Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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Query: EC:3.4.21.73 (
urokinase-type plasminogen activator
)
10,685
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Pro-opiomelanocortin-derived peptides,
alpha-MSH
and beta-endorphin, are synthesized and secreted by Leydig cells, and are believed to have paracrine effects on Sertoli cells in the testis. Peptides with MSH activity stimulate adenylate cyclase and cAMP accumulation in Sertoli cell-enriched cultures. The purpose of the present study was to determine whether such peptides would affect Sertoli cell parameters, such as aromatase and plasminogen activator activities, that are known to be regulated by cAMP.
alpha-MSH
stimulated aromatase activity in Sertoli cell-enriched cultures prepared from 10-day-old rats and this effect was potentiated by methyl isobutylxanthine (MIX). The combination of
alpha-MSH
plus MIX was not as potent as FSH.
alpha-MSH
, des-acetyl-
alpha-MSH
, beta-MSH, ACTH(1-13), and ACTH(1-24) stimulated aromatase activity to a similar extent, suggesting that Sertoli cells do not distinguish between the activities of these peptides.
alpha-MSH
potentiated the action of dbcAMP and forskolin on Sertoli cell aromatase, but unexpectedly had no effect on the action of either half-maximal or maximal doses of FSH. The regulation of plasminogen activator was examined next;
urokinase
was markedly suppressed by FSH in 10-day-old Sertoli cells. Although neither
alpha-MSH
nor MIX alone had an effect on
urokinase
secretion, in combination they were as effective as FSH. In 10-day-old Sertoli cells each of these peptides had little or no effect on tissue plasminogen activator.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Estradiol and plasminogen activator secretion by cultured rat Sertoli cells in response to melanocyte-stimulating hormones. 247 57
The presence of the ancient anti-inflammatory peptide alpha-melanocyte-stimulating hormone [
alpha-MSH
(1-13), SYSMEHFRWGKPV] in barrier organs such as gut and skin suggests a role in the nonspecific (innate) host defense.
alpha-MSH
and and its carboxy-terminal tripeptide (11-13, KPV) were determined to have antimicrobial influences against two major and representative pathogens: Staphylococcus aureus and Candida albicans.
alpha-MSH
peptides significantly inhibited S. aureus colony formation and reversed the enhancing effect of
urokinase
on colony formation. Antimicrobial effects occurred over a broad range of concentrations including the physiological (picomolar) range. Small concentrations of
alpha-MSH
peptides likewise reduced viability and germ tube formation of the yeast C. albicans. Antimicrobial influences of
alpha-MSH
peptides could be mediated by their capacity to increase cellular cAMP. Indeed, this messenger was significantly augmented in peptide-treated yeast and the potent adenylyl cyclase inhibitor dideoxyadenosine (ddAdo) partly reversed the killing activity of
alpha-MSH
peptides. Reduced killing of pathogens is a detrimental consequence of therapy with anti-inflammatory drugs. Because
alpha-MSH
has potent anti-inflammatory effects we determined influences of
alpha-MSH
on C. albicans and S. aureus killing by human neutrophils.
alpha-MSH
peptides did not reduce killing but rather enhanced it, likely as a consequence of the direct antimicrobial activity.
alpha-MSH
peptides that combine antipyretic, anti-inflammatory, and antimicrobial effects could be useful in treatment of disorders in which infection and inflammation coexist.
...
PMID:Antimicrobial effects of alpha-MSH peptides. 1909 31