Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression

Pavan Atluri; Kevin J. Morine; George P. Liao; Corinna M. Panlilio; Mark F. Berry; Vivian M. Hsu; William Hiesinger; Jeffrey E. Cohen; Y. Joseph Woo

doi:10.2478/s11658-006-0058-7

Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression

Pavan Atluri, Kevin J. Morine, George P. Liao, Corinna M. Panlilio, Mark F. Berry, Vivian M. Hsu, William Hiesinger, Jeffrey E. Cohen, Y. Joseph Woo

Research output: Contribution to journal › Article › peer-review

94 Scopus citations

Abstract

Apelin interacts with the APJ receptor to enhance inotropy. In heart failure, apelin-APJ coupling may provide a means of enhancing myocardial function. The alterations in apelin and APJ receptor concentrations with ischemic cardiomyopathy are poorly understood. We investigated the compensatory changes in endogenous apelin and APJ levels in the setting of ischemic cardiomyopathy. Male, Lewis rats underwent LAD ligation and progressed into heart failure over 6 weeks. Corresponding animals underwent sham thoracotomy as control. Six weeks after initial surgery, the animals underwent hemodynamic functional analysis in the presence of exogenous apelin-13 infusion and the hearts were explanted for western blot and enzyme immunoassay analysis. Western blot analysis of myocardial APJ concentration demonstrated increased APJ receptor protein levels with heart failure (1890750±133500 vs. 901600±143120 intensity units, n=8, p=0.00001). Total apelin protein levels increased with ischemic heart failure as demonstrated by enzyme immunoassay (12.0±4.6 vs. 1.0±1.2 ng/ml, n=5, p=0.006) and western blot (1579400±477733 vs. 943000±157600 intensity units, n=10, p=0.008). Infusion of apelin-13 significantly enhanced myocardial function in sham and failing hearts. We conclude that total myocardial apelin and APJ receptor levels increase in compensation for ischemic cardiomyopathy.

Original language	English
Pages (from-to)	127-138
Number of pages	12
Journal	Cellular and Molecular Biology Letters
Volume	12
Issue number	1
DOIs	https://doi.org/10.2478/s11658-006-0058-7
State	Published - 2007
Externally published	Yes

Keywords

APJ
Apelin
G protein coupled receptor
Inotrope

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10.2478/s11658-006-0058-7

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@article{072a0f34d7404832a9c9945f6944fc6c,

title = "Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression",

abstract = "Apelin interacts with the APJ receptor to enhance inotropy. In heart failure, apelin-APJ coupling may provide a means of enhancing myocardial function. The alterations in apelin and APJ receptor concentrations with ischemic cardiomyopathy are poorly understood. We investigated the compensatory changes in endogenous apelin and APJ levels in the setting of ischemic cardiomyopathy. Male, Lewis rats underwent LAD ligation and progressed into heart failure over 6 weeks. Corresponding animals underwent sham thoracotomy as control. Six weeks after initial surgery, the animals underwent hemodynamic functional analysis in the presence of exogenous apelin-13 infusion and the hearts were explanted for western blot and enzyme immunoassay analysis. Western blot analysis of myocardial APJ concentration demonstrated increased APJ receptor protein levels with heart failure (1890750±133500 vs. 901600±143120 intensity units, n=8, p=0.00001). Total apelin protein levels increased with ischemic heart failure as demonstrated by enzyme immunoassay (12.0±4.6 vs. 1.0±1.2 ng/ml, n=5, p=0.006) and western blot (1579400±477733 vs. 943000±157600 intensity units, n=10, p=0.008). Infusion of apelin-13 significantly enhanced myocardial function in sham and failing hearts. We conclude that total myocardial apelin and APJ receptor levels increase in compensation for ischemic cardiomyopathy.",

keywords = "APJ, Apelin, G protein coupled receptor, Inotrope",

author = "Pavan Atluri and Morine, {Kevin J.} and Liao, {George P.} and Panlilio, {Corinna M.} and Berry, {Mark F.} and Hsu, {Vivian M.} and William Hiesinger and Cohen, {Jeffrey E.} and Woo, {Y. Joseph}",

note = "Funding Information: Acknowledgements. This work was supported in part by grants from the NIH National Heart Lung and Blood Institute/Thoracic Surgery Foundation for Research and Education HL072812 (Y. Joseph Woo, M.D.) and NIH Ruth L. Kirschstein National Research Service Award, Individual Fellowship 1 F32 HL79769-01 (Pavan Atluri, M.D.).",

year = "2007",

doi = "10.2478/s11658-006-0058-7",

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journal = "Cellular and Molecular Biology Letters",

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T1 - Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression

AU - Atluri, Pavan

AU - Morine, Kevin J.

AU - Liao, George P.

AU - Panlilio, Corinna M.

AU - Berry, Mark F.

AU - Hsu, Vivian M.

AU - Hiesinger, William

AU - Cohen, Jeffrey E.

AU - Woo, Y. Joseph

N1 - Funding Information: Acknowledgements. This work was supported in part by grants from the NIH National Heart Lung and Blood Institute/Thoracic Surgery Foundation for Research and Education HL072812 (Y. Joseph Woo, M.D.) and NIH Ruth L. Kirschstein National Research Service Award, Individual Fellowship 1 F32 HL79769-01 (Pavan Atluri, M.D.).

PY - 2007

Y1 - 2007

N2 - Apelin interacts with the APJ receptor to enhance inotropy. In heart failure, apelin-APJ coupling may provide a means of enhancing myocardial function. The alterations in apelin and APJ receptor concentrations with ischemic cardiomyopathy are poorly understood. We investigated the compensatory changes in endogenous apelin and APJ levels in the setting of ischemic cardiomyopathy. Male, Lewis rats underwent LAD ligation and progressed into heart failure over 6 weeks. Corresponding animals underwent sham thoracotomy as control. Six weeks after initial surgery, the animals underwent hemodynamic functional analysis in the presence of exogenous apelin-13 infusion and the hearts were explanted for western blot and enzyme immunoassay analysis. Western blot analysis of myocardial APJ concentration demonstrated increased APJ receptor protein levels with heart failure (1890750±133500 vs. 901600±143120 intensity units, n=8, p=0.00001). Total apelin protein levels increased with ischemic heart failure as demonstrated by enzyme immunoassay (12.0±4.6 vs. 1.0±1.2 ng/ml, n=5, p=0.006) and western blot (1579400±477733 vs. 943000±157600 intensity units, n=10, p=0.008). Infusion of apelin-13 significantly enhanced myocardial function in sham and failing hearts. We conclude that total myocardial apelin and APJ receptor levels increase in compensation for ischemic cardiomyopathy.

AB - Apelin interacts with the APJ receptor to enhance inotropy. In heart failure, apelin-APJ coupling may provide a means of enhancing myocardial function. The alterations in apelin and APJ receptor concentrations with ischemic cardiomyopathy are poorly understood. We investigated the compensatory changes in endogenous apelin and APJ levels in the setting of ischemic cardiomyopathy. Male, Lewis rats underwent LAD ligation and progressed into heart failure over 6 weeks. Corresponding animals underwent sham thoracotomy as control. Six weeks after initial surgery, the animals underwent hemodynamic functional analysis in the presence of exogenous apelin-13 infusion and the hearts were explanted for western blot and enzyme immunoassay analysis. Western blot analysis of myocardial APJ concentration demonstrated increased APJ receptor protein levels with heart failure (1890750±133500 vs. 901600±143120 intensity units, n=8, p=0.00001). Total apelin protein levels increased with ischemic heart failure as demonstrated by enzyme immunoassay (12.0±4.6 vs. 1.0±1.2 ng/ml, n=5, p=0.006) and western blot (1579400±477733 vs. 943000±157600 intensity units, n=10, p=0.008). Infusion of apelin-13 significantly enhanced myocardial function in sham and failing hearts. We conclude that total myocardial apelin and APJ receptor levels increase in compensation for ischemic cardiomyopathy.

KW - APJ

KW - Apelin

KW - G protein coupled receptor

KW - Inotrope

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DO - 10.2478/s11658-006-0058-7

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SN - 1425-8153

VL - 12

SP - 127

EP - 138

JO - Cellular and Molecular Biology Letters

JF - Cellular and Molecular Biology Letters

IS - 1

ER -

Ischemic heart failure enhances endogenous myocardial apelin and APJ receptor expression

Abstract

Keywords

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