TGF-β1-induced airway smooth muscle cell proliferation involves TRPM7-dependent calcium influx via TGFβR/SMAD3 (Revision)

Publication date: November 2018

Source: Molecular Immunology, Volume 103

Author(s): Ming Chen, Wei Zhang, Jianting Shi, Shanping Jiang

Abstract

Background

TRPM7 in mast cells plays a key role in asthma. However, the effect of TRPM7 on TGF-β1-induced airway smooth muscle cell (ASMC) proliferation remains unclear. Therefore, we designed this study to explore whether TRPM7 is involved in TGF-β1-induced ASMC proliferation.

Methods

An asthmatic mouse model was established, and the expressions of TGF-β1 and TRPM7 in mice lungs were detected using enzyme-linked immunosorbent assay (ELISA) and western blotting. In addition, murine ASMCs were cultured and stimulated with TGF-β1. Possible TGF-β1 and TRPM7 interactions were examined using RT-PCR and western blotting analyses with ASMCs. The effect of TRPM7 knockdown on ASMC calcium influx was assessed by the fluorescent indicator indo-1. MTT and flow cytometry were applied to evaluate the effects of TRPM7 knockdown on ASMC proliferation and apoptosis.

Results

TGF-β1 elevated the expression of TRPM7 via TGFβR/SMAD3. Knocking down TRPM7 decreased the intracellular Ca²⁺ concentration and cellular proliferation of ASMCs, although apoptosis remained unaffected.

Conclusions

Our initial findings suggest that TRPM7 inhibition may prevent asthma-induced airway remodeling.

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