Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion.

Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Research Abstract Details 

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Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Abstract Text:

D-Y Li,L Tao,H Liu,T A Christopher,B L Lopez,X L Ma,

Objective: Experimental results from cultured cells suggest that there is cross-talk between nitric oxide (NO) and extracellular signal-regulated kinase (ERK) in their anti-apoptotic effect. However, the cross-talk between these two molecules in either direction has not been confirmed in the whole organ or whole animal level. The aim of the present study was to determine whether ERK may play a role in the anti-apoptotic and cardioprotective effects of NO in myocardial ischemia/reperfusion (MI/R). Methods: Isolated perfused mouse hearts were subjected to 20 min of global ischemia and 120 min of reperfusion and treated with vehicle or an NO donor (SNAP, 10 muM) during reperfusion. To determine the role of ERK1/2 in the anti-apoptotic and cardioprotective effects of NO, hearts were pre-treated (10 min before ischemia) with U0126, a selective MEK1/2 inhibitor (1 muM). Results: Treatment with SNAP exerted significant cardioprotective effects as evidenced by reduced cardiac apoptosis (TUNEL and caspase 3 activity, p < 0.01), and improved cardiac functional recovery (p < 0.01). In addition, treatment with SNAP resulted in a 2.5-fold increase in ERK activation when compared with heart receiving vehicle. Pre-treatment with U0126 slightly increased post-ischemic myocardial apoptosis but had no significant effect on cardiac functional recovery in this isolated perfused heart model. However, treatment with U0126 completely blocked SNAP-induced ERK activation and markedly, although not completely, inhibited the cardioprotection exerted by SNAP. Conclusion: These results demonstrate that nitric oxide exerts its anti-apoptotic and cardioprotective effects, at least in part, by activation of ERK in ischemic/reperfused heart.

Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Publishing Authors By Initials

DY Li,L Tao,H Liu,TA Christopher,BL Lopez,XL Ma,

For similar inorganic chemicals: free radicals: nitric oxide research abstracts see: inorganic chemicals: free radicals: nitric oxide research

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Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Apoptosis : an international journal on programmed

VOLUME: 11

Page Numbers: 923-30

Journal Abbreviation: Apoptosis

ISSN: 1360-8185

DAY: 3

MONTH: Jun

YEAR: 2006

Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9712129

Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Keywords Mesh Terms:

KEYWORDS: Nitric Oxide

MESH TERMS: physiology

Chemical & Substance for Abstract: Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion. Information

Substance Name: Extracellular Signal-Regulated MAP Kinas

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Role of ERK1/2 in the anti-apoptotic and cardioprotective effects of nitric oxide after myocardial ischemia and reperfusion.

AFFILIATION: Department of Emergency Medicine, Thomas Jefferson University, 1020 Sansom Street, PA 19107, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-63828

ACRONYM: HL

MEDLINETA: Apoptosis

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