Document Detail

TGF-β mediates suppression of adipogenesis by estradiol through connective tissue growth factor induction.
MedLine Citation:
PMID:  22067314     Owner:  NLM     Status:  MEDLINE    
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.
Ashok Kumar; Ming Ruan; Kari Clifton; Farhan Syed; Sundeep Khosla; Merry Jo Oursler
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-08
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-23     Completed Date:  2012-03-05     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  254-63     Citation Subset:  AIM; IM    
Endocrine Research Unit and Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA.
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MeSH Terms
3T3-L1 Cells
Adipogenesis / drug effects*,  genetics,  physiology*
Base Sequence
Cell Line
Connective Tissue Growth Factor / biosynthesis*
DNA Primers / genetics
Estradiol / pharmacology*
Gene Expression / drug effects
Mesenchymal Stromal Cells / cytology,  drug effects,  metabolism
Multipotent Stem Cells / cytology,  drug effects,  metabolism
Osteoblasts / cytology,  drug effects,  metabolism
Thiazolidinediones / pharmacology
Transforming Growth Factor beta / antagonists & inhibitors,  metabolism*
Grant Support
P01 AG004875/AG/NIA NIH HHS; R01 AG028936/AG/NIA NIH HHS
Reg. No./Substance:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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