PMID- 27392713
OWN - NLM
STAT- MEDLINE
DCOM- 20170523
LR  - 20171126
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 477
IP  - 4
DP  - 2016 Sep 2
TI  - Androgen-androgen receptor system improves chronic inflammatory conditions by 
      suppressing monocyte chemoattractant protein-1 gene expression in adipocytes via 
      transcriptional regulation.
PG  - 895-901
LID - S0006-291X(16)31109-3 [pii]
LID - 10.1016/j.bbrc.2016.06.155 [doi]
AB  - Age-related decreases in sex hormones are closely related to chronic inflammation 
      in obesity and metabolic diseases. Particularly, the molecular basis of androgen 
      activity in regulating inflammation and controlling metabolism remains largely 
      unknown. Obese adipocytes secrete monocyte chemoattractant protein-1 (MCP-1), a 
      key chemokine that promotes the infiltration of monocytes/macrophages into 
      adipose tissue, thereby leading to metabolic disorders. Here, we studied the role 
      of androgen-androgen receptor (AR) action in regulating MCP-1 expression in 
      adipose tissue. We observed the induction of Mcp-1 expression in 3T3-L1 
      adipocytes co-cultured with RAW264.7 macrophages. Additionally, Mcp-1 expression 
      was upregulated by culturing in conditioned medium derived from inflammatory 
      macrophages (M1-Mphi) containing tumor necrosis factor-alpha (TNF-alpha). We found that 
      sex hormones downregulated TNF-alpha-induced Mcp-1 and interleukin (Il)-6 expression 
      in 3T3-L1 adipocytes. Furthermore, luciferase-reporter analysis indicated that 
      MCP-1 promoter activity was predominantly suppressed by dihydrotestosterone 
      (DHT)-AR interactions through functional canonical nuclear factor-kappa B (NF-kappaB) 
      sites, whereas non-canonical NF-kappaB site containing important flanking sequences 
      exhibited minor contributions to DHT-AR transcriptional repression. These 
      findings suggested that androgen-AR suppressed obesity-induced chronic 
      inflammation in adipose tissue.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - Morooka, Nobukatsu
AU  - Morooka N
AD  - Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 
      Showa-machi, Maebashi, Gunma, 371-8512, Japan. Electronic address: 
      amorooka@gunma-u.ac.jp.
FAU - Ueguri, Kei
AU  - Ueguri K
AD  - Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 
      Showa-machi, Maebashi, Gunma, 371-8512, Japan.
FAU - Yee, Karen Kar Lye
AU  - Yee KKL
AD  - Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 
      Showa-machi, Maebashi, Gunma, 371-8512, Japan; Human Resources Cultivation 
      Center, Gunma University, 1-5-1 Tenjin-cho, Kiryushi, Gunma, 376-8515, Japan.
FAU - Yanase, Toshihiko
AU  - Yanase T
AD  - Department of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka 
      University, Jonan-ku, Fukuoka, 814-0180, Japan.
FAU - Sato, Takashi
AU  - Sato T
AD  - Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 
      Showa-machi, Maebashi, Gunma, 371-8512, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160705
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (AR protein, mouse)
RN  - 0 (Androgens)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, Androgen)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/*metabolism
MH  - Androgens/*metabolism
MH  - Animals
MH  - Chemokine CCL2/*metabolism
MH  - Chronic Disease
MH  - Gene Expression Regulation
MH  - Inflammation/*metabolism
MH  - Mice
MH  - RAW 264.7 Cells
MH  - Receptors, Androgen/*metabolism
MH  - *Transcriptional Activation
OTO - NOTNLM
OT  - Adipocyte
OT  - Androgen
OT  - Androgen receptor, AR
OT  - Chronic inflammation
OT  - MCP-1
OT  - Macrophage
EDAT- 2016/07/10 06:00
MHDA- 2017/05/24 06:00
CRDT- 2016/07/10 06:00
PHST- 2016/06/20 00:00 [received]
PHST- 2016/06/29 00:00 [accepted]
PHST- 2016/07/10 06:00 [entrez]
PHST- 2016/07/10 06:00 [pubmed]
PHST- 2017/05/24 06:00 [medline]
AID - S0006-291X(16)31109-3 [pii]
AID - 10.1016/j.bbrc.2016.06.155 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2016 Sep 2;477(4):895-901. doi: 
      10.1016/j.bbrc.2016.06.155. Epub 2016 Jul 5.