PMID- 25678844
OWN - NLM
STAT- MEDLINE
DCOM- 20151120
LR  - 20181113
IS  - 1449-2288 (Electronic)
IS  - 1449-2288 (Linking)
VI  - 11
IP  - 3
DP  - 2015
TI  - High-density lipoprotein increases the uptake of oxidized low density lipoprotein 
      via PPARgamma/CD36 pathway in inflammatory adipocytes.
PG  - 256-65
LID - 10.7150/ijbs.10258 [doi]
AB  - AIM: Previous studies have demonstrated that the dysregulated-secretion of 
      adipokines by adipocytes may contribute to obesity-associated atherosclerosis 
      (As) and high density lipoprotein (HDL) may protect against atherogenesis through 
      multiple pathways. This study was to explore the effect of HDL on the oxLDL 
      uptake in inflammatory adipocytes stimulated by endotoxin lipopolysaccharide 
      (LPS) and the possible mechanism. METHODS AND RESULTS: 3T3-L1 adipocytes were 
      cultured and induced to differentiation and maturation. Acute inflammation in 
      adipocytes was induced by LPS (100 ng/ml) for 6 hours. The adipocytes were 
      pretreated with HDL in various concentrations (10, 50, 100 mug/ml) for 16 hours or 
      with specific PPARgamma antagonist (GW9662, 10 muM) or agonist (Rosiglitazone, 10 muM) 
      for 30 min before administration of LPS. The results showed that LPS 
      significantly increased the release of inflammation-related adipokines, such as 
      monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor 1 
      (PAI-1), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-8 and IL-6, while 
      decreasing the release of leptin and adiponectin. Meanwhile, LPS reduced the 
      uptake and degradation of 125I-oxLDL, and down-regulated the expression of PPARgamma 
      and CD36. Pretreatment with HDL dose-dependently affected the release of IL-8 and 
      IL-6 and the reduced uptake and degradation of oxLDL of adipocytes stimulated by 
      LPS, accompanied with marked upregulation of PPARgamma and CD36 expression. 
      Pretreatment with GW9662 markedly inhibited the upregulation of CD36 expression 
      mediated by HDL (100 mug/ml), while the effects of Rosiglitazone were opposite to 
      GW9662. CONCLUSIONS: HDL may increase oxLDL uptake of inflammatory adipocytes 
      stimulated by LPS via upregulation of PPARgamma/CD36 pathway, which may be a new 
      mechanism of anti-atherosclerosis mediated by HDL.
FAU - Zhong, Qiaoqing
AU  - Zhong Q
AD  - 1. Post-doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular 
      Disease and Key Lab for Arteriosclerology of Hunan Province, University of South 
      China, Hengyang, Hunan, 421001, China ; 2. Department of Cardiology, First 
      People's Hospital of Chenzhou, Chenzhou, 423000, China ; 3. Department of 
      Cardiology, The second Xiangya Hospital of Central South University, Changsha, 
      410011, China.
FAU - Zhao, Shuiping
AU  - Zhao S
AD  - 3. Department of Cardiology, The second Xiangya Hospital of Central South 
      University, Changsha, 410011, China.
FAU - Yu, Bilian
AU  - Yu B
AD  - 3. Department of Cardiology, The second Xiangya Hospital of Central South 
      University, Changsha, 410011, China.
FAU - Wang, Xing
AU  - Wang X
AD  - 4. Department of Cardiology, the First Affiliated Hospital of Sun Yat-sen 
      University, Guangzhou, 510080, China.
FAU - Matyal, Robina
AU  - Matyal R
AD  - 5. Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical 
      Center, Harvard Medical School, Boston, MA 02215, USA.
FAU - Li, Yunping
AU  - Li Y
AD  - 5. Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical 
      Center, Harvard Medical School, Boston, MA 02215, USA.
FAU - Jiang, Zhisheng
AU  - Jiang Z
AD  - 1. Post-doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular 
      Disease and Key Lab for Arteriosclerology of Hunan Province, University of South 
      China, Hengyang, Hunan, 421001, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150115
PL  - Australia
TA  - Int J Biol Sci
JT  - International journal of biological sciences
JID - 101235568
RN  - 0 (Adipokines)
RN  - 0 (CD36 Antigens)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (PPAR gamma)
SB  - IM
MH  - 3T3 Cells
MH  - Adipocytes/*metabolism
MH  - Adipokines/metabolism
MH  - Animals
MH  - CD36 Antigens/*metabolism
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - Lipoproteins, HDL/metabolism/*physiology
MH  - Lipoproteins, LDL/metabolism
MH  - Metabolic Networks and Pathways
MH  - Mice
MH  - Oxidation-Reduction
MH  - PPAR gamma/*metabolism
PMC - PMC4323365
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Inflammation
OT  - Lipopolysaccharide
OT  - Lipoprotein
COIS- Competing Interests: The authors have declared that no competing interest exists.
EDAT- 2015/02/14 06:00
MHDA- 2015/12/15 06:00
PMCR- 2015/01/01
CRDT- 2015/02/14 06:00
PHST- 2014/08/04 00:00 [received]
PHST- 2014/12/18 00:00 [accepted]
PHST- 2015/02/14 06:00 [entrez]
PHST- 2015/02/14 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - ijbsv11p0256 [pii]
AID - 10.7150/ijbs.10258 [doi]
PST - epublish
SO  - Int J Biol Sci. 2015 Jan 15;11(3):256-65. doi: 10.7150/ijbs.10258. eCollection 
      2015.