Binding of progesterone to cell surfaces of human granulosa-lutein cells
Autor: | Edward V. Younglai, Yanjing Wu, Thomas M Price, Warren G. Foster, Derek K. Lobb |
---|---|
Rok vydání: | 2006 |
Předmět: |
endocrine system
medicine.medical_specialty Endocrinology Diabetes and Metabolism Blotting Western Clinical Biochemistry Granulosa cell tumour Biology Biochemistry Cell membrane Endocrinology Cell surface receptor Internal medicine Progesterone receptor medicine Humans Ovarian follicle Granulosa Lutein Cell Receptor Molecular Biology Progesterone Binding Sites Granulosa Cells urogenital system Cell Membrane Lutein Cell Biology medicine.disease Cell biology medicine.anatomical_structure Molecular Medicine Female Luteinizing hormone |
Zdroj: | The Journal of Steroid Biochemistry and Molecular Biology. 101:61-67 |
ISSN: | 0960-0760 |
DOI: | 10.1016/j.jsbmb.2006.06.018 |
Popis: | Progesterone is produced by granulosa cells under the influence of luteinizing hormone. Nuclear progesterone receptors have been found in rat granulosa cells. Human granulosa-lutein cells rapidly respond to progesterone with an increase in intracellular calcium suggesting the existence of a nongenomic mechanism. This study was conducted to determine whether binding of progesterone to granulosa cells could occur at the membrane. Granulosa cells were obtained from an in vitro fertilization program and examined immunohistochemically with an antiserum to membrane progesterone receptors. Approximately 14-70% of freshly harvested or cultured granulosa cells of six patients showed a positive reaction to the antiserum, limited to the cell membrane. Western blot analysis of homogenates of granulosa cells and a granulosa cell tumour confirmed the presence of progesterone receptors A, B and C and low amounts of a putative membrane receptor. These results demonstrate that the plasma membranes of human granulosa cells possess binding components for progesterone which may be involved in its nongenomic mechanism of action. |
Databáze: | OpenAIRE |
Externí odkaz: |