Estrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometrium
| Autor: | Thaís F.G. Lucas, Carine Royer, Vivian C. Konigame, Catarina S. Porto, Fernando Maurício Francis Abdalla, Erica Rosanna Siu |
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| Rok vydání: | 2011 |
| Předmět: |
Agonist
medicine.medical_specialty Time Factors medicine.drug_class Inositol Phosphates Clinical Biochemistry Active Transport Cell Nucleus Estrogen receptor Stimulation In Vitro Techniques Biology Phosphatidylinositols Endometrium Biochemistry Endocrinology Internal medicine medicine Animals RNA Messenger Rats Wistar Receptor Molecular Biology Cell Nucleus Pharmacology Estradiol Phospholipase C Hydrolysis Organic Chemistry Rats Enzyme Activation medicine.anatomical_structure Receptors Estrogen Type C Phospholipases Myometrium Female Estrogen receptor alpha GPER hormones hormone substitutes and hormone antagonists Signal Transduction |
| Zdroj: | Steroids. 76:1582-1589 |
| ISSN: | 0039-128X |
| DOI: | 10.1016/j.steroids.2011.09.013 |
| Popis: | The aim of the present study was to investigate the activation of rapid signaling events by 17β-estradiol in the rat uterus. 17β-Estradiol induced a rapid increase of total [3H]-inositol phosphate accumulation in the whole uterus and endometrium, but not in the myometrium. The effect of 17β-estradiol in the endometrium was blocked by phospholipase C (PLC) inhibitor (U73122), estrogen receptors antagonist (ICI 182,780), exportin CRM1 inhibitor (leptomycin B) and selective inhibitor of the SRC family of protein tyrosine kinases (PP2). Furthermore, a selective agonist of ESR1 (PPT) and a selective agonist of GPER (G-1) also induced a rapid increase of total [(3)H]-inositol phosphate accumulation in the endometrium. The G-1 effects were blocked by GPER antagonist (G-15). 17β-Estradiol and G-1 promoted an additive effect on total [3H]-inositol phosphate accumulation. In conclusion, the present results indicate that a rapid activation of the PLC-mediated phosphoinositide hydrolysis occurred in the rat endometrium after 17β-estradiol stimulation, and this effect was mediated by ESR1 that underwent nuclear export after hormone stimulation, and that GPER activation may play an additive role for this response. These rapid actions might be one of the key steps that mediate the estrogen-dependent activation of cellular events in the endometrium. |
| Databáze: | OpenAIRE |
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