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Esculetin regulates the phenotype switching of airway smooth muscle cells
Author(s) -
Xie Chundan,
Li Yanyang,
Gao Jie,
Wang Yingying
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6483
Subject(s) - platelet derived growth factor receptor , phenotype , pi3k/akt/mtor pathway , platelet derived growth factor , calponin , fibronectin , extracellular matrix , protein kinase b , microbiology and biotechnology , phenotypic switching , signal transduction , chemistry , growth factor , cancer research , biology , biochemistry , receptor , actin , gene
Airway remodeling is one important feature of childhood asthma, which is one of the most common chronic childhood diseases. Phenotype switching of airway smooth muscle cells (ASMCs), defined as a reversible switching between contractile and proliferative phenotypes, plays an important role in the process of airway remodeling. Esculetin has shown antiinflammatory action in animal models of asthma; however, the effects of esculetin on ASMC phenotype switching have not been investigated. In the present study, platelet‐derived growth factor (PDGF) was used to induce the phenotype modulation of ASMCs. The results demonstrated that esculetin pretreatment mitigated the PDGF‐caused inhibitory effects on expressions of contractile phenotype protein markers, including calponin and SM22α. Esculetin also inhibited PDGF‐induced migration and proliferation of ASMCs. Besides, the PDGF‐induced expressions of extracellular matrix components, collagen I and fibronectin, were attenuated by esculetin pretreatment. Furthermore, PDGF‐caused activation of PI3K/Akt pathway in ASMCs was inhibited by esculetin. These findings suggest that esculetin might exert its inhibitory effect on PDGF‐induced ASMC phenotype switching through inhibition of PI3K/Akt pathway.