Dataset Information

Transcriptomic profile of cationic channels in human pulmonary arterial hypertension.

ABSTRACT: The dysregulation of K⁺ channels is a hallmark of pulmonary arterial hypertension (PAH). Herein, the channelome was analyzed in lungs of patients with PAH in a public transcriptomic database. Sixty six (46%) mRNA encoding cationic channels were dysregulated in PAH with most of them downregulated (83%). The principal component analysis indicated that dysregulated cationic channel expression is a signature of the disease. Changes were very similar in idiopathic, connective tissue disease and congenital heart disease associated PAH. This analysis 1) is in agreement with the widely recognized pathophysiological role of TASK1 and K_V1.5, 2) supports previous preliminary reports pointing to the dysregulation of several K⁺ channels including the downregulation of K_V1.1, K_V1.4, K_V1.6, K_V7.1, K_V7.4, K_V9.3 and TWIK2 and the upregulation of K_Ca1.1 and 3) points to other cationic channels dysregulated such as Kv7.3, TALK2, Ca_V1 and TRPV4 which might play a pathophysiological role in PAH. The significance of other changes found in Na⁺ and TRP channels remains to be investigated.

SUBMITTER: Perez-Vizcaino F

PROVIDER: S-EPMC8338963 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature

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Transcriptomic profile of cationic channels in human pulmonary arterial hypertension.

Perez-Vizcaino Francisco F Cogolludo Angel A Mondejar-Parreño Gema G

Scientific reports 20210804 1

The dysregulation of K<sup>+</sup> channels is a hallmark of pulmonary arterial hypertension (PAH). Herein, the channelome was analyzed in lungs of patients with PAH in a public transcriptomic database. Sixty six (46%) mRNA encoding cationic channels were dysregulated in PAH with most of them downregulated (83%). The principal component analysis indicated that dysregulated cationic channel expression is a signature of the disease. Changes were very similar in idiopathic, connective tissue diseas ...[more]

PMID: 34349187

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Project description:Pulmonary arterial hypertension (PAH) is a rare, fatal, and incurable disorder. Although advances in the understanding of the PAH pathobiology have been seen in recent years, molecular processes underlying heart remodelling over the course of PAH are still insufficiently understood. Therefore, the aim of this study was to investigate myocardial proteomic profile of rats at different stages of monocrotaline-induced PAH. Samples of left and right ventricle (LV and RV) free wall collected from 32 Wistar rats were subjected to proteomic analysis using an isobaric tag for relative quantitation method. Hemodynamic parameters indicated development of mild elevation of pulmonary artery pressure in the early PAH group (27.00 ± 4.93 mmHg) and severe elevation in the end-stage PAH group (50.50 ± 11.56 mmHg). In early PAH LV myocardium proteins that may be linked to an increase in inflammatory response, apoptosis, glycolytic process and decrease in myocardial structural proteins were differentially expressed compared to controls. During end-stage PAH an increase in proteins associated with apoptosis, fibrosis and cardiomyocyte Ca2+ currents as well as decrease in myocardial structural proteins were observed in LV. In RV during early PAH, especially proteins associated with myocardial structural components and fatty acid beta-oxidation pathway were upregulated. During end-stage PAH significant changes in RV proteins abundance related to the increased myocardial structural components, intensified fibrosis and glycolytic processes as well as decreased proteins related to cardiomyocyte Ca2+ currents were observed. At both PAH stages changes in RV proteins linked to apoptosis inhibition were observed. In conclusion, we identified changes of the levels of several proteins and thus of the metabolic pathways linked to the early and late remodelling of the left and right ventricle over the course of monocrotaline-induced PAH to delineate potential therapeutic targets for the treatment of this severe disease.

Dataset Information

Transcriptomic profile of cationic channels in human pulmonary arterial hypertension.

Publications

Transcriptomic profile of cationic channels in human pulmonary arterial hypertension.

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