Cardioprotective effect of VEGF and venom VEGF-like protein in acute myocardial ischemia in mice: effect on mitochondrial function.

Erij Messadi; Zohra Aloui; Elise Belaidi; Marie-Pascale Vincent; Elisabeth Couture-Lepetit; Ludovic Waeckel; Johanna Decorps; Nadine Bouby; Ammar Gasmi; Habib Karoui; Michel Ovize; François Alhenc-Gelas; Christine Richer

doi:10.1097/FJC.0000000000000045

Cardioprotective effect of VEGF and venom VEGF-like protein in acute myocardial ischemia in mice: effect on mitochondrial function.

Erij Messadi ^{1, 2, 3} Zohra Aloui ^{1, 4} Elise Belaidi ⁵ Marie-Pascale Vincent ³ Elisabeth Couture-Lepetit ⁵ Ludovic Waeckel ³ Johanna Decorps ⁵ Nadine Bouby ³ Ammar Gasmi ^{1, 4} Habib Karoui ^{1, 4} Michel Ovize ⁵ François Alhenc-Gelas ³ Christine Richer ³

1 UTM - Université Tunis El Manar

2 LR11IPT08 - Laboratoire des Venins et Biomolécules Thérapeutiques

3 Centre de Recherche des Cordeliers

4 LR11IPT04 - Laboratoire d'Epidémiologie Moléculaire et de Pathologie Expérimentale Appliquée aux Maladies Infectieuses

5 CarMeN - Laboratoire de recherche en cardiovasculaire, métabolisme, diabétologie et nutrition

Abstract : Coronary endothelial dysfunction is involved in cardiac ischemia-reperfusion (IR) injury. Vascular endothelial growth factor (VEGF) activates endothelial cells and exerts cardioprotective effects in isolated hearts. The recently discovered viper venom protein called increasing capillary permeability protein (ICPP) exerts VEGF-like effects in endothelial cells. We examined whether VEGF or ICPP can influence IR outcome in vivo in mice. Dosages of VEGF and ICPP were determined by preliminary blood pressure study. In IR, both the proteins administered intravenously at reperfusion reduced infarct size (IS) by 57% for VEGF and 52% for ICPP (P < 0.01). Pretreatment with a selective VEGFR2 receptor antagonist abolished the reduction in IS. VEGF and ICPP induced ERK phosphorylation in the myocardium. IR triggered mitochondrial pore opening and impaired mitochondrial respiratory function. These effects of IR were prevented by VEGF or ICPP, which increased mitochondrial calcium retention capacity by 37% compared with saline (P < 0.05) and improved mitochondrial respiratory function (by 71% and 65%, respectively for state 3, and 51% and 38% for state 4, P < 0.01 for VEGF). Thus, intravenous administration of VEGF or ICPP at reperfusion largely reduces IS in IR, through stimulation of VEGFR2 receptors. This effect is mediated, at least in part, by improvement of IR-induced mitochondrial dysfunction.

Keywords : cardiac ischemia reperfusion VEGF mitochondria myocardial infarction

Type de document :

Article dans une revue

Journal of Cardiovascular Pharmacology, Lippincott, Williams & Wilkins, 2014, 63 (3), pp.274-81. 〈10.1097/FJC.0000000000000045〉

Domaine :

Sciences du Vivant [q-bio]

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Soumis le : mardi 5 septembre 2017 - 11:18:23
Dernière modification le : mercredi 21 mars 2018 - 18:57:30

Cardioprotective effect of VEGF and venom VEGF-like protein in acute myocardial ischemia in mice: effect on mitochondrial function.

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Cardioprotective effect of VEGF and venom VEGF-like protein in acute myocardial ischemia in mice: effect on mitochondrial function.

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