6533b7cffe1ef96bd125873e

RESEARCH PRODUCT

Inducibility of the avidin gene by progesterone is suppressed during estrogen-induced cytodifferentiation.

S. SalomaaMarkku S. KulomaaMarkku S. KulomaaH. AlhoTimo YlikomiPekka ViljaPentti TuohimaaA. NiemeläTarja KunnasTimo Joensuu

subject

medicine.medical_specialtymedicine.drug_classOvalbuminEndocrinology Diabetes and MetabolismClinical BiochemistryDiethylstilbestrolEstrogen receptorOviductsBiologyBiochemistryEpitheliumImmunoenzyme TechniquesEndocrinologystomatognathic systemInternal medicineProgesterone receptormedicineAnimalsTubular glandMolecular BiologyDiethylstilbestrolIn Situ HybridizationProgesteroneEstradiolCell DifferentiationEpithelial CellsCell BiologyAvidinEpitheliummedicine.anatomical_structureEndocrinologyGene Expression RegulationEstrogenbiology.proteinMolecular MedicineOviductChickenshormones hormone substitutes and hormone antagonistsmedicine.drugAvidin

description

Abstract We have studied epithelial differentiation of the chick oviduct as induced by diethylstilbestrol (DES) and 17β-estradiol (E 2 ). The proportion of goblet cells in the oviduct was slightly higher after E 2 than after DES treatment. Also avidin induction by progesterone was stronger following DES than E 2 priming. In the estrogen pretreated oviduct epithelium, avidin expression was induced by progesterone in the surface epithelial cells, protodifferentiated gland cells and tubular gland cells, but not in goblet cells. During prolonged estrogen treatment, however, the inducibility of avidin by progesterone ceased in tubular gland cells but not in surface epithelial cells. The estrogen action on the expression of avidin could be explained by estrogen-induced terminal differentiation of the epithelial gland cells or by a direct effect of estrogen on the progesterone action, for instance interaction of estrogen receptor and progesterone receptor in the regulation of transcription.

10.1016/0960-0760(92)90285-qhttps://pubmed.ncbi.nlm.nih.gov/1472452