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Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes.

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Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes. / El-Armouche, Ali; Rau, Thomas; Zolk, Oliver; Ditz, Diana; Pamminger, Torsten; Zimmermann, Wolfram-H; Jäckel, Elmar; Harding, Sian E; Boknik, Peter; Neumann, Joachim; Eschenhagen, Thomas.

In: FASEB J, Vol. 17, No. 3, 3, 2003, p. 437-439.

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

Harvard

El-Armouche, A, Rau, T, Zolk, O, Ditz, D, Pamminger, T, Zimmermann, W-H, Jäckel, E, Harding, SE, Boknik, P, Neumann, J & Eschenhagen, T 2003, 'Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes.', FASEB J, vol. 17, no. 3, 3, pp. 437-439. <http://www.ncbi.nlm.nih.gov/pubmed/12514122?dopt=Citation>

APA

El-Armouche, A., Rau, T., Zolk, O., Ditz, D., Pamminger, T., Zimmermann, W-H., Jäckel, E., Harding, S. E., Boknik, P., Neumann, J., & Eschenhagen, T. (2003). Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes. FASEB J, 17(3), 437-439. [3]. http://www.ncbi.nlm.nih.gov/pubmed/12514122?dopt=Citation

Vancouver

El-Armouche A, Rau T, Zolk O, Ditz D, Pamminger T, Zimmermann W-H et al. Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes. FASEB J. 2003;17(3):437-439. 3.

Bibtex

@article{1b0dc4152aa8499bb4961150ea72c948,
title = "Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes.",
abstract = "The protein phosphatase inhibitor-1 (PPI-1) inhibits phosphatase type-1 (PP1) only when phosphorylated by protein kinase A and could play a pivotal role in the phosphorylation/dephosphorylation balance. Rat cardiac PPI-1 was cloned by reverse transcriptase-polymerase chain reaction, expressed in Eschericia coli, evaluated in phosphatase assays, and used to generate an antiserum. An adenovirus was constructed encoding PPI-1 and green fluorescent protein (GFP) under separate cytomegalovirus promotors (AdPPI-1/GFP). A GFP-only virus (AdGFP) served as control. Engineered heart tissue (EHT) from neonatal rat cardiomyocytes and adult rat cardiac myocytes (ARCMs) were used as model systems. PPI-1 expression was determined in human ventricular samples by Northern blots. Compared with AdGFP, AdPPI-1/GFP-infected neonatal rat cardiomyocytes displayed a 73% reduction in PP1 activity. EHTs infected with AdPPI-1/GFP exhibited a fivefold increase in isoprenaline sensitivity. AdPPI-1/GFP-infected ARCMs displayed enhanced cell shortening as well as enhanced phospholamban phosphorylation when stimulated with 1 nM isoprenaline. PPI-1 mRNA levels were reduced by 57+/-12% in failing hearts with dilated and ischemic cardiomyopathy (n=8 each) compared with nonfailing hearts (n=8). In summary, increased PPI-1 expression enhances myocyte sensitivity to isoprenaline, indicating that PPI-1 acts as an amplifier in beta-adrenergic signaling. Decreased PPI-1 in failing human hearts could participate in desensitization of the cAMP pathway.",
author = "Ali El-Armouche and Thomas Rau and Oliver Zolk and Diana Ditz and Torsten Pamminger and Wolfram-H Zimmermann and Elmar J{\"a}ckel and Harding, {Sian E} and Peter Boknik and Joachim Neumann and Thomas Eschenhagen",
year = "2003",
language = "Deutsch",
volume = "17",
pages = "437--439",
journal = "FASEB J",
issn = "0892-6638",
publisher = "FASEB",
number = "3",

}

RIS

TY - JOUR

T1 - Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes.

AU - El-Armouche, Ali

AU - Rau, Thomas

AU - Zolk, Oliver

AU - Ditz, Diana

AU - Pamminger, Torsten

AU - Zimmermann, Wolfram-H

AU - Jäckel, Elmar

AU - Harding, Sian E

AU - Boknik, Peter

AU - Neumann, Joachim

AU - Eschenhagen, Thomas

PY - 2003

Y1 - 2003

N2 - The protein phosphatase inhibitor-1 (PPI-1) inhibits phosphatase type-1 (PP1) only when phosphorylated by protein kinase A and could play a pivotal role in the phosphorylation/dephosphorylation balance. Rat cardiac PPI-1 was cloned by reverse transcriptase-polymerase chain reaction, expressed in Eschericia coli, evaluated in phosphatase assays, and used to generate an antiserum. An adenovirus was constructed encoding PPI-1 and green fluorescent protein (GFP) under separate cytomegalovirus promotors (AdPPI-1/GFP). A GFP-only virus (AdGFP) served as control. Engineered heart tissue (EHT) from neonatal rat cardiomyocytes and adult rat cardiac myocytes (ARCMs) were used as model systems. PPI-1 expression was determined in human ventricular samples by Northern blots. Compared with AdGFP, AdPPI-1/GFP-infected neonatal rat cardiomyocytes displayed a 73% reduction in PP1 activity. EHTs infected with AdPPI-1/GFP exhibited a fivefold increase in isoprenaline sensitivity. AdPPI-1/GFP-infected ARCMs displayed enhanced cell shortening as well as enhanced phospholamban phosphorylation when stimulated with 1 nM isoprenaline. PPI-1 mRNA levels were reduced by 57+/-12% in failing hearts with dilated and ischemic cardiomyopathy (n=8 each) compared with nonfailing hearts (n=8). In summary, increased PPI-1 expression enhances myocyte sensitivity to isoprenaline, indicating that PPI-1 acts as an amplifier in beta-adrenergic signaling. Decreased PPI-1 in failing human hearts could participate in desensitization of the cAMP pathway.

AB - The protein phosphatase inhibitor-1 (PPI-1) inhibits phosphatase type-1 (PP1) only when phosphorylated by protein kinase A and could play a pivotal role in the phosphorylation/dephosphorylation balance. Rat cardiac PPI-1 was cloned by reverse transcriptase-polymerase chain reaction, expressed in Eschericia coli, evaluated in phosphatase assays, and used to generate an antiserum. An adenovirus was constructed encoding PPI-1 and green fluorescent protein (GFP) under separate cytomegalovirus promotors (AdPPI-1/GFP). A GFP-only virus (AdGFP) served as control. Engineered heart tissue (EHT) from neonatal rat cardiomyocytes and adult rat cardiac myocytes (ARCMs) were used as model systems. PPI-1 expression was determined in human ventricular samples by Northern blots. Compared with AdGFP, AdPPI-1/GFP-infected neonatal rat cardiomyocytes displayed a 73% reduction in PP1 activity. EHTs infected with AdPPI-1/GFP exhibited a fivefold increase in isoprenaline sensitivity. AdPPI-1/GFP-infected ARCMs displayed enhanced cell shortening as well as enhanced phospholamban phosphorylation when stimulated with 1 nM isoprenaline. PPI-1 mRNA levels were reduced by 57+/-12% in failing hearts with dilated and ischemic cardiomyopathy (n=8 each) compared with nonfailing hearts (n=8). In summary, increased PPI-1 expression enhances myocyte sensitivity to isoprenaline, indicating that PPI-1 acts as an amplifier in beta-adrenergic signaling. Decreased PPI-1 in failing human hearts could participate in desensitization of the cAMP pathway.

M3 - SCORING: Zeitschriftenaufsatz

VL - 17

SP - 437

EP - 439

JO - FASEB J

JF - FASEB J

SN - 0892-6638

IS - 3

M1 - 3

ER -