| 17β-Estradiol regulates rat growth plate chondrocyte apoptosis through a mitochondrial pathway not involving nitric oxide or MAPKs. | |
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MedLine Citation:
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PMID: 21068162 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Estrogens cause growth plate closure in both males and females, by decreasing proliferation and inducing apoptosis of postproliferative growth plate chondrocytes. In vitro studies using 17β-estradiol (E(2)) conjugated to bovine serum albumin (E(2)-BSA) show that rat costochondral growth plate resting zone chondrocytes also respond to E(2). Moreover, they are regulated by E(2)-BSA via a protein kinase C and ERK MAPK signaling pathway that is functional only in female cells. To better understand how E(2) regulates apoptosis of growth plate chondrocytes, rat resting zone chondrocytes cells were treated with E(2) or E(2)-BSA. E(2) caused apoptosis in male and female resting zone and growth zone chondrocytes in a dose-dependent manner, based on elevated DNA fragmentation, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and caspase-3 activation. E(2) also up-regulated p53 and Bax protein (Bcl-2-associated X protein) levels and induced release of cytochrome C from the mitochondria, indicating a mitochondrial apoptotic pathway. The apoptotic effect of E(2) did not involve elevated nitric oxide production or MAPKs. It was reduced by ICI 182780, which is an estrogen receptor (ER) antagonist and blocked by antibodies to Erα36, a membrane-associated ER. E(2)-BSA reduced cell viability and increased caspase-3 activity; ICI 182780 had no effect, but anti-ERα36 antibodies blocked the effect. The results indicate that estrogen is able to directly affect the cell population kinetics of growth plate chondrocytes by regulating apoptosis, as well as proliferation and differentiation in both resting zone and growth zone cells. They also have provided further information about the physiological functions of estrogen on longitudinal bone growth. |
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Authors:
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M Zhong; D H Carney; B D Boyan; Z Schwartz |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-11-10 |
Journal Detail:
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Title: Endocrinology Volume: 152 ISSN: 1945-7170 ISO Abbreviation: Endocrinology Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-24 Completed Date: 2011-01-31 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 82-92 Citation Subset: AIM; IM |
Affiliation:
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Department of Biomedical Engineering, Georgia Institute of Technology, 315 Ferst Drive NW, Atlanta, Georgia 30332-0363, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology* Cell Membrane Cell Nucleus Cells, Cultured Chondrocytes / physiology* DNA Fragmentation Epiphyses / physiology* Estradiol / metabolism, pharmacology* Female Foscarnet / pharmacology Gene Expression Regulation, Enzymologic Male Mitochondria / metabolism* Mitogen-Activated Protein Kinases / genetics, metabolism* Nitric Oxide / metabolism* Peptide Fragments / pharmacology Rats Rats, Sprague-Dawley Receptors, Estrogen / metabolism Sex Characteristics Thrombin / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Peptide Fragments; 0/Receptors, Estrogen; 0/rusalatide acetate; 10102-43-9/Nitric Oxide; 4428-95-9/Foscarnet; 50-28-2/Estradiol; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.21.5/Thrombin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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