Neuregulin-1beta1 rapidly modulates nitric oxide synthesis and calcium handling in rat cardiomyocytes.

Aims: The ErbB-neuregulin-1β1 (Nrg1β1) pathway is required for cardiac development and exerts chronic effects on the postnatal adult heart. Long-term application of Nrg1β1 results in hypertrophy and protection against oxidative stress and cytotoxic agents. We performed experiments with acute Nrg1β1 treatment to find evidence for a further protective role due to rapid modulation of adult cardiomyocyte function.

Growth hormone-releasing hormone promotes survival of cardiac myocytes in vitro and protects against ischaemia-reperfusion injury in rat heart.

Aims: The hypothalamic neuropeptide growth hormone-releasing hormone (GHRH) stimulates GH synthesis and release in the pituitary. GHRH also exerts proliferative effects in extrapituitary cells, whereas GHRH antagonists have been shown to suppress cancer cell proliferation. We investigated GHRH effects on cardiac myocyte cell survival and the underlying signalling mechanisms.

Homing of annexin-labeled stem cells to apoptotic cells.

Ischemic diseases are characterized by the presence of pro-apoptotic stimuli, which initiate a cascade of processes that lead to cell injury and death. Several molecules and events represent detectable indicators of the different stages of apoptosis. Among these indicators is phosphatidylserine (PS) translocation from the inner to the outer leaflet of the plasma membrane, which can be detected by annexinV (ANXA5) conjugation.

Endothelium-derived nitric oxide mediates the antiadrenergic effect of human vasostatin-1 in rat ventricular myocardium.

Vasostatins (VSs) are vasoactive peptides derived from chromogranin A (CgA), a protein contained in secretory granules of chromaffin and other cells. The negative inotropic effect and the reduction of isoproterenol (Iso)-dependent inotropism induced by VSs in the heart suggest that they have an antiadrenergic function. However, further investigation of the mechanisms of action of VSs is needed.