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Angiocidin, a tumor-inhibiting novel protein discovered by Temple University researchers, may also have a role as a new therapeutic application in treating leukemia, according to a study by the researchers. The study, "The Novel Angiogenic Inhibitor, Angiocidin, Induces Differentiation of Monocytes to Macropahges," will be published in the July 15 issue of the journal Cancer Research (http://cancerres.aacrjournals.org/future/68.14.shtml). The research was done by Temple biology doctoral student Anita Gaurnier-Hausser under the direction of George Tuszynski, a professor of neuroscience in Temple's School of Medicine and a professor of biology in Temple's College of Science and Technology.
Source: Cyclic GMP-linked pathway for renin secretion., Kidney international, Volume 46, Issue 6, UNITED STATES (1995)
ISBN: 0085-2538
Call Number: 7700014
Accession Number: 7700014
URL:http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=7700014&retmode=ref&cmd=prlinks
Keywords: Cyclic-GMP Phosphodiesterases Aminoquinolines Animals Atrial Natriuretic Factor; Cyclic GMP; Guanylate Cyclase; Kidney Cortex; Methylene Blue; Nitroprusside; Peptide Fragments; Purinones; Rats; Renin; Second Messenger Systems;
Abstract: The role of cGMP as a second messenger for renin secretion is contentious. This was investigated using a superfused collagenase-dispersed rat kidney cortex cell preparation devoid of indirect influences on renin secretion. Nitroprusside, atriopeptin II and 8-Br-cGMP all increased renin release but the dose-response relationships were biphasic. At low dose ranges there was a positive correlation between increasing drug concentration and renin secretion, but at high drug concentrations, a negative correlation was apparent. Methylene blue, a guanylate cyclase inhibitor, also suppressed baseline renin release at 10(-5) and 10(-6) M, but stimulated release at 10(-3) M. Using mid-range drug concentrations, the cGMP specific phosphodiesterase inhibitor MB22948 potentiated renin release in response to nitroprusside and 8-Br-cGMP. Inhibition of guanylate cyclase with either methylene blue or LY83583 attenuated renin release in response to nitroprusside, but, as expected, had no effect on 8-Br-cGMP induced release. We conclude that, under physiological conditions, cGMP is a stimulatory second messenger for renin release. This activity is mimicked at low dose ranges by 8-Br-cGMP, nitroprusside and atriopeptin II. In response to high doses of these drugs an unknown inhibitory pathway is activated and this opposes, in a dose-related manner, the stimulatory actions of cGMP for renin release.
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