TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk

Introduction: Tumour Necrosis Factor alpha (TNFα) contributes to cardiac dysfunction following ischaemia-reperfusion. Nonetheless, brief exposure to exogenous low doses of TNFα can mimic ischaemic preconditioning and thus be cardio-protective. The extracellular signal-regulated kinase (Erk) has been...

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Autores principales:	Sarin Somers, Aurelien Engerer, Sandrine Lecour
Formato:	article
Lenguaje:	EN
Publicado:	South African Heart Association 2017
Materias:	tumour necrosis factor alpha (tnfα) extracellular signal-regulated kinase (erk) ischaemic preconditioning Diseases of the circulatory (Cardiovascular) system RC666-701
Acceso en línea:	https://doaj.org/article/84d0d950263a4a23b28975884a299afd
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spelling	oai:doaj.org-article:84d0d950263a4a23b28975884a299afd2021-11-22T08:43:05ZTNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk10.24170/6-3-19861996-67412071-4602https://doaj.org/article/84d0d950263a4a23b28975884a299afd2017-04-01T00:00:00Zhttps://www.journals.ac.za/index.php/SAHJ/article/view/1986https://doaj.org/toc/1996-6741https://doaj.org/toc/2071-4602Introduction: Tumour Necrosis Factor alpha (TNFα) contributes to cardiac dysfunction following ischaemia-reperfusion. Nonetheless, brief exposure to exogenous low doses of TNFα can mimic ischaemic preconditioning and thus be cardio-protective. The extracellular signal-regulated kinase (Erk) has been implicated in the protection against ischaemia-reperfusion and is known to be activated by TNFα. However, whether Erk activation contributes to TNFα-induced cardio-protection remains unknown. Methods: PD 98059 (10μM), an Erk inhibitor, was used to evaluate the role of this prosurvival kinase with respect to infarct size (expressed as a percentage of the area at risk) in isolated rat hearts subjected to ischaemic preconditioning (IPC) or TNFα preconditioning (TNFαP). Western blot analyses were used to determine the degree of Erk phosphorylation after the application of the preconditioning stimulus. Results: Pre-treatment of the hearts with 0.5ng/ml of TNFα (for 7min) or 2 cycles of 5min ischaemia-reperfusion prior to 30min regional index ischaemia and 2h of reperfusion reduced the infarct size by 76% and 88%, respectively, versus control. Western blot analysis of isolated rat hearts revealed that IPC but not TNFαP activated phosphorylation of Erk (+54% for IPC vs. control). Coadministration of PD 98059 during the preconditioning stimulus did not influence the infarct size. Conclusion: These findings confirm that activation of TNFα may be considered as a novel therapeutic approach against ischaemic heart disease and that its effect is independent of the activation of the classic prosurvival factor Erk.Sarin SomersAurelien EngererSandrine LecourSouth African Heart Associationarticletumour necrosis factor alpha (tnfα)extracellular signal-regulated kinase (erk)ischaemic preconditioningDiseases of the circulatory (Cardiovascular) systemRC666-701ENSA Heart Journal, Vol 6, Iss 3, Pp 168-172 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	tumour necrosis factor alpha (tnfα) extracellular signal-regulated kinase (erk) ischaemic preconditioning Diseases of the circulatory (Cardiovascular) system RC666-701
spellingShingle	tumour necrosis factor alpha (tnfα) extracellular signal-regulated kinase (erk) ischaemic preconditioning Diseases of the circulatory (Cardiovascular) system RC666-701 Sarin Somers Aurelien Engerer Sandrine Lecour TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
description	Introduction: Tumour Necrosis Factor alpha (TNFα) contributes to cardiac dysfunction following ischaemia-reperfusion. Nonetheless, brief exposure to exogenous low doses of TNFα can mimic ischaemic preconditioning and thus be cardio-protective. The extracellular signal-regulated kinase (Erk) has been implicated in the protection against ischaemia-reperfusion and is known to be activated by TNFα. However, whether Erk activation contributes to TNFα-induced cardio-protection remains unknown. Methods: PD 98059 (10μM), an Erk inhibitor, was used to evaluate the role of this prosurvival kinase with respect to infarct size (expressed as a percentage of the area at risk) in isolated rat hearts subjected to ischaemic preconditioning (IPC) or TNFα preconditioning (TNFαP). Western blot analyses were used to determine the degree of Erk phosphorylation after the application of the preconditioning stimulus. Results: Pre-treatment of the hearts with 0.5ng/ml of TNFα (for 7min) or 2 cycles of 5min ischaemia-reperfusion prior to 30min regional index ischaemia and 2h of reperfusion reduced the infarct size by 76% and 88%, respectively, versus control. Western blot analysis of isolated rat hearts revealed that IPC but not TNFαP activated phosphorylation of Erk (+54% for IPC vs. control). Coadministration of PD 98059 during the preconditioning stimulus did not influence the infarct size. Conclusion: These findings confirm that activation of TNFα may be considered as a novel therapeutic approach against ischaemic heart disease and that its effect is independent of the activation of the classic prosurvival factor Erk.
format	article
author	Sarin Somers Aurelien Engerer Sandrine Lecour
author_facet	Sarin Somers Aurelien Engerer Sandrine Lecour
author_sort	Sarin Somers
title	TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
title_short	TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
title_full	TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
title_fullStr	TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
title_full_unstemmed	TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk
title_sort	tnfα-induced cardioprotection is independent of the activation of the prosurvival kinase erk
publisher	South African Heart Association
publishDate	2017
url	https://doaj.org/article/84d0d950263a4a23b28975884a299afd
work_keys_str_mv	AT sarinsomers tnfainducedcardioprotectionisindependentoftheactivationoftheprosurvivalkinaseerk AT aurelienengerer tnfainducedcardioprotectionisindependentoftheactivationoftheprosurvivalkinaseerk AT sandrinelecour tnfainducedcardioprotectionisindependentoftheactivationoftheprosurvivalkinaseerk
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TNFα-induced cardioprotection is independent of the activation of the prosurvival kinase Erk

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