Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes

β-Adrenergic stimulation increases cAMP in cardiac cells to induce PKA-mediated phosphorylation of various proteins regulating heart function, such as the L-type Ca 2+ channels which carry I Ca,L and trigger cardiac contraction. Phosphodiesterases (PDEs) 3 and 4 are the main cAMP degrading enzymes i...

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Main Author: Leroy, Jerome (author)
Other Authors: Abi-Gerges, Aniella (author), Richter, Wito (author), Nikolaev, Viacheslav O. (author), Engelhardt, Stefan (author), Lohse, Martin J. (author), Conti, Marco (author), Fischmeister, Rodolphe (author), Vandecasteele, Gregoire (author)
Format: article
Published: 2007
Online Access:http://hdl.handle.net/10725/6362
http://dx.doi.org/10.1117/j.yjmcc.2007.03.139
http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php
https://www.jmmc-online.com/article/S0022-2828(07)00195-2/abstract#articleInformation
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author Leroy, Jerome
author2 Abi-Gerges, Aniella
Richter, Wito
Nikolaev, Viacheslav O.
Engelhardt, Stefan
Lohse, Martin J.
Conti, Marco
Fischmeister, Rodolphe
Vandecasteele, Gregoire
author2_role author
author
author
author
author
author
author
author
author_facet Leroy, Jerome
Abi-Gerges, Aniella
Richter, Wito
Nikolaev, Viacheslav O.
Engelhardt, Stefan
Lohse, Martin J.
Conti, Marco
Fischmeister, Rodolphe
Vandecasteele, Gregoire
author_role author
dc.creator.none.fl_str_mv Leroy, Jerome
Abi-Gerges, Aniella
Richter, Wito
Nikolaev, Viacheslav O.
Engelhardt, Stefan
Lohse, Martin J.
Conti, Marco
Fischmeister, Rodolphe
Vandecasteele, Gregoire
dc.date.none.fl_str_mv 2007
2017-10-19T12:43:47Z
2017-10-19T12:43:47Z
2017-10-19
dc.identifier.none.fl_str_mv 0022-2828
http://hdl.handle.net/10725/6362
http://dx.doi.org/10.1117/j.yjmcc.2007.03.139
Leroy, J., Abi-Gerges, A., Richter, W., Nikolaev, V. O., Engelhardt, S., Lohse, M. J., ... & Vandecasteele, G. (2007). Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa, L in adult rat ventricular myocytes. Journal of Molecular and Cellular Cardiology, 42(6), S49.
http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php
https://www.jmmc-online.com/article/S0022-2828(07)00195-2/abstract#articleInformation
dc.language.none.fl_str_mv en
dc.relation.none.fl_str_mv Journal of Molecular and Cellular Cardiology
dc.rights.*.fl_str_mv info:eu-repo/semantics/openAccess
dc.title.none.fl_str_mv Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
dc.type.none.fl_str_mv Article
info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/article
description β-Adrenergic stimulation increases cAMP in cardiac cells to induce PKA-mediated phosphorylation of various proteins regulating heart function, such as the L-type Ca 2+ channels which carry I Ca,L and trigger cardiac contraction. Phosphodiesterases (PDEs) 3 and 4 are the main cAMP degrading enzymes in cardiomyocytes and modulate the β-adrenergic regulation of I Ca,L but the significance of this dual regulation remains elusive. Here, we compared the participation of PDE3 and PDE4 in the β-adrenergic regulation of intracellular cAMP and I Ca,L using the FRET-based indicator Epac2-cAMPS and the whole-cell patch-clamp technique in adult rat ventricular myocytes. Isoprenaline (Iso, 100 nM, 15 s) induced a transient increase in both [cAMP] i and I Ca,L. PDE3 inhibition with cilostamide (1 μM) neither modified [cAMP] i nor I Ca,L transients, whereas PDE4 inhibition with Ro-201724 (10 μM) prolonged both signals. When both PDE3 and PDE4 were blocked, [cAMP] i and I Ca,L signals became nearly stable. PKA inhibition with PKI prolonged the β-adrenergic cAMP transient and this effect was not additive with that of Ro201724. Thus, PDE4 is predominant to terminate β-adrenergic induced [cAMP] i increase and I Ca,L stimulation in adult rat cardiomyocytes.
eu_rights_str_mv openAccess
format article
id LAURepo_e93efcc919cdd2fc0f9bf14c98278f6b
identifier_str_mv 0022-2828
Leroy, J., Abi-Gerges, A., Richter, W., Nikolaev, V. O., Engelhardt, S., Lohse, M. J., ... & Vandecasteele, G. (2007). Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa, L in adult rat ventricular myocytes. Journal of Molecular and Cellular Cardiology, 42(6), S49.
language_invalid_str_mv en
network_acronym_str LAURepo
network_name_str Lebanese American University repository
oai_identifier_str oai:laur.lau.edu.lb:10725/6362
publishDate 2007
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spelling Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytesLeroy, JeromeAbi-Gerges, AniellaRichter, WitoNikolaev, Viacheslav O.Engelhardt, StefanLohse, Martin J.Conti, MarcoFischmeister, RodolpheVandecasteele, Gregoireβ-Adrenergic stimulation increases cAMP in cardiac cells to induce PKA-mediated phosphorylation of various proteins regulating heart function, such as the L-type Ca 2+ channels which carry I Ca,L and trigger cardiac contraction. Phosphodiesterases (PDEs) 3 and 4 are the main cAMP degrading enzymes in cardiomyocytes and modulate the β-adrenergic regulation of I Ca,L but the significance of this dual regulation remains elusive. Here, we compared the participation of PDE3 and PDE4 in the β-adrenergic regulation of intracellular cAMP and I Ca,L using the FRET-based indicator Epac2-cAMPS and the whole-cell patch-clamp technique in adult rat ventricular myocytes. Isoprenaline (Iso, 100 nM, 15 s) induced a transient increase in both [cAMP] i and I Ca,L. PDE3 inhibition with cilostamide (1 μM) neither modified [cAMP] i nor I Ca,L transients, whereas PDE4 inhibition with Ro-201724 (10 μM) prolonged both signals. When both PDE3 and PDE4 were blocked, [cAMP] i and I Ca,L signals became nearly stable. PKA inhibition with PKI prolonged the β-adrenergic cAMP transient and this effect was not additive with that of Ro201724. Thus, PDE4 is predominant to terminate β-adrenergic induced [cAMP] i increase and I Ca,L stimulation in adult rat cardiomyocytes.PublishedN/A2017-10-19T12:43:47Z2017-10-19T12:43:47Z20072017-10-19Articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article0022-2828http://hdl.handle.net/10725/6362http://dx.doi.org/10.1117/j.yjmcc.2007.03.139Leroy, J., Abi-Gerges, A., Richter, W., Nikolaev, V. O., Engelhardt, S., Lohse, M. J., ... & Vandecasteele, G. (2007). Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa, L in adult rat ventricular myocytes. Journal of Molecular and Cellular Cardiology, 42(6), S49.http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.phphttps://www.jmmc-online.com/article/S0022-2828(07)00195-2/abstract#articleInformationenJournal of Molecular and Cellular Cardiologyinfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/63622021-03-19T10:43:10Z
spellingShingle Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
Leroy, Jerome
status_str publishedVersion
title Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
title_full Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
title_fullStr Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
title_full_unstemmed Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
title_short Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
title_sort Role of PDE3 and PDE4 for β-adrenergic control of cAMP and ICa,L in adult rat ventricular myocytes
url http://hdl.handle.net/10725/6362
http://dx.doi.org/10.1117/j.yjmcc.2007.03.139
http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php
https://www.jmmc-online.com/article/S0022-2828(07)00195-2/abstract#articleInformation