| Estrogen increases the permeability of the cultured human cervical epithelium by modulating cell deformability. | |
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MedLine Citation:
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PMID: 9730974 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Estrogens increase secretion of cervical mucus in females. The objective of this research was to study the mechanisms of estrogen action. The experimental models were human CaSki (endocervical) and hECE (ectocervical) epithelial cells cultured on filters. Incubation in steroid-free medium increased transepithelial electrical resistance (RTE) and decreased epithelial permeability to the cell-impermeant acid pyranine. Estrogen treatment reversed the effects, indicating estrogen decreases epithelial paracellular resistance. The estrogen effect was time and dose related (EC50 approximately 1 nM) and specific (estradiol = diethylstilbestrol > estrone, estriol; no effect by progesterone, testosterone, or cortisol) and was blocked by progesterone, tamoxifen, and ICI-182780 (an estrogen receptor antagonist). Estrogen treatment did not modulate dilution potential or changes in RTE in response to diC8 or to low extracellular Ca2+ (modulators of tight junctional resistance). In contrast, estrogen augmented decreases in RTE in response to hydrostatic and hypertonic gradients [modulators of resistance of lateral intercellular space (RLIS)], suggesting estrogen decreases RLIS. Estrogen decreased cervical cell size, shortened response time relative to changes in cell size after hypertonic challenge, and augmented the decrease in cell size in response to hypertonic and hydrostatic gradients. Lowering luminal NaCl had no significant effect on RTE, and the Cl- channel blocker diphenylamine-2-carboxylate attenuated the hypertonicity-induced decrease in cell size to the same degree in control and estrogen-treated cells, suggesting estrogen effects on permeability and cell size are not mediated by modulating Na+ or Cl- transport. In contrast, estrogen increased cellular G-actin levels, suggesting estrogens shift actin steady-state toward G-actin and the cervical cell cytoskeleton toward a more flexible structure. We suggest that the mechanism by which estrogens decrease RLIS and increase permeability is by fragmenting the cytoskeleton and facilitating deformability and decreases in cervical cell size. |
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Authors:
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G I Gorodeski |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of physiology Volume: 275 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1998 Sep |
Date Detail:
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Created Date: 1998-10-05 Completed Date: 1998-10-05 Revised Date: 2013-06-11 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: C888-99 Citation Subset: IM |
Affiliation:
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Department of Reproductive Biology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism Cell Line Cell Membrane Permeability / drug effects, physiology* Cells, Cultured Cervix Uteri / cytology, physiology* Chlorides / metabolism Diethylstilbestrol / pharmacology Egtazic Acid / pharmacology Epithelial Cells / cytology, drug effects, physiology* Estradiol / analogs & derivatives, pharmacology Estriol / pharmacology Estrogen Antagonists / pharmacology Estrogens / pharmacology* Estrone / pharmacology Female Humans Kinetics Progesterone / pharmacology Sodium / metabolism Tamoxifen / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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HD-00977/HD/NICHD NIH HHS; HD-29924/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Chlorides; 0/Estrogen Antagonists; 0/Estrogens; 10540-29-1/Tamoxifen; 22X328QOC4/fulvestrant; 50-27-1/Estriol; 50-28-2/Estradiol; 53-16-7/Estrone; 56-53-1/Diethylstilbestrol; 57-83-0/Progesterone; 67-42-5/Egtazic Acid; 7440-23-5/Sodium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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