Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension
AffiliationUniv Arizona, Dept Med
MetadataShow full item record
CitationExpression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension 2017, 21 (3):353 The Korean Journal of Physiology & Pharmacology
RightsCopyright © 2017 The Korean Physiological Society and The Korean Society of Pharmacology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at email@example.com.
AbstractSeveral human diseases have been associated with mitochondria! voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology. First, we identified the genes differentially expressed between wild-type and Vdac1 knockout mouse embryonic fibroblasts in hypoxic conditions. These genes were deemed to be influenced by VDAC1 deficiency. Gene ontology analysis indicates that the VDAC1 influenced genes are significantly associated with PAH pathobiology. Second, a molecular signature derived from the VDAC1 influenced genes was developed. We suggest that, VDAC1 has a protective role in PAH and the gene expression signature of VDAC1 influenced genes can be used to i) predict severity of pulmonary hypertension secondary to pulmonary diseases, ii) differentiate idiopathic pulmonary artery hypertension (IPAH) patients from controls, and iii) differentiate IPAH from connective tissue disease associated PAH.
NoteOpen Access Journal
VersionFinal published version
- Voltage-dependent anion channel-2 interaction with nitric oxide synthase enhances pulmonary artery endothelial cell nitric oxide production.
- Authors: Alvira CM, Umesh A, Husted C, Ying L, Hou Y, Lyu SC, Nowak J, Cornfield DN
- Issue date: 2012 Nov
- Expression profiling of mitochondrial voltage-dependent anion channel-1 associated genes predicts recurrence-free survival in human carcinomas.
- Authors: Ko JH, Gu W, Lim I, Zhou T, Bang H
- Issue date: 2014
- The mitochondrial voltage-dependent anion channel 1 in tumor cells.
- Authors: Shoshan-Barmatz V, Ben-Hail D, Admoni L, Krelin Y, Tripathi SS
- Issue date: 2015 Oct
- Buffered l-ascorbic acid, alone or bound to KMUP-1 or sildenafil, reduces vascular endothelium growth factor and restores endothelium nitric oxide synthase in hypoxic pulmonary artery.
- Authors: Wu JR, Kao LP, Wu BN, Dai ZK, Wang YY, Chai CY, Chen IJ
- Issue date: 2015 May
- Activated CD47 promotes pulmonary arterial hypertension through targeting caveolin-1.
- Authors: Bauer PM, Bauer EM, Rogers NM, Yao M, Feijoo-Cuaresma M, Pilewski JM, Champion HC, Zuckerbraun BS, Calzada MJ, Isenberg JS
- Issue date: 2012 Mar 15