Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias. / Gardner, R T; Wang, L; Lang, B T; Cregg, J M; Dunbar, C L; Woodward, W R; Silver, J; Ripplinger, C M; Habecker, B A.

In: Nature Communications, Vol. 6, 6235, 02.02.2015.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Gardner, RT, Wang, L, Lang, BT, Cregg, JM, Dunbar, CL, Woodward, WR, Silver, J, Ripplinger, CM & Habecker, BA 2015, 'Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias', Nature Communications, vol. 6, 6235. https://doi.org/10.1038/ncomms7235

APA

Gardner, R. T., Wang, L., Lang, B. T., Cregg, J. M., Dunbar, C. L., Woodward, W. R., Silver, J., Ripplinger, C. M., & Habecker, B. A. (2015). Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias. Nature Communications, 6, [6235]. https://doi.org/10.1038/ncomms7235

Vancouver

Gardner RT, Wang L, Lang BT, Cregg JM, Dunbar CL, Woodward WR et al. Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias. Nature Communications. 2015 Feb 2;6. 6235. https://doi.org/10.1038/ncomms7235

Author

Gardner, R T ; Wang, L ; Lang, B T ; Cregg, J M ; Dunbar, C L ; Woodward, W R ; Silver, J ; Ripplinger, C M ; Habecker, B A. / Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias. In: Nature Communications. 2015 ; Vol. 6.

Bibtex

@article{84233a0a3d3b426ca86724e18e142463,
title = "Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias",
abstract = "Millions of people suffer a myocardial infarction (MI) every year, and those who survive have increased risk of arrhythmias and sudden cardiac death. Recent clinical studies have identified sympathetic denervation as a predictor of increased arrhythmia susceptibility. Chondroitin sulfate proteoglycans present in the cardiac scar after MI prevent sympathetic reinnervation by binding the neuronal protein tyrosine phosphatase receptor σ (PTPσ). Here we show that the absence of PTPσ, or pharmacologic modulation of PTPσ by the novel intracellular sigma peptide (ISP) beginning 3 days after injury, restores sympathetic innervation to the scar and markedly reduces arrhythmia susceptibility. Using optical mapping we observe increased dispersion of action potential duration, supersensitivity to β-adrenergic receptor stimulation and Ca(2+) mishandling following MI. Sympathetic reinnervation prevents these changes and renders hearts remarkably resistant to induced arrhythmias. ",
keywords = "Animals, Arrhythmias, Cardiac/prevention & control, Calcium/metabolism, Electrocardiography, Female, Male, Mice, Mice, Inbred BALB C, Mice, Transgenic, Myocardial Infarction/drug therapy, Peptides/therapeutic use, Receptor-Like Protein Tyrosine Phosphatases, Class 2/antagonists & inhibitors, Receptors, Adrenergic, beta/metabolism, Sympathetic Nervous System/metabolism",
author = "Gardner, {R T} and L Wang and Lang, {B T} and Cregg, {J M} and Dunbar, {C L} and Woodward, {W R} and J Silver and Ripplinger, {C M} and Habecker, {B A}",
year = "2015",
month = feb,
day = "2",
doi = "10.1038/ncomms7235",
language = "English",
volume = "6",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias

AU - Gardner, R T

AU - Wang, L

AU - Lang, B T

AU - Cregg, J M

AU - Dunbar, C L

AU - Woodward, W R

AU - Silver, J

AU - Ripplinger, C M

AU - Habecker, B A

PY - 2015/2/2

Y1 - 2015/2/2

N2 - Millions of people suffer a myocardial infarction (MI) every year, and those who survive have increased risk of arrhythmias and sudden cardiac death. Recent clinical studies have identified sympathetic denervation as a predictor of increased arrhythmia susceptibility. Chondroitin sulfate proteoglycans present in the cardiac scar after MI prevent sympathetic reinnervation by binding the neuronal protein tyrosine phosphatase receptor σ (PTPσ). Here we show that the absence of PTPσ, or pharmacologic modulation of PTPσ by the novel intracellular sigma peptide (ISP) beginning 3 days after injury, restores sympathetic innervation to the scar and markedly reduces arrhythmia susceptibility. Using optical mapping we observe increased dispersion of action potential duration, supersensitivity to β-adrenergic receptor stimulation and Ca(2+) mishandling following MI. Sympathetic reinnervation prevents these changes and renders hearts remarkably resistant to induced arrhythmias.

AB - Millions of people suffer a myocardial infarction (MI) every year, and those who survive have increased risk of arrhythmias and sudden cardiac death. Recent clinical studies have identified sympathetic denervation as a predictor of increased arrhythmia susceptibility. Chondroitin sulfate proteoglycans present in the cardiac scar after MI prevent sympathetic reinnervation by binding the neuronal protein tyrosine phosphatase receptor σ (PTPσ). Here we show that the absence of PTPσ, or pharmacologic modulation of PTPσ by the novel intracellular sigma peptide (ISP) beginning 3 days after injury, restores sympathetic innervation to the scar and markedly reduces arrhythmia susceptibility. Using optical mapping we observe increased dispersion of action potential duration, supersensitivity to β-adrenergic receptor stimulation and Ca(2+) mishandling following MI. Sympathetic reinnervation prevents these changes and renders hearts remarkably resistant to induced arrhythmias.

KW - Animals

KW - Arrhythmias, Cardiac/prevention & control

KW - Calcium/metabolism

KW - Electrocardiography

KW - Female

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Transgenic

KW - Myocardial Infarction/drug therapy

KW - Peptides/therapeutic use

KW - Receptor-Like Protein Tyrosine Phosphatases, Class 2/antagonists & inhibitors

KW - Receptors, Adrenergic, beta/metabolism

KW - Sympathetic Nervous System/metabolism

U2 - 10.1038/ncomms7235

DO - 10.1038/ncomms7235

M3 - Journal article

C2 - 25639594

VL - 6

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 6235

ER -

ID: 248114734