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dc.contributor.authorZhou, Tong
dc.contributor.authorTang, Haiyang
dc.contributor.authorHan, Ying
dc.contributor.authorFraidenburg, Dustin
dc.contributor.authorKim, Young-Won
dc.contributor.authorLee, Donghee
dc.contributor.authorChoi, Jeongyoon
dc.contributor.authorBang, Hyoweon
dc.contributor.authorKo, Jae-Hong
dc.date.accessioned2017-06-23T23:53:54Z
dc.date.available2017-06-23T23:53:54Z
dc.date.issued2017
dc.identifier.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 & Pharmacologyen
dc.identifier.issn1226-4512
dc.identifier.issn2093-3827
dc.identifier.pmid28461778
dc.identifier.doi10.4196/kjpp.2017.21.3.353
dc.identifier.urihttp://hdl.handle.net/10150/624396
dc.description.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.
dc.description.sponsorshipChung-Ang Universityen
dc.language.isoenen
dc.publisherKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGYen
dc.relation.urlhttps://synapse.koreamed.org/DOIx.php?id=10.4196/kjpp.2017.21.3.353en
dc.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.en
dc.subjectGene expressionen
dc.subjectHypoxiaen
dc.subjectMolecular signatureen
dc.subjectPulmonary hypertensionen
dc.subjectVDAC1en
dc.titleExpression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertensionen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Dept Meden
dc.identifier.journalThe Korean Journal of Physiology & Pharmacologyen
dc.description.noteOpen Access Journalen
dc.description.collectioninformationThis 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 repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
dc.contributor.institutionDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.
dc.contributor.institutionDepartment of Medicine, University of Arizona, Tucson, AZ 85721, USA.
dc.contributor.institutionDepartment of Physiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
dc.contributor.institutionSection of Pulmonary, Critical Care, Sleep & Allergy, Department of Medicine, The University of Illinois at Chicago, Chicago, IL 60612, USA.
dc.contributor.institutionDepartment of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea.
dc.contributor.institutionDepartment of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea.
dc.contributor.institutionDepartment of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea.
dc.contributor.institutionDepartment of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea.
dc.contributor.institutionDepartment of Physiology, College of Medicine, Chung-Ang University, Seoul 06974, Korea.
refterms.dateFOA2018-06-04T15:54:45Z
html.description.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.


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