Inhibition of prostacyclin-induced Ca2+ mobilization by phorbol esters in Ob1771 preadipocytes.
Vassaux G., Far DF., Gaillard D., Ailhaud G., Negrel R.
Animal Study, published in Prostaglandins (1993) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Prostaglandins (1993)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 7506432
- DOI
- 10.1016/0090-6980(93)90080-q
Abstract (original English)
In addition to cAMP production, a transient elevation of intracellular free Ca2+ has been shown to take place in preadipose cells upon stimulation by carbaprostacyclin (cPGI2), both messengers acting in synergy to initiate adipose cell differentiation (Vassaux, G., Gaillard, D., Ailhaud, G., and Négrel, R. (1992) J. Biol. Chem.267, 11092-11097). Further studies reported herein show that this Ca2+ transient is i) elicited by the natural prostaglandin PGI2, ii) independent of the presence of extracellular Ca2+, suggesting a mobilization of Ca2+ from intracellular pools and ii) unaffected by cAMP elevating agents. Moreover, and in contrast to the InsP3-dependent Ca2+ signal evoked by PGF2 alpha, that induced by PGI2 is fully abolished by pretreatment with phorbol esters (EC50: 1-5 nM). Furthermore, experiments designed to empty the Ca2+ pools, using PGI2 or PGF2 alpha as Ca2+ mobilizing agents as well as pretreatments with drugs, allow to conclude that PGI2 mobilizes Ca2+ from an InsP3 sensitive, ryanodine insensitive intracellular pool. Altogether, these results strongly suggest that PGI2 mobilizes Ca2+ from an intracellular store common to that affected by InsP3, by means of a mechanism which remains to be elucidated.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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