PMID- 27246393
OWN - NLM
STAT- MEDLINE
DCOM- 20180405
LR  - 20190423
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 6
DP  - 2016 Jun 1
TI  - Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor.
PG  - 27026
LID - 10.1038/srep27026 [doi]
LID - 27026
AB  - The present study was designed to determine whether sulfur dioxide (SO2) could be 
      endogenously produced in adipocyte and served as a novel adipocyte-derived 
      inflammatory inhibitor. SO2 was detected in adipose tissue using high-performance 
      liquid chromatography with fluorescence detection. SO2 synthase aspartate 
      aminotransferase (AAT1 and AAT2) mRNA and protein expressions in adipose tissues 
      were measured. For in vitro study, 3T3-L1 adipocytes were cultured, infected with 
      adenovirus carrying AAT1 gene or lentivirus carrying shRNA to AAT1, and then 
      treated with tumor necrosis factor-alpha (TNF-alpha). We found that endogenous SO2/AAT 
      pathway existed in adipose tissues including perivascular, perirenal, epididymal, 
      subcutaneous and brown adipose tissue. AAT1 overexpression significantly 
      increased SO2 production and inhibited TNF-alpha-induced inflammatory factors, 
      monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion 
      from 3T3-L1 adipocytes. By contrast, AAT1 knockdown decreased SO2 production and 
      exacerbated TNF-alpha-stimulated MCP-1 and IL-8 secretion. Mechanistically, AAT1 
      overexpression attenuated TNF-alpha-induced IkappaBalpha phosphorylation and degradation, and 
      nuclear factor-kappaB (NF-kappaB) p65 phosphorylation, while AAT1 knockdown aggravated 
      TNF-alpha-activated NF-kappaB pathway, which was blocked by SO2. NF-kappaB inhibitors, PDTC 
      or Bay 11-7082, abolished excessive p65 phosphorylation and adipocyte 
      inflammation induced by AAT1 knockdown. This is the first report to suggest that 
      endogenous SO2 is a novel adipocyte-derived inflammatory inhibitor.
FAU - Zhang, Heng
AU  - Zhang H
AD  - Department of Endocrinology, Beijing Chaoyang Hospital, Capital Medical 
      University, Beijing, China.
FAU - Huang, Yaqian
AU  - Huang Y
AD  - Department of Pediatrics, Peking University First Hospital, Beijing 100034, 
      China.
FAU - Bu, Dingfang
AU  - Bu D
AD  - Research Center, Peking University First Hospital, Beijing 100034, China.
FAU - Chen, Selena
AU  - Chen S
AD  - University of California, San Diego, La Jolla, California, 92093, United States 
      of America.
FAU - Tang, Chaoshu
AU  - Tang C
AD  - Department of Physiology and Pathophysiology, Peking University Health Science 
      Center, Beijing 100191, China.
AD  - Key Lab. of Ministry of Education of China, Beijing, China.
FAU - Wang, Guang
AU  - Wang G
AD  - Department of Endocrinology, Beijing Chaoyang Hospital, Capital Medical 
      University, Beijing, China.
FAU - Du, Junbao
AU  - Du J
AD  - Department of Pediatrics, Peking University First Hospital, Beijing 100034, 
      China.
AD  - Key Lab. of Ministry of Education of China, Beijing, China.
FAU - Jin, Hongfang
AU  - Jin H
AD  - Department of Pediatrics, Peking University First Hospital, Beijing 100034, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160601
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (3-(4-methylphenylsulfonyl)-2-propenenitrile)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Isoenzymes)
RN  - 0 (Nitriles)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Sulfones)
RN  - 0 (Thiocarbamates)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0UZA3422Q4 (Sulfur Dioxide)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 9DLQ4CIU6V (Proline)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/cytology/*metabolism
MH  - Adipose Tissue, Brown/cytology/*metabolism
MH  - Adipose Tissue, White/cytology/*metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*metabolism
MH  - Aspartate Aminotransferases/antagonists & inhibitors/genetics/metabolism
MH  - Chemokine CCL2/genetics/metabolism
MH  - Gene Expression Regulation
MH  - Interleukin-8/genetics/metabolism
MH  - Isoenzymes/antagonists & inhibitors/genetics/metabolism
MH  - Male
MH  - Mice
MH  - NF-KappaB Inhibitor alpha/genetics/metabolism
MH  - Nitriles/pharmacology
MH  - Phosphorylation/drug effects
MH  - Proline/analogs & derivatives/pharmacology
MH  - RNA, Small Interfering/genetics/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - Sulfones/pharmacology
MH  - Sulfur Dioxide/*metabolism
MH  - Thiocarbamates/pharmacology
MH  - Transcription Factor RelA/antagonists & inhibitors/genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
PMC - PMC4887903
COIS- The authors declare no competing financial interests.
EDAT- 2016/06/02 06:00
MHDA- 2018/04/06 06:00
PMCR- 2016/06/01
CRDT- 2016/06/02 06:00
PHST- 2016/02/05 00:00 [received]
PHST- 2016/05/12 00:00 [accepted]
PHST- 2016/06/02 06:00 [entrez]
PHST- 2016/06/02 06:00 [pubmed]
PHST- 2018/04/06 06:00 [medline]
PHST- 2016/06/01 00:00 [pmc-release]
AID - srep27026 [pii]
AID - 10.1038/srep27026 [doi]
PST - epublish
SO  - Sci Rep. 2016 Jun 1;6:27026. doi: 10.1038/srep27026.