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Published on: June 8, 2022
The effects of transient receptor potential channel (TRPC) on airway smooth muscle cell isolated from asthma model
Xiaoyu Zhang1, Zhixin Zhao1, Lijun Ma1
1Department of Respiratory Medicine, People's Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Abstract:
This study aimed to validate whether transient receptor potential channel1 (TRPC1) and TRPC3 participate in the regulation the proliferation of airway smooth muscle cells (ASMCs) through modulating calcium ion (Ca2+ ) influx in vitro. Chronic model of murine asthma was induced and ASMCs isolated from asthmatic mice were used in this whole study. TRPC1 and TRPC3 were upregulated in asthmatic mouse ASMCs and selected for further investigation. Ca2+ concentration and the cell viability of asthmatic mouse ASMCs were significantly higher than that from non- asthma mice, however, TRPC channels blocker SKF96365 alleviated these effects. Furthermore, TRPC1 or TRPC3 overexpression markedly increased Ca2+ concentration and significantly induced the viability of ASMCs; whereas TRPC1 or TRPC3 knockdown exerted the completely conversed effects. Moreover, knockdown of TRPC1 and TRPC3 also exerted different effects on the protein expression of growth-related proteins p-p38, p-JNK, cleaved caspase-3 and Bcl-2, as well as on cell cycle. Finally, we found Ca2+ chelator EGTA or BAPTA-AM significantly diminished the effects of si-TRPC1 and si-TRPC3 on the cell viability, cell cycle, and the protein expression of p-p38, p-JNK, cleaved caspase-3, and Bcl-2 in asthmatic mouse ASMCs. Our findings demonstrated that the effects of TRPC1 and TRPC3 on the cell viability and cell cycle of ASMCs were, at least partially, through regulating Ca2+ influx.
Insights
Transient receptor potential channel 1 (TRPC1) and TRPC3 regulate airway smooth muscle cell (ASMC) proliferation by modulating calcium ion (Ca2+) influx. Targeting these channels may offer new asthma therapies.
Area of Science:
- Physiology
- Cell Biology
- Pharmacology
Background:
- Airway smooth muscle cell (ASMC) proliferation is a key feature of asthma.
- The role of specific transient receptor potential (TRP) channels, particularly TRPC1 and TRPC3, in ASMC proliferation and calcium (Ca2+) influx in asthma remains to be fully elucidated.
Purpose of the Study:
- To investigate the involvement of TRPC1 and TRPC3 in regulating ASMC proliferation via Ca2+ influx in a murine asthma model.
- To determine the effects of TRPC1 and TRPC3 modulation on ASMC viability, cell cycle, and related protein expression.
Main Methods:
- Induced a chronic asthma model in mice and isolated ASMCs.
- Assessed Ca2+ concentration, cell viability, and protein expression (p-p38, p-JNK, cleaved caspase-3, Bcl-2) following TRPC1/TRPC3 manipulation (overexpression/knockdown) and pharmacological inhibition (SKF96365).
- Utilized Ca2+ chelators (EGTA, BAPTA-AM) to confirm the role of Ca2+ influx.
Main Results:
- TRPC1 and TRPC3 were upregulated in asthmatic mouse ASMCs.
- Overexpression of TRPC1/TRPC3 increased Ca2+ concentration and ASMC viability, while knockdown reduced them.
- SKF96365 and Ca2+ chelators attenuated the observed effects, indicating a critical role for Ca2+ influx.
Conclusions:
- TRPC1 and TRPC3 play a significant role in regulating ASMC proliferation and viability in asthma.
- The observed effects are mediated, at least in part, by modulating Ca2+ influx through TRPC1 and TRPC3 channels.
- These findings suggest TRPC1 and TRPC3 as potential therapeutic targets for managing airway remodeling in asthma.
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