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Effect of peptide f-MDP-1 on calcium transient and contractility of cardiomyocytes isolated from adult rats

Grant number: 17/16804-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): December 01, 2017
Effective date (End): November 30, 2018
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Julio Cesar Batista Ferreira
Grantee:Lisley Santos Ramalho
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil


Despite scientific and therapeutic advances, ischemic heart disease is still the leading cause of death worldwide. This pathology is caused by decreased blood flow (ischemia), which promotes tissue damage and cell death according to the intensity and time of ischemia, thus causing biochemical and functional changes to the myocardium. Among these changes, the increase in intracellular calcium (Ca2+) levels is highlighted, since it is the key player in the cardiomyocyte contractility. In addition, the high levels of Ca2+ observed during the ischemic insult become exacerbated after tissue reperfusion, thus potentializing the injury and causing cell dysfunction and death by apoptosis and necrosis. Thus, the maintenance of cardiomyocytes calcium transient and contractility homeostasis is crucial to the heart. Recent experiments performed in our laboratory identified by mass spectrometry a single formylated peptide (named f-MDP-1), derived from a mitochondrial-encoded protein, which was present in all hearts submitted to ischemia/reperfusion injury, but not in the control group hearts (Normoxia). Next, our group synthesized this peptide and observed an important role of this synthetic peptide in preventing cell death induced by ischemia/reperfusion (unpublished data). However, its mechanism of action is still unknown. Considering the relevance of calcium homeostasis in the development and progression of cardiac damage induced by ischemia/reperfusion and its role in maintaining myocardium viability and contractile function, in the present study we will test the hypothesis that the peptide f-MDP-1 modulates positively the calcium transient and contractility in cardiomyocytes isolated from adult rats exposed to an ex vivo protocol of ischemia/reperfusion injury, thus being a possible mechanism associated with its protective effect against myocardial infarction. (AU)

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