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Thrombin, phorbol ester, and cAMP regulate thrombin receptor protein and mRNA expression by different pathways
1INSERM U 64, Paris, France.
The Journal of Biological Chemistry
|January 13, 1995
Summary
Thrombin receptor regulation differs: homologous down-regulation involves protein degradation, while heterologous down-regulation, via protein kinase C or cAMP pathways, affects receptor mRNA expression.
Area of Science:
- Cellular signaling
- Molecular biology
- Renal physiology
Background:
- Thrombin receptors mediate cellular responses.
- Understanding receptor regulation is crucial for cellular function.
Purpose of the Study:
- Investigate thrombin receptor protein and mRNA regulation.
- Differentiate homologous and heterologous down-regulation mechanisms.
Main Methods:
- Utilized human mesangial cells.
- Stimulated cells with thrombin, phorbol 12-myristate 13-acetate (PMA), and prostaglandin E1 (PGE1).
- Assessed receptor protein and mRNA levels, and employed protein kinase C inhibitors.
Main Results:
- Thrombin caused homologous down-regulation of thrombin receptor protein without affecting mRNA.
- PMA and PGE1 induced heterologous down-regulation, reducing both protein and mRNA levels.
- Homologous regulation was independent of protein kinase C; heterologous regulation involved protein kinase C and cAMP pathways.
Conclusions:
- Homologous and heterologous down-regulation of thrombin receptors employ distinct mechanisms.
- Protein degradation underlies homologous down-regulation.
- Inhibition of mRNA expression contributes to heterologous down-regulation.