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Amphotericin B inhibits the serum-induced expression of tissue transglutaminase in murine peritoneal macrophages
Abstract:
Culture of mouse resident peritoneal macrophages (PM) in serum-containing medium causes a rapid and marked induction of the enzyme tissue transglutaminase (tissue TGase). Coculture of PM with amphotericin B (AmpB) inhibited the serum-induced expression and accumulation of tissue TGase. The AmpB-mediated inhibition of tissue TGase was specific and was due to inhibition of enzyme synthesis. The serum-dependent induction of tissue TGase was inhibited in a dose-dependent fashion, and a complete inhibition was observed at 1.5 microgram/ml dose of AmpB. The inhibition was reversible; however, the time of recovery depended on the dose and time of exposure of the cells to AmpB. The present studies suggest that AmpB-mediated inhibition of tissue TGase is due to inhibition of the uptake of serum retinoids by PM.
Insights
Amphotericin B (AmpB) inhibits the production of tissue transglutaminase (tTG) in mouse macrophages by blocking serum retinoid uptake. This inhibition is dose-dependent and reversible, impacting enzyme synthesis.
Area of Science:
- Cell Biology
- Enzymology
- Pharmacology
Background:
- Serum-containing media rapidly induce tissue transglutaminase (tTG) in mouse peritoneal macrophages (PM).
- Understanding the regulation of tTG expression is crucial for cellular processes.
Purpose of the Study:
- To investigate the effect of amphotericin B (AmpB) on serum-induced tissue transglutaminase (tTG) expression in PM.
- To elucidate the mechanism behind AmpB-mediated inhibition of tTG synthesis.
Main Methods:
- Culture of mouse resident peritoneal macrophages (PM).
- Treatment with amphotericin B (AmpB) at varying doses and durations.
- Measurement of tissue transglutaminase (tTG) expression and accumulation.
Main Results:
- AmpB significantly inhibited serum-induced tTG expression and accumulation in PM.
- The inhibition was dose-dependent, with complete suppression at 1.5 µg/ml AmpB.
- AmpB's effect was specific to enzyme synthesis and reversible, with recovery time dependent on exposure.
Conclusions:
- AmpB inhibits tTG synthesis in PM by interfering with the uptake of serum retinoids.
- This mechanism highlights a novel regulatory pathway for tTG expression.
- AmpB's action provides insights into retinoid metabolism and its impact on enzyme production.