| TGF-β mediates suppression of adipogenesis by estradiol through connective tissue growth factor induction. | |
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MedLine Citation:
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PMID: 22067314 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In the bone marrow cavity, adipocyte numbers increase, whereas osteoblast progenitor numbers decrease with aging. Because adipocytes and osteoblasts share a common progenitor, it is possible that this shift is due to an increase in adipocyte-lineage cells at the expense of osteoblast-lineage commitment. Estrogens inhibit adipocyte differentiation, and in both men and women, circulating estrogens correlate with bone loss with aging. In bone cells, estrogens stimulate expression of TGF-β and suppress mesenchymal cell adipogenesis. Using a tripotential mesenchymal cell line, we have examined whether estradiol suppression of adipocyte differentiation is due to stimulation of TGF-β and the mechanism by which TGF-β suppresses adipogenesis. We observed that estradiol-mediated suppression of adipogenic gene expression required at least 48 h treatment. TGF-β expression increased within 24 h of estradiol treatment, and TGF-β inhibition reversed estradiol influences on adipogenesis and adipocyte gene expression. Connective tissue growth factor (CTGF) mediates TGF-β suppression of adipogenesis in mouse 3T3-L1 cells. CTGF expression was induced within 24 h of TGF-β treatment, whereas estradiol-mediated induction required 48 h treatment. Moreover, estradiol-mediated induction of CTGF was abrogated by TGF-β inhibition. These data support that estradiol effects on adipogenesis involves TGF-β induction, which then induces CTGF to suppress adipogenesis. |
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Authors:
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Ashok Kumar; Ming Ruan; Kari Clifton; Farhan Syed; Sundeep Khosla; Merry Jo Oursler |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-11-08 |
Journal Detail:
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Title: Endocrinology Volume: 153 ISSN: 1945-7170 ISO Abbreviation: Endocrinology Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-23 Completed Date: 2012-03-05 Revised Date: 2013-05-23 |
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: 254-63 Citation Subset: AIM; IM |
Affiliation:
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Endocrine Research Unit and Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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3T3-L1 Cells Adipogenesis / drug effects*, genetics, physiology* Animals Base Sequence Cell Line Connective Tissue Growth Factor / biosynthesis* DNA Primers / genetics Estradiol / pharmacology* Female Gene Expression / drug effects Humans Male Mesenchymal Stromal Cells / cytology, drug effects, metabolism Mice Multipotent Stem Cells / cytology, drug effects, metabolism Osteoblasts / cytology, drug effects, metabolism Thiazolidinediones / pharmacology Transforming Growth Factor beta / antagonists & inhibitors, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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P01 AG004875/AG/NIA NIH HHS; R01 AG028936/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Ctgf protein, mouse; 0/DNA Primers; 0/Thiazolidinediones; 0/Transforming Growth Factor beta; 122320-73-4/rosiglitazone; 139568-91-5/Connective Tissue Growth Factor; 50-28-2/Estradiol |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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