Document Detail


Estrogen increases the permeability of the cultured human cervical epithelium by modulating cell deformability.
MedLine Citation:
PMID:  9730974     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
G I Gorodeski
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  275     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1998 Sep 
Date Detail:
Created Date:  1998-10-05     Completed Date:  1998-10-05     Revised Date:  2013-06-11    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  C888-99     Citation Subset:  IM    
Affiliation:
Department of Reproductive Biology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
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MeSH Terms
Descriptor/Qualifier:
Actins / 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:
HD-00977/HD/NICHD NIH HHS; HD-29924/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
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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