THE DIFFERENTIAL EXPRESSION OF TRPV1 IN PULMONARY ARTERY SMOOTH MUSCLE CELLS AND PULMONARY ENDOTHELIAL CELLS
Pulmonary arterial hypertension (PAH) is a fatal microvascular disease that ultimately leads to right heart failure. Enhanced cytosolic calcium concentration ([Ca2+]cyt) originating from the extracellular environment via predominantly Ca2+-permeable channels such as transient receptor potential (TRP...
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| Language: | en_US |
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The University of Arizona.
2016
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| Online Access: | http://hdl.handle.net/10150/612827 http://arizona.openrepository.com/arizona/handle/10150/612827 |
| Summary: | Pulmonary arterial hypertension (PAH) is a fatal microvascular disease that ultimately leads to right heart failure. Enhanced cytosolic calcium concentration ([Ca2+]cyt) originating from the extracellular environment via predominantly Ca2+-permeable channels such as transient receptor potential (TRP) channels is one method which can lead to the pulmonary vascular remodeling observed in PAH patients. Although Ca2+ signaling has been extensively studied in pulmonary artery smooth muscle cells (PASMCs), it has been somewhat neglected in pulmonary artery endothelial cells (PAECs). In this study, we determined the expression of TRPV1 channels in PASMCs and PAECs from normal and idiopathic pulmonary arterial hypertension (IPAH) patients and lung tissues from animal models of pulmonary hypertension (PH). TRPV1 expression is enhanced in IPAH PASMCs versus normal PASMCs. Interestingly, TRPV1 is decreased in IPAH PAECs and in monocrotaline (MCT)-induced PH rat lung tissues, compared with their respective controls. Additionally, Ca2+ influx is increased in IPAH PASMCs versus control. IPAH PASMC proliferation is attenuated; yet, normal PAEC proliferation is enhanced by the TRPV1 antagonist capsazepine (CPZ). These results suggest that TRPV1 may have a differential role in PASMCs and PAECs. Establishing a link between TRPV1 in these two cell types may potentially underlie new pharmacological treatments for PAH. |
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