Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis.

Abstract

The ability of human choriogonadotropin (hCG) to regulate its receptors and target cell responses has been studied in a clonal strain of cultured Leydig tumor cells (MA-10). Exposure of the MA-10 cells to hCG results in decrease in hCG binding activity which is dependent on time and the concentration of hCG. This decrease is due to a change in the number of receptors rather than in the affinity of the receptors, and it is accompanied by a corresponding reduction in the ability of hCG to stimulate steroidogenesis. Exposure of the MA-10 cells to hCG also resulted in a reduction of the steroidogenic responses to cholera toxin and 8-Br-adenosine cyclic 3',5'-monophosphate. The hCG-induced loss of steroidogenic responses to these stimuli seems to be due to the stimulation of steroidogenesis rather than to the decrease in hCG receptors because it also can be induced when steroidogenesis is stimulated with cholera toxin or 8-Br-adenosine 3',5'-monophosphate under conditions such that the number of hCG receptors is not reduced.

• Authors: D A Freeman, M Ascoli
• Journal: Proceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 78 Issue 10 Pg. 6309-13 (Oct 1981) ISSN: 0027-8424 [Print] United States
• PMID: 6273862 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Chorionic Gonadotropin
• DNA, Neoplasm
• Receptors, Cell Surface
• Receptors, LH
• 8-Bromo Cyclic Adenosine Monophosphate
• Progesterone
• Cholera Toxin
• Cyclic AMP

Topics

• 8-Bromo Cyclic Adenosine Monophosphate
• Cells, Cultured
• Cholera Toxin (pharmacology)
• Chorionic Gonadotropin (pharmacology, physiology)
• Cyclic AMP (analogs & derivatives, pharmacology)
• DNA, Neoplasm (biosynthesis)
• Female
• Humans
• Kinetics
• Leydig Cell Tumor (physiopathology)
• Ovarian Neoplasms (physiopathology)
• Progesterone (biosynthesis)
• Receptors, Cell Surface (physiology)
• Receptors, LH