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Revista chilena de cardiología

versión On-line ISSN 0718-8560

Resumen

ESPINOZA, Cristián et al. Policystin-1 protects cardiomyocytes from mechanical stress induced necrosis. Rev Chil Cardiol [online]. 2019, vol.38, n.1, pp.29-36. ISSN 0718-8560.  http://dx.doi.org/10.4067/S0718-85602019000100029.

Background:

Cardiomyocytes death is a determining factor in the development of cardiac dysfunction after myocardial infarction and heart failure. The change in BCL-2 family protein expression regulates both cell death and survival pathways, whereas BCL-2 is an anti-apoptotic protein and NIX induces necrosis and/or apoptosis. Polycystin-1 (PC1) is a crucial mechanosensor for cardiac contractile function. However, its role in cardiomyocyte survival during mechanical stress is unknown.

Aim:

To study the relationship of PC1 with mechanical stretch-death in cardiomyocytes and the BCL-2, and NIX proteins. Methods. Controls or deficient expression of PC1 neonatal rat ventricular myocytes were stimulated with hypoosmotic solution (HS) and used as a model of mechanical stress. Necrosis or apoptosis cell death, BCL-2 and NIX protein levels were measured.

Results:

Deficient expression of PC1 increases cardiomyocyte necrosis and NIX protein levels in cells stimulated with HS. Mechanical stress induces basal apoptosis related to a decrease in BCL-2, independent of PC1 expression.

Conclusion:

PC1 protects cardiomyocytes from mechanical stress necrosis, at least in part, by regulating NIX protein levels.

Palabras clave : cardiomyocyte; cell death; mechanical stretch; Polycystin-1.

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