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Inhibitory effect of mabuterol on proliferation of rat ASMCs induced by PDGF-BB via regulating [Ca2+]i and mitochondrial fission/fusion.

Abstract：

:This study is aimed to investigate whether Mabuterol (Mab) inhibits proliferation of airway smooth muscle cells (ASMCs) induced by platelet-derived growth factor BB (PDGF-BB) and how far it is related to mitochondrial fission/fusion and intracellular calcium if it comes into play. To explore the mechanism of Mab's antagonizing the proliferation, Mdivi-1, DRP1 inhibitor, which has an inhibitory effect on mitochondrial fission, is used to compare with Mab. Cell viability was measured by either MTT or CCK-8. The inhibitory effect of Mab on S phase of ASM cell cycle induced by PDGF-BB was analyzed by flow cytometry (FCM). Fluo-3/AM, Ca2+ fluorescent probe, was used to detect Ca2+ fluorescence intensity by inverted microscope and flow cytometry. The gene expression of Drp-1 and Mfn-2 was observed with Real time PCR and the proteins of Drp-1, Mfn-2, PCNA and cyclin D1 were assessed by Western Blot. Mab and Mdivi-1 both suppressed the proliferation induced by PDGF-BB. The results from inverted microscope and flow cytometry showed that Mab inhibited [Ca2+]i in rat ASMCs induced by PDGF-BB. Cell cycle concept map illustrated that Mab significantly controlled the S phase of ASM cell cycle induced by PDGF-BB. As a consequence, Real time PCR and Western blot revealed the fact that Mab decreased the expression of Drp-1 mRNA and protein, and promoted the expression of Mfn-2 mRNA and protein. These findings suggested that Mab placed restrictions on the proliferation of rat ASMCs induced by PDGF-BB and the mechanism might be associated with the intracellular calcium inhibited and the mitochondrial fission/fusion regulated by Mab.

journal_name

Chem Biol Interact

journal_title

Chemico-biological interactions

authors

Gu Y,Yu X,Li X,Wang X,Gao X,Wang M,Wang S,Li X,Zhang Y

doi

10.1016/j.cbi.2019.04.023

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

63-72

eissn

0009-2797

issn

1872-7786

pii

S0009-2797(18)31680-6

journal_volume

307

pub_type

杂志文章

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