Open AccessKnockdown of FSTL1 inhibits PDGF-BB-induced human airway smooth muscle cell proliferation and migration
Author(s) -
Yuting Deng,
Yao Zhang,
Huajie Wu,
Zhaoling Shi,
Xin Sun
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6439
Subject(s) - platelet derived growth factor receptor , gene knockdown , cell growth , microbiology and biotechnology , downregulation and upregulation , protein kinase b , mapk/erk pathway , follistatin , cell cycle , cell migration , platelet derived growth factor , biology , growth factor , signal transduction , cell , cancer research , cell culture , receptor , biochemistry , genetics , gene
Abnormal proliferation and migration of airway smooth muscle (ASM) cells serve roles in airway remodeling, and contribute to airway hyper‑responsiveness. Follistatin‑like protein 1 (FSTL1) is a secreted glycoprotein that belongs to the follistatin family of proteins. It was reported that in the lungs of patients suffering from severe asthma, FSTL1 is highly expressed by macrophages. However, the role of FSTL1 in ASM cell proliferation and migration remains unknown. The present study aimed to investigate the role of FSTL1 in cell proliferation and migration mediated by platelet‑derived growth factor subunit B (PDGF‑BB) in human ASM cells. The results of the present study demonstrated that PDGF‑BB stimulation upregulated FSTL1 expression levels in ASM cells in vitro. Knockdown of FSTL1 inhibited cell proliferation and arrested the cell cycle in the G2/M phase in PDGF‑BB‑stimulated ASM cells. Additionally, knockdown of FSTL1 inhibited PDGF‑BB‑induced ASM cell migration. Furthermore, FSTL1 knockdown caused the downregulation of phosphorylated (p)‑extracellular signal‑regulated kinase (ERK) and p‑protein kinase B (AKT) expression levels induced by PDGF‑BB in ASM cells. In conclusion, the present study demonstrated that knockdown of FSTL1 inhibited ASM cell proliferation and migration induced by PDGF‑BB, at least partially via inhibiting the activation of ERK and AKT. FSTL1 may therefore represent a novel therapeutic target for airway remodeling in childhood asthma.