Document Detail


Infarction-induced cytokines cause local depletion of tyrosine hydroxylase in cardiac sympathetic nerves.
MedLine Citation:
PMID:  19880537     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial infarction causes a heterogeneity of noradrenergic transmission that contributes to the development of ventricular arrhythmias and sudden cardiac death. Ischaemia-induced alterations in sympathetic transmission include regional variations in cardiac noradrenaline (NA) and in tyrosine hydroxylase, the rate-limiting enzyme in NA synthesis. Inflammatory cytokines that act through gp130 are elevated in the heart after myocardial infarction. These cytokines decrease expression of tyrosine hydroxylase in sympathetic neurons, and indirect evidence suggests that they contribute to the local depletion of tyrosine hydroxylase in the damaged left ventricle. However, gp130 cytokines are also important for the survival of cardiac myocytes following damage to the heart. To examine the effect of cytokines on tyrosine hydroxylase and NA content in cardiac nerves we used gp130(DBH-Cre/lox) mice, which have a deletion of the gp130 receptor in neurons expressing dopamine beta-hydroxylase. The absence of neuronal gp130 prevented the loss of tyrosine hydroxylase in cardiac sympathetic nerves innervating the left ventricle 1 week after ischaemia-reperfusion compared with wild-type C57BL/6J mice. Surprisingly, restoration of tyrosine hydroxylase in the damaged ventricle did not return neuronal NA content to normal levels. Noradrenaline uptake into cardiac nerves was significantly lower in gp130 knockout mice, contributing to the lack of neuronal NA stores. There were no significant differences in left ventricular peak systolic pressure, dP/dt(max) or dP/dt(min) between the two genotypes after myocardial infarction, but ganglionic blockade revealed differences in autonomic tone between the genotypes. Stimulation of the heart with dobutamine or release of endogenous NA with tyramine generated similar responses in both genotypes. Thus, the removal of gp130 from sympathetic neurons prevents the post-infarct depletion of tyrosine hydroxylase in the left ventricle, but does not alter NA content or cardiac function.
Authors:
Diana C Parrish; Eric N Alston; Hermann Rohrer; Paul Nkadi; William R Woodward; Günther Schütz; Beth A Habecker
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-10-30
Journal Detail:
Title:  Experimental physiology     Volume:  95     ISSN:  1469-445X     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-12     Completed Date:  2010-05-06     Revised Date:  2013-03-12    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  304-14     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cytokine Receptor gp130 / metabolism*
Cytokines / metabolism*
Heart Ventricles / innervation,  metabolism*
Mice
Mice, Knockout
Myocardial Infarction / metabolism*
Sodium / metabolism*
Sympathetic Nervous System / metabolism*
Tyrosine 3-Monooxygenase / metabolism*
Grant Support
ID/Acronym/Agency:
R01 HL068231/HL/NHLBI NIH HHS; R01 HL068231/HL/NHLBI NIH HHS; R01 HL068231-08/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 133483-10-0/Cytokine Receptor gp130; 7440-23-5/Sodium; EC 1.14.16.2/Tyrosine 3-Monooxygenase
Comments/Corrections

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