THE DIFFERENTIAL EXPRESSION OF TRPV1 IN PULMONARY ARTERY SMOOTH MUSCLE CELLS AND PULMONARY ENDOTHELIAL CELLS

Persistent Link:
http://hdl.handle.net/10150/612827
Title:
THE DIFFERENTIAL EXPRESSION OF TRPV1 IN PULMONARY ARTERY SMOOTH MUSCLE CELLS AND PULMONARY ENDOTHELIAL CELLS
Author:
DASH, SWETALEENA
Issue Date:
2016
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
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.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
Bachelors
Degree Program:
Honors College; Physiology
Degree Grantor:
University of Arizona
Advisor:
Yuan, Jason X.-J.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleTHE DIFFERENTIAL EXPRESSION OF TRPV1 IN PULMONARY ARTERY SMOOTH MUSCLE CELLS AND PULMONARY ENDOTHELIAL CELLSen_US
dc.creatorDASH, SWETALEENAen
dc.contributor.authorDASH, SWETALEENAen
dc.date.issued2016-
dc.publisherThe University of Arizona.en
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en
dc.description.abstractPulmonary 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.en
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.nameB.S.en
thesis.degree.levelBachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplinePhysiologyen
thesis.degree.grantorUniversity of Arizonaen
dc.contributor.advisorYuan, Jason X.-J.en
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