Androgen receptor agonism promotes an osteogenic gene program in preadipocytes

Sean M. Hartig; Qin Feng; Scott A. Ochsner; Rui Xiao; Neil J. McKenna; Sean E. McGuire; Bin He

doi:10.1016/j.bbrc.2013.03.078

Androgen receptor agonism promotes an osteogenic gene program in preadipocytes

Sean M. Hartig, Qin Feng, Scott A. Ochsner, Rui Xiao, Neil J. McKenna, Sean E. McGuire, Bin He

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

Androgens regulate body composition by interacting with the androgen receptor (AR) to control gene expression in a tissue-specific manner. To identify novel regulatory roles for AR in preadipocytes, we created a 3T3-L1 cell line stably expressing human AR. We found AR expression is required for androgen-mediated inhibition of 3T3-L1 adipogenesis. This inhibition is characterized by decreased lipid accumulation, reduced expression of adipogenic genes, and induction of genes associated with osteoblast differentiation. Collectively, our results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation.

Original language	English (US)
Pages (from-to)	357-362
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	434
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2013.03.078
State	Published - May 3 2013

Keywords

Adipocyte
Androgen receptor
Gene regulation
Osteoblast

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2013.03.078

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title = "Androgen receptor agonism promotes an osteogenic gene program in preadipocytes",

abstract = "Androgens regulate body composition by interacting with the androgen receptor (AR) to control gene expression in a tissue-specific manner. To identify novel regulatory roles for AR in preadipocytes, we created a 3T3-L1 cell line stably expressing human AR. We found AR expression is required for androgen-mediated inhibition of 3T3-L1 adipogenesis. This inhibition is characterized by decreased lipid accumulation, reduced expression of adipogenic genes, and induction of genes associated with osteoblast differentiation. Collectively, our results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation.",

keywords = "Adipocyte, Androgen receptor, Gene regulation, Osteoblast",

author = "Hartig, {Sean M.} and Qin Feng and Ochsner, {Scott A.} and Rui Xiao and McKenna, {Neil J.} and McGuire, {Sean E.} and Bin He",

note = "Funding Information: We thank Lisa White for expert assistance with microarray experiments. This work was funded by NIH 1F32DK85979 (S.M.H.), NIH 1 K01DK096093 (S.M.H.), Caroline Weiss Law Foundation (S.E.M.), NIH 3U19DK062434 NURSA (N.J.M.), NIH 5K01DK084209 (Q.F.), and NIH 5 K01DK081446 (B.H.). The Genomic and RNA Profiling Core at Baylor College of Medicine is supported by P30-CA125123. This work was also partly supported by the Diabetes and Endocrinology Research Center ( P30-DK079638 ) at Baylor College of Medicine. ",

year = "2013",

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day = "3",

doi = "10.1016/j.bbrc.2013.03.078",

language = "English (US)",

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T1 - Androgen receptor agonism promotes an osteogenic gene program in preadipocytes

AU - Hartig, Sean M.

AU - Feng, Qin

AU - Ochsner, Scott A.

AU - Xiao, Rui

AU - McKenna, Neil J.

AU - McGuire, Sean E.

AU - He, Bin

N1 - Funding Information: We thank Lisa White for expert assistance with microarray experiments. This work was funded by NIH 1F32DK85979 (S.M.H.), NIH 1 K01DK096093 (S.M.H.), Caroline Weiss Law Foundation (S.E.M.), NIH 3U19DK062434 NURSA (N.J.M.), NIH 5K01DK084209 (Q.F.), and NIH 5 K01DK081446 (B.H.). The Genomic and RNA Profiling Core at Baylor College of Medicine is supported by P30-CA125123. This work was also partly supported by the Diabetes and Endocrinology Research Center ( P30-DK079638 ) at Baylor College of Medicine.

PY - 2013/5/3

Y1 - 2013/5/3

N2 - Androgens regulate body composition by interacting with the androgen receptor (AR) to control gene expression in a tissue-specific manner. To identify novel regulatory roles for AR in preadipocytes, we created a 3T3-L1 cell line stably expressing human AR. We found AR expression is required for androgen-mediated inhibition of 3T3-L1 adipogenesis. This inhibition is characterized by decreased lipid accumulation, reduced expression of adipogenic genes, and induction of genes associated with osteoblast differentiation. Collectively, our results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation.

AB - Androgens regulate body composition by interacting with the androgen receptor (AR) to control gene expression in a tissue-specific manner. To identify novel regulatory roles for AR in preadipocytes, we created a 3T3-L1 cell line stably expressing human AR. We found AR expression is required for androgen-mediated inhibition of 3T3-L1 adipogenesis. This inhibition is characterized by decreased lipid accumulation, reduced expression of adipogenic genes, and induction of genes associated with osteoblast differentiation. Collectively, our results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation.

KW - Adipocyte

KW - Androgen receptor

KW - Gene regulation

KW - Osteoblast

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Androgen receptor agonism promotes an osteogenic gene program in preadipocytes

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Keywords

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