smooth muscle cells (ASMCs). Eight-week-old mice were sensitized with OVA to simulate pediatric asthma. The expression patterns of RMRP, microRNA-206 (miR-206) and C-C motif ligand 2 (CCL2) in pulmonary tissues were evaluated by qPCR. In addition, the concentrations of interleukin (IL)-4, IL-5 and IL-13 cytokines in bronchoalveolar lavage fluid were detected by ELISA. The expression of RMRP and CCL2 was elevated, while miR-206 was reduced in OVA-induced mice. Our findings indicated that administration of RMRP overexpression in ASMCs increased the levels of biomarkers in asthma. RMRP functioned as a sponge for miR-206 to upregulate CCL2 expression. Blockade of the TGF-β/Smad2 signaling pathway in ASMCs overexpressing RMRP suppressed the inflammatory cytokines and cell viability, while enhancing apoptosis. The RMRP/miR-206/CCL2 regulatory axis is implicated in the occurrence of pediatric asthma.