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Updated: Jul 1, 2026
Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
Published on: January 14, 2014
Functional expression of transient receptor potential vanilloid-related channels in chronically hypoxic human
Yue Xiu Wang1, Jun Wang, Cong Wang
1Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, People's Republic of China.
Abstract:
Transient receptor potential vanilloid (TRPV) channels are nonselective cation channels pertinent to diverse physiological functions. Multiple TRPV channel subtypes have been identified in different tissues and cloned. The aim of this study was to investigate the role of TRPV channels in hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (PASMCs) and its possible signal pathway. Reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, and Western blot analysis were used to detect the expression of TRPV in human PASMCs. Cell number was determined with a hemocytometer. Cytosolic Ca2+ concentration ([Ca2+]cyt) was measured with a dynamic digital Ca2+ imaging system. The mRNA of TRPV1-4 was detected in human PASMCs and chronic hypoxia up-regulated expression levels of the TRPV1 gene and protein. The ability to proliferate, the resting [Ca2+]cyt, and cyclopiazonic acid-induced capacitative Ca2+ entry in human PASMCs were enhanced significantly by chronic hypoxia compared with the control, and these effects were inhibited in a dose-dependent manner by capsazepine, a TRPV1 channel inhibitor. These results suggest that TRPV1 may be a critical pathway or mediator in chronic hypoxia-induced proliferation of human PASMCs.
Insights
Chronic hypoxia enhances human pulmonary artery smooth muscle cell proliferation via TRPV1 channels. Inhibiting TRPV1 with capsazepine blocks this effect, suggesting TRPV1
Area of Science:
- Physiology
- Molecular Biology
- Cell Biology
Background:
- Transient receptor potential vanilloid (TRPV) channels are crucial nonselective cation channels involved in various physiological processes.
- TRPV channel subtypes are expressed in different tissues, playing roles in cellular function.
- Pulmonary artery smooth muscle cells (PASMCs) are key regulators of vascular tone and proliferation.
Purpose of the Study:
- To investigate the role of TRPV channels in hypoxia-induced proliferation of human PASMCs.
- To explore the potential signaling pathway involved in this process.
Main Methods:
- Gene and protein expression analysis using RT-PCR, real-time PCR, and Western blot.
- Cell proliferation assessment using a hemocytometer.
- Intracellular calcium ([Ca2+]cyt) measurement via digital imaging systems.
- Pharmacological inhibition using capsazepine, a TRPV1 channel inhibitor.
Main Results:
- TRPV1-4 mRNA detected in human PASMCs; chronic hypoxia upregulated TRPV1 gene and protein expression.
- Chronic hypoxia significantly enhanced PASMC proliferation, resting [Ca2+]cyt, and capacitative Ca2+ entry.
- Capsazepine dose-dependently inhibited hypoxia-induced proliferation and calcium signaling.
- TRPV1 expression and function are upregulated by chronic hypoxia in human PASMCs.
Conclusions:
- TRPV1 channels are implicated in the proliferation of human PASMCs under chronic hypoxic conditions.
- TRPV1 may act as a critical pathway or mediator in chronic hypoxia-induced PASMC proliferation.
- Targeting TRPV1 could offer therapeutic potential for pulmonary vascular diseases associated with hypoxia.
