Hydrogen sulphide increases pulmonary veins and atrial arrhythmogenesis with activation of protein kinase C

Chao Shun Chan, Yung Kuo Lin, Yu Hsun Kao, Yao Chang Chen, Shih Ann Chen, Yi Jen Chen

Research output: Contribution to journalArticle

Abstract

Hydrogen sulphide (H2S), one of the most common toxic air pollutants, is an important aetiology of atrial fibrillation (AF). Pulmonary veins (PVs) and left atrium (LA) are the most important AF trigger and substrate. We investigated whether H2S may modulate the arrhythmogenesis of PVs and atria. Conventional microelectrodes and whole-cell patch clamp were performed in rabbit PV, sinoatrial node (SAN) or atrial cardiomyocytes before and after the perfusion of NaHS with or without chelerythrine (a selective PKC inhibitor), rottlerin (a specific PKC δ inhibitor) or KB-R7943 (a NCX inhibitor). NaHS reduced spontaneous beating rates, but increased the occurrences of delayed afterdepolarizations and burst firing in PVs and SANs. NaHS (100 μmol/L) increased IKATP and INCX in PV and LA cardiomyocytes, which were attenuated by chelerythrine (3 μmol/L). Chelerythrine, rottlerin (10 μmol/L) or KB-R7943 (10 μmol/L) attenuated the arrhythmogenic effects of NaHS on PVs or SANs. NaHS shortened the action potential duration in LA, but not in right atrium or in the presence of chelerythrine. NaHS increased PKC activity, but did not translocate PKC isoforms α, ε to membrane in LA. In conclusion, through protein kinase C signalling, H2S increases PV and atrial arrhythmogenesis, which may contribute to air pollution-induced AF.

Original languageEnglish
JournalJournal of Cellular and Molecular Medicine
DOIs
Publication statusAccepted/In press - Jan 1 2018

Fingerprint

Hydrogen Sulfide
Pulmonary Veins
Protein Kinase C
Heart Atria
Atrial Fibrillation
Cardiac Myocytes
Air Pollutants
Sinoatrial Node
Poisons
Air Pollution
Microelectrodes
Action Potentials
sodium bisulfide
Protein Isoforms
Perfusion
Rabbits
Membranes
chelerythrine

Keywords

  • Atrial fibrillation
  • Hydrogen sulphide
  • Protein kinase C

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology

Cite this

@article{b2109daa331a41fda5b3c7e3dbc5e761,
title = "Hydrogen sulphide increases pulmonary veins and atrial arrhythmogenesis with activation of protein kinase C",
abstract = "Hydrogen sulphide (H2S), one of the most common toxic air pollutants, is an important aetiology of atrial fibrillation (AF). Pulmonary veins (PVs) and left atrium (LA) are the most important AF trigger and substrate. We investigated whether H2S may modulate the arrhythmogenesis of PVs and atria. Conventional microelectrodes and whole-cell patch clamp were performed in rabbit PV, sinoatrial node (SAN) or atrial cardiomyocytes before and after the perfusion of NaHS with or without chelerythrine (a selective PKC inhibitor), rottlerin (a specific PKC δ inhibitor) or KB-R7943 (a NCX inhibitor). NaHS reduced spontaneous beating rates, but increased the occurrences of delayed afterdepolarizations and burst firing in PVs and SANs. NaHS (100 μmol/L) increased IKATP and INCX in PV and LA cardiomyocytes, which were attenuated by chelerythrine (3 μmol/L). Chelerythrine, rottlerin (10 μmol/L) or KB-R7943 (10 μmol/L) attenuated the arrhythmogenic effects of NaHS on PVs or SANs. NaHS shortened the action potential duration in LA, but not in right atrium or in the presence of chelerythrine. NaHS increased PKC activity, but did not translocate PKC isoforms α, ε to membrane in LA. In conclusion, through protein kinase C signalling, H2S increases PV and atrial arrhythmogenesis, which may contribute to air pollution-induced AF.",
keywords = "Atrial fibrillation, Hydrogen sulphide, Protein kinase C",
author = "Chan, {Chao Shun} and Lin, {Yung Kuo} and Kao, {Yu Hsun} and Chen, {Yao Chang} and Chen, {Shih Ann} and Chen, {Yi Jen}",
year = "2018",
month = "1",
day = "1",
doi = "10.1111/jcmm.13627",
language = "English",
journal = "Journal of Cellular and Molecular Medicine",
issn = "1582-1838",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Hydrogen sulphide increases pulmonary veins and atrial arrhythmogenesis with activation of protein kinase C

AU - Chan, Chao Shun

AU - Lin, Yung Kuo

AU - Kao, Yu Hsun

AU - Chen, Yao Chang

AU - Chen, Shih Ann

AU - Chen, Yi Jen

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Hydrogen sulphide (H2S), one of the most common toxic air pollutants, is an important aetiology of atrial fibrillation (AF). Pulmonary veins (PVs) and left atrium (LA) are the most important AF trigger and substrate. We investigated whether H2S may modulate the arrhythmogenesis of PVs and atria. Conventional microelectrodes and whole-cell patch clamp were performed in rabbit PV, sinoatrial node (SAN) or atrial cardiomyocytes before and after the perfusion of NaHS with or without chelerythrine (a selective PKC inhibitor), rottlerin (a specific PKC δ inhibitor) or KB-R7943 (a NCX inhibitor). NaHS reduced spontaneous beating rates, but increased the occurrences of delayed afterdepolarizations and burst firing in PVs and SANs. NaHS (100 μmol/L) increased IKATP and INCX in PV and LA cardiomyocytes, which were attenuated by chelerythrine (3 μmol/L). Chelerythrine, rottlerin (10 μmol/L) or KB-R7943 (10 μmol/L) attenuated the arrhythmogenic effects of NaHS on PVs or SANs. NaHS shortened the action potential duration in LA, but not in right atrium or in the presence of chelerythrine. NaHS increased PKC activity, but did not translocate PKC isoforms α, ε to membrane in LA. In conclusion, through protein kinase C signalling, H2S increases PV and atrial arrhythmogenesis, which may contribute to air pollution-induced AF.

AB - Hydrogen sulphide (H2S), one of the most common toxic air pollutants, is an important aetiology of atrial fibrillation (AF). Pulmonary veins (PVs) and left atrium (LA) are the most important AF trigger and substrate. We investigated whether H2S may modulate the arrhythmogenesis of PVs and atria. Conventional microelectrodes and whole-cell patch clamp were performed in rabbit PV, sinoatrial node (SAN) or atrial cardiomyocytes before and after the perfusion of NaHS with or without chelerythrine (a selective PKC inhibitor), rottlerin (a specific PKC δ inhibitor) or KB-R7943 (a NCX inhibitor). NaHS reduced spontaneous beating rates, but increased the occurrences of delayed afterdepolarizations and burst firing in PVs and SANs. NaHS (100 μmol/L) increased IKATP and INCX in PV and LA cardiomyocytes, which were attenuated by chelerythrine (3 μmol/L). Chelerythrine, rottlerin (10 μmol/L) or KB-R7943 (10 μmol/L) attenuated the arrhythmogenic effects of NaHS on PVs or SANs. NaHS shortened the action potential duration in LA, but not in right atrium or in the presence of chelerythrine. NaHS increased PKC activity, but did not translocate PKC isoforms α, ε to membrane in LA. In conclusion, through protein kinase C signalling, H2S increases PV and atrial arrhythmogenesis, which may contribute to air pollution-induced AF.

KW - Atrial fibrillation

KW - Hydrogen sulphide

KW - Protein kinase C

UR - http://www.scopus.com/inward/record.url?scp=85045742274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85045742274&partnerID=8YFLogxK

U2 - 10.1111/jcmm.13627

DO - 10.1111/jcmm.13627

M3 - Article

JO - Journal of Cellular and Molecular Medicine

JF - Journal of Cellular and Molecular Medicine

SN - 1582-1838

ER -