Contact stimulation of the proliferation of cultured chick embryo cells

It was reported elsewhere (Gasparian, Grigorian, 1989a) that in the secondary chick embryo cell culture, after its superinoculation with additional homologous cells, the cell population density increased and the cell proliferation was activated. It has been shown in the present paper that the cell proliferation rate increase after inoculation of fixed cells, as well. The results obtained are discussed as a direct evidence for growth-stimulating effect of contacts between homologous cells.     

Adrenal cortex cytochrome c]

The method of preparation of highly purified cytochrome c from bovine adrenal cortex is described. Absolute spectra of the protein in reduced and oxidized states and some its physico-chemical properties are investigated.     

Biochemical features of platelet alpha2-adrenergic receptors and their connection with an increase in concentration of intracellular Ca2+

Epinephrine (E) and norepinephrine (NE) alone did not increase free intracellular Ca2+ ([Ca2+]i) in human platelets loaded with Quin-2 or Fura-2; however, they did potentiate the effects of vasopressin (VP), serotonin (S) and platelet activating factor (PAF). The synergism in [Ca2+]i increase was also obtained in the presence of VP together with PAF, S with PAF as well as VP with S. The effect of E or NE was blocked by yohimbine and phentolamine. Prazosin was less effective, while propranolol had no effect at all. Clonidine did not potentiate the effects of VP, S or PAF on [Ca2+]i; however, it did block the potentiation induced by E or NE. E potentiated the VP-induced 45Ca2+ uptake as well as VP-stimulated inositol 1,4,5-trisphosphate (IP3) formation. E alone did not change significantly the level of IP3 in platelets, nor did it influence the cyclic AMP level. The experimental results suggest that both Ca2+ influx and polyphosphoinositide breakdown underlie the mechanism of potentiation.     

Effects of hypoxia on phosphoinositide turnover and adenylate cyclase system in cultured endothelial cells]

By studying the effects of oxygen deficiency upon signal-transducing system it has been shown that in long hypobaric hypoxia activates PI-turnover in cultured human endothelial cells. The sensitivity of cells to histamine was decreased as well as the adenylate cyclase activity in membranes of this cells. The amount of beta-adrenoreceptors was not influenced significantly. Incubation of endothelial cells with histamine (10(-5) M) and phorbol ester (10(-9) M) = activator of protein kinase C within 1-2 h resulted in desensitization of cellular responses which can be seen not only as a disappearance of histamine-induced activation of PI-turnover but also as a decrease of beta-adrenoreceptor amount and adenylate cyclase activity. It seems that hypoxia may change the action of Ca-mobilizing hormones on PI-turnover and suppress adenylate cyclase in human endothelial cells. However the effects of hypoxia on signal-transducing systems in this cells are developed slower than those of Ca-mobilizing hormones.