ArticlePhysiological research2021
MiR-18a Inhibits PI3K/AKT Signaling Pathway to Regulate PDGF BB-Induced Airway Smooth Muscle Cell Proliferation and Phenotypic Transformation.
Article in Physiological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- The Role of MicroRNAs Implicated in the Regulation of PI3K/AKT and Focal Adhesion Signaling Pathways in Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- Fibrinogen-like protein 2 regulates inflammatory and metabolic reprogramming of airway smooth muscle cells through PI3K/Akt activation.Frontiers in medicine · 2026Article
- miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway.Frontiers in genetics · 2026Article
- Midkine promotes PDGF-BB-induced proliferation, migration, and glycolysis of airway smooth muscle cells via the PI3K Akt pathway.Physiological reports · 2025Article
- Noncoding RNAs in asthmatic airway smooth muscle cells.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- CST1 promotes the proliferation and migration of PDGF-BB-treated airway smooth muscle cells via the PI3K/AKT signaling pathway.The Kaohsiung journal of medical sciences · 2023Article
- Ellagic acid attenuates muscle atrophy in STZ-induced diabetic mice.Physiological research · 2022Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increased proliferation and migration of airway smooth muscle cells (ASMCs) is a key process in the formation of airway remodeling in asthma. In this study, we focused on the expression of mircoRNA-18a (miR-18a) in airway remodeling in bronchial asthma and its related mechanisms. ASMCs are induced by platelet-derived growth factor BB (PDGF-BB) for in vitro airway remodeling. The expression of miR-18a in sputum of asthmatic patients and healthy volunteers was detected by qRT-PCR. The expression of miR-18a was over-expressed or interfered with in PDGF-BB-treated ASMCs. Cell proliferation, apoptosis and migration were detected by MTT, flow cytometry and Transwell, respectively; the expression of contractile phenotype marker proteins (SM-22?, ?-SM-actin, calponin) and key molecules of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K, p-PI3K, AKT and p-AKT) in ASMCs were detected by Western blot. The expression of miR-18a was down-regulated in the sputum and PDGF-BB-treated ASMCs of asthma patients. PDGF-BB could promote the proliferation and migration of ASMCs and inhibit their apoptosis; it could also promote the phenotypic transformation of ASMCs and activate the PI3K/AKT pathway. MiR-18a could inhibit the proliferation, migration ability and phenotypic transformation of ASMCs induced by PDGF-BB to a certain extent and alleviate the effect of PDGF-BB in supressing apoptosis, while miR-18a could inhibit the activation of the PI3K/AKT pathway. MiR-18a inhibits PDGF-BB-induced proliferation, migration and phenotypic conversion of ASMCs by inhibiting the PI3K/AKT pathway, thus attenuating airway remodeling in asthma.
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Registered trials
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