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Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint

BACKGROUND: Estrogen is known to play role in temporomandibular joint (TMJ) disorders and estrogen effects can be mediated by estrogen receptor (ER) alpha present in the TMJ. Cells expressing the estrogen receptor ERalpha are present in the temporomandibular joint (TMJ) but changes in expression due...

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Autores principales: Puri, Jyoti, Hutchins, Bob, Bellinger, Larry L, Kramer, Phillip R
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811708/
https://www.ncbi.nlm.nih.gov/pubmed/20043825
http://dx.doi.org/10.1186/1477-7827-7-155
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author Puri, Jyoti
Hutchins, Bob
Bellinger, Larry L
Kramer, Phillip R
author_facet Puri, Jyoti
Hutchins, Bob
Bellinger, Larry L
Kramer, Phillip R
author_sort Puri, Jyoti
collection PubMed
description BACKGROUND: Estrogen is known to play role in temporomandibular joint (TMJ) disorders and estrogen effects can be mediated by estrogen receptor (ER) alpha present in the TMJ. Cells expressing the estrogen receptor ERalpha are present in the temporomandibular joint (TMJ) but changes in expression due to estrogen and inflammation have not been characterized. In this study, ERalpha protein content and the number of cells expressing ERalpha was measured in 17 beta-estradiol-treated rats after inflammation was induced in the TMJ. METHODS: Sixteen ovariectomized female rats were divided into two groups such that one group received 17 beta estradiol (E2) and the other was given vehicle (VEH). Groups were then subdivided further, one received injections of saline and the other received Complete Freund's adjuvant (CFA) within the superior joint space of the TMJ. Thus the four groups include no E2/saline, E2/saline, no E2/CFA and E2/CFA. After treatment, the rats were sacrificed, and the TMJ anterior, disc, retrodiscal and synovial tissues were analyzed by western blot and immunocytochemistry. Positive stained cells were counted using a Nikon epifluorescent microscope. RESULTS: The western blot showed that ERalpha protein significantly decreased with inflammation. The number of ERalpha-positive cells in the TMJ was not affected by inflammation or 17 beta-estradiol with exception of the retrodiscal tissue. In the retrodiscal tissue 17 beta-estradiol significantly decreased the number of ERalpha-positive cells but only in a non-inflamed joint. CONCLUSIONS: In conclusion, inflammation and 17 beta-estradiol can modulate ERalpha expression in the TMJ but the effects are tissue specific.
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spelling pubmed-28117082010-01-27 Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint Puri, Jyoti Hutchins, Bob Bellinger, Larry L Kramer, Phillip R Reprod Biol Endocrinol Research BACKGROUND: Estrogen is known to play role in temporomandibular joint (TMJ) disorders and estrogen effects can be mediated by estrogen receptor (ER) alpha present in the TMJ. Cells expressing the estrogen receptor ERalpha are present in the temporomandibular joint (TMJ) but changes in expression due to estrogen and inflammation have not been characterized. In this study, ERalpha protein content and the number of cells expressing ERalpha was measured in 17 beta-estradiol-treated rats after inflammation was induced in the TMJ. METHODS: Sixteen ovariectomized female rats were divided into two groups such that one group received 17 beta estradiol (E2) and the other was given vehicle (VEH). Groups were then subdivided further, one received injections of saline and the other received Complete Freund's adjuvant (CFA) within the superior joint space of the TMJ. Thus the four groups include no E2/saline, E2/saline, no E2/CFA and E2/CFA. After treatment, the rats were sacrificed, and the TMJ anterior, disc, retrodiscal and synovial tissues were analyzed by western blot and immunocytochemistry. Positive stained cells were counted using a Nikon epifluorescent microscope. RESULTS: The western blot showed that ERalpha protein significantly decreased with inflammation. The number of ERalpha-positive cells in the TMJ was not affected by inflammation or 17 beta-estradiol with exception of the retrodiscal tissue. In the retrodiscal tissue 17 beta-estradiol significantly decreased the number of ERalpha-positive cells but only in a non-inflamed joint. CONCLUSIONS: In conclusion, inflammation and 17 beta-estradiol can modulate ERalpha expression in the TMJ but the effects are tissue specific. BioMed Central 2009-12-31 /pmc/articles/PMC2811708/ /pubmed/20043825 http://dx.doi.org/10.1186/1477-7827-7-155 Text en Copyright ©2009 Puri et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Puri, Jyoti
Hutchins, Bob
Bellinger, Larry L
Kramer, Phillip R
Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title_full Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title_fullStr Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title_full_unstemmed Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title_short Estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
title_sort estrogen and inflammation modulate estrogen receptor alpha expression in specific tissues of the temporomandibular joint
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811708/
https://www.ncbi.nlm.nih.gov/pubmed/20043825
http://dx.doi.org/10.1186/1477-7827-7-155
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