Title

Decreased bioavailability of hydrogen sulfide links vascular endothelium and atrial remodeling in atrial fibrillation

Authors

Megan Watts, The Departments of Medicine, And Molecular and Cellular Physiology and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Gopi K. Kolluru, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Parinita Dherange, The Departments of Medicine, And Molecular and Cellular Physiology and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Sibile Pardue, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Man Si, The Departments of Cellular Biology and Anatomy and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States; The Department of Biological Sciences, Southern Methodist University, Dallas, TX, USA.
Xinggui Shen, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Krystle Trosclair, The Departments of Cellular Biology and Anatomy and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States; The Department of Neurosurgery and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
John Glawe, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Zaki Al-Yafeai, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Mazen Iqbal, The Departments of Medicine, And Molecular and Cellular Physiology and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Brenna H. Pearson, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Kathryn A. Hamilton, The Departments of Cellular Biology and Anatomy and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
A Wayne Orr, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Edward Glasscock, The Departments of Cellular Biology and Anatomy and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States; The Department of Biological Sciences, Southern Methodist University, Dallas, TX, USA.
Christopher G. Kevil, The Departments of Pathology, Molecular and Cellular Physiology, Cellular Biology and Anatomy And Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States.
Paari Dominic, The Departments of Medicine, And Molecular and Cellular Physiology and Center of Excellence for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center-Shreveport, Louisiana, United States. Electronic address: pdomi2@lsuhsc.edu.

Document Type

Article

Publication Date

1-1-2021

Abstract

Oxidative stress drives the pathogenesis of atrial fibrillation (AF), the most common arrhythmia. In the cardiovascular system, cystathionine γ-lyase (CSE) serves as the primary enzyme producing hydrogen sulfide (HS), a mammalian gasotransmitter that reduces oxidative stress. Using a case control study design in patients with and without AF and a mouse model of CSE knockout (CSE-KO), we evaluated the role of HS in the etiology of AF. Patients with AF (n = 51) had significantly reduced plasma acid labile sulfide levels compared to patients without AF (n = 65). In addition, patients with persistent AF (n = 25) showed lower plasma free sulfide levels compared to patients with paroxysmal AF (n = 26). Consistent with an important role for HS in AF, CSE-KO mice had decreased atrial sulfide levels, increased atrial superoxide levels, and enhanced propensity for induced persistent AF compared to wild type (WT) mice. Rescuing HS signaling in CSE-KO mice by Diallyl trisulfide (DATS) supplementation or reconstitution with endothelial cell specific CSE over-expression significantly reduced atrial superoxide, increased sulfide levels, and lowered AF inducibility. Lastly, low HS levels in CSE KO mice was associated with atrial electrical remodeling including longer effective refractory periods, slower conduction velocity, increased myocyte calcium sparks, and increased myocyte action potential duration that were reversed by DATS supplementation or endothelial CSE overexpression. Our findings demonstrate an important role of CSE and HS bioavailability in regulating electrical remodeling and susceptibility to AF.

Publication Source (Journal or Book title)

Redox biology

First Page

101817

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