PMID- 22262711
OWN - NLM
STAT- MEDLINE
DCOM- 20120731
LR  - 20211021
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Print)
IS  - 0091-6765 (Linking)
VI  - 120
IP  - 4
DP  - 2012 Apr
TI  - Inflammatory pathway genes belong to major targets of persistent organic 
      pollutants in adipose cells.
PG  - 508-14
LID - 10.1289/ehp.1104282 [doi]
AB  - BACKGROUND: Epidemiological studies emphasize the possible role of persistent 
      organic pollutants (POPs) in obesity and the metabolic syndrome. These pollutants 
      are stored in adipose tissue (AT). OBJECTIVES: Our aim was to study the effects 
      of POPs on human adipose cells and rodent AT. METHODS: Using human multipotent 
      adipose-derived stem cells, we carried out large-scale gene expression analysis 
      to identify the major pathways modified by 2,3,7,8-tetrachlorodibenzo-p-dioxin 
      (TCDD), polychlorinated biphenyl (PCB) congener 126 (PCB-126), and PCB-153 and to 
      evaluate their toxic effects. The effects of TCDD on gene expression and AT 
      histology were also assessed in mice. RESULTS: The most significantly regulated 
      genes in both precursor cells and adipocytes were those involved in the 
      inflammatory/immune response, cancer, and metabolism pathways. Interestingly, the 
      fold induction and the number of modulated genes were higher in precursors than 
      in adipocytes, suggesting that the former could be more sensitive to the effect 
      of pollutants. When cells were treated with combinations of pollutants, the 
      effects of the AhR ligands TCDD and PCB-126 were dominant compared with those of 
      the non-dioxin-like PCB-153. The effects of AhR ligands were reduced by the AhR 
      antagonist alpha-naphthoflavone. The regulation of inflammatory pathway was observed 
      in wild-type AT but not in AhR-knockout mice. CONCLUSIONS: Both in vitro and in 
      vivo studies showed that adipose cells were targets of AhR ligands and suggest 
      that inflammation is one of the main regulated pathways. These observations 
      suggest a possible contribution of pollutants to low-grade AT inflammation that 
      accompanies the pathogenesis of metabolic diseases.
FAU - Kim, Min Ji
AU  - Kim MJ
AD  - INSERM UMR-S 747, Universite Paris Descartes, Centre Universitaire des 
      Saints-Peres, Paris, France.
FAU - Pelloux, Veronique
AU  - Pelloux V
FAU - Guyot, Erwan
AU  - Guyot E
FAU - Tordjman, Joan
AU  - Tordjman J
FAU - Bui, Linh-Chi
AU  - Bui LC
FAU - Chevallier, Aline
AU  - Chevallier A
FAU - Forest, Claude
AU  - Forest C
FAU - Benelli, Chantal
AU  - Benelli C
FAU - Clement, Karine
AU  - Clement K
FAU - Barouki, Robert
AU  - Barouki R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120119
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Benzoflavones)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 604-59-1 (alpha-naphthoflavone)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
RN  - ZRU0C9E32O (2,4,5,2',4',5'-hexachlorobiphenyl)
SB  - IM
CIN - Environ Health Perspect. 2012 Apr;120(4):A164. PMID: 22469859
MH  - Adipocytes/cytology/*drug effects
MH  - Adipose Tissue/cytology/drug effects
MH  - Animals
MH  - Benzoflavones/pharmacology
MH  - Body Weight/drug effects
MH  - *Cell Differentiation
MH  - Cytokines/metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Multipotent Stem Cells/cytology/drug effects
MH  - Obesity/*chemically induced/pathology
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Polychlorinated Dibenzodioxins/*toxicity
MH  - Real-Time Polymerase Chain Reaction
MH  - Receptors, Aryl Hydrocarbon/genetics/physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Weight Gain/drug effects
PMC - PMC3339464
COIS- The authors declare they have no actual or potential competing financial 
      interests.
EDAT- 2012/01/21 06:00
MHDA- 2012/08/01 06:00
PMCR- 2012/04/01
CRDT- 2012/01/21 06:00
PHST- 2011/07/30 00:00 [received]
PHST- 2012/01/19 00:00 [accepted]
PHST- 2012/01/21 06:00 [entrez]
PHST- 2012/01/21 06:00 [pubmed]
PHST- 2012/08/01 06:00 [medline]
PHST- 2012/04/01 00:00 [pmc-release]
AID - ehp.1104282 [pii]
AID - 10.1289/ehp.1104282 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2012 Apr;120(4):508-14. doi: 10.1289/ehp.1104282. Epub 
      2012 Jan 19.