Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension
Authors
Zhou, Tong
Tang, Haiyang
Han, Ying
Fraidenburg, Dustin
Kim, Young-Won
Lee, Donghee
Choi, Jeongyoon
Bang, Hyoweon
Ko, Jae-Hong
Issue Date
2017
Type
Article
Language
Keywords
Alternative Title
Abstract
Several 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.
Description
Citation
Zhou, T., Tang, H., Han, Y., Fraidenburg, D., Kim, Y.-W., Lee, D., … Ko, J.-H. (2017). Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension. The Korean Journal of Physiology & Pharmacology, 21(3), 353. doi:10.4196/kjpp.2017.21.3.353
Publisher
License
Creative Commons Attribution-NonCommercial 4.0 International
Journal
Volume
Issue
PubMed ID
ISSN
1226-4512