Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The generation of T-cell colonies from human peripheral blood lymphocytes is a sensitive in vitro measure of cell-mediated immunity, considered to be under different and/or additional regulatory controls than short-term liquid cultures. The influences of steroids (aldosterone, estradiol, diethylstilbestrol, hydrocortisone, prednisolone, progesterone, testosterone), prostaglandins (PGA1, PGA2, PGB1, PGB2, PGE1, PGE2, PGF1 alpha), bradykinin, cyclic adenosine monophosphate (AMP), cyclic guanosine monophosphate (GMP), epinephrine, glucagon, histamine, insulin, luteinizing hormone, luteotropic hormone, serotonin, and thyroxin on the generation of both T-cell colonies in semisolid phase and induction of transformation in liquid culture was assessed in parallel assays. Steroids uniformly suppressed both types of culture systems, although colony formation appeared more sensitive by several hours of magnitude. In contrast, significant differences in the response of lymphocytes in colony formation assay, compared to liquid transformation, was noted for the other agents. Prostaglandins significantly inhibited colony formation even in the presence of as little as 10(-12) M PGE2; however, liquid culture responses were suppressed only by higher concentrations (10(-5) M) and enhanced transformation was found at lower concentrations (10(-9) M). Bradykinin, glucagon, and luteinizing hormone did not significantly influence either colony formation or liquid transformation. In contrast, cyclic AMP inhibited and cyclic GMP stimulated colony formation and liquid transformation. Histamine, insulin, epinephrine, and serotonin all had significant positive or negative influences on colony formation in concentrations that produced no detectable effects using conventional liquid transformation assays. Finally, correlation analysis of drug effects for each system extends the thesis that these assays quantitate different parameters of T-cell function. T-lymphocyte colony formation is a promising diagnostic tool for rapid screening of immune modulating agents.
 ...
PMID:Pharmacologic and biochemical modulation of human T-lymphocyte colony formation: hormonal influences. 697 65

Experimental evidence has recently accumulated indicating that administration of some prostaglandins (PGs), particularly those of the E series, can evoke release of glucagon by the pancreatic alpha-cells. Virtually, all the in vitro studies (isolated perfused rat pancreas, isolated guinea-pig islets) agree that PGs can increase both basal and stimulated glucagon release. On the other hand, inhibition of PG synthesis with indomethacin blocks glucagon release. In rats and in normal humans, PGE1, but not PGA2 or PGF2a, causes a progressive rise of plasma glucagon levels. While in the rat this response seems independent of the adrenergic nervous system, in man the hyperglucagonemia induced by PGE1 is easily suppressed by propranolol, suggesting an interaction between the prostaglandin and the beta-receptors of the alpha-cell. Studies with inhibitors of PG synthesis in vivo have yielded conflicting results, depending on the particular experimental protocol used and on the type of inhibitor tested. In normal humans, it seems that acetylsalicylic acid (ASA) has no effect on glucagon response to arginine, tolbutamide and insulin-induced hypoglycemia. Conversely, a stimulator of PG synthesis, such as furosemide, increases glucagon response to an arginine pulse in man. In insulin-dependent diabetics, who present an exaggerated glucagon response to stimulants, ASA fails to alter glucagon response to arginine, but completely blunts the glucagon response to salbutamol, a weak beta-2 receptor agonist. In conclusion, these observations provide evidence in support to a role for PGs, at least PGE, in the contro of glucagon release.
 ...
PMID:Prostaglandins and the alpha-cell. 701 76