PMID- 27098798
OWN - NLM
STAT- MEDLINE
DCOM- 20170307
LR  - 20181202
IS  - 2542-5641 (Electronic)
IS  - 0366-6999 (Print)
IS  - 0366-6999 (Linking)
VI  - 129
IP  - 9
DP  - 2016 May 5
TI  - L-4F Inhibits Oxidized Low-density Lipoprotein-induced Inflammatory Adipokine 
      Secretion via Cyclic AMP/Protein Kinase A-CCAAT/Enhancer Binding Protein beta 
      Signaling Pathway in 3T3-L1 Adipocytes.
PG  - 1108-12
LID - 10.4103/0366-6999.180519 [doi]
AB  - BACKGROUND: Adipocytes behave like a rich source of pro-inflammatory cytokines 
      including monocyte chemoattractant protein-1 (MCP-1). Oxidized low-density 
      lipoprotein (oxLDL) participates in the local chronic inflammatory response, and 
      high-density lipoprotein could counterbalance the proinflammatory function of 
      oxLDL, but the underlying mechanism is not completely understood. This study 
      aimed to evaluate the effect of apolipoprotein A-I mimetic peptide L-4F on the 
      secretion and expression of MCP-1 in fully differentiated 3T3-L1 adipocytes 
      induced by oxLDL and to elucidate the possible mechanisms. METHODS: Fully 
      differentiated 3T3-L1 adipocytes were incubated in the medium containing various 
      concentration of L-4F (0-50 mug/ml) with oxLDL (50 mug/ml) stimulated, with/without 
      protein kinase A (PKA) inhibitor H-89 (10 mumol/L) preincubated. The 
      concentrations of MCP-1 in the supernatant, the mRNA expression of MCP-1, the 
      levels of CCAAT/enhancer binding protein alpha (C/EBPalpha), and CCAAT/enhancer binding 
      protein beta (C/EBPbeta) were evaluated. The monocyte chemotaxis assay was performed by 
      micropore filter method using a modified Boyden chamber. RESULTS: OxLDL 
      stimulation induced a significant increase of MCP-1 expression and secretion in 
      3T3-L1 adipocytes, which were inhibited by L-4F preincubation in a dose-dependent 
      manner. PKA inhibitor H-89 markedly reduced the oxLDL-induced MCP-1 expression, 
      but no further decrease was observed when H-89 was used in combination with L-4F 
      (50 mug/ml) (P > 0.05). OxLDL stimulation showed no significant effect on C/EBPalpha 
      protein level but increased C/EBPbeta protein level in a time-dependent manner. H-89 
      and L-4F both attenuated C/EBPbeta protein level in oxLDL-induced 3T3-L1 adipocytes. 
      CONCLUSIONS: OxLDL induces C/EBPbeta protein synthesis in a time-dependent manner 
      and enhances MCP-1 secretion and expression in 3T3-L1 adipocytes. L-4F 
      dose-dependently counterbalances the pro-inflammatory effect of oxLDL, and cyclic 
      AMP/PKA-C/EBPbeta signaling pathway may participate in it.
FAU - Xie, Xiang-Zhu
AU  - Xie XZ
FAU - Huang, Xin
AU  - Huang X
FAU - Zhao, Shui-Ping
AU  - Zhao SP
FAU - Yu, Bi-Lian
AU  - Yu BL
FAU - Zhong, Qiao-Qing
AU  - Zhong QQ
FAU - Cao, Jian
AU  - Cao J
AD  - Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (CCAAT-Enhancer-Binding Protein-beta)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (L-4F peptide)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Peptides)
RN  - 0 (oxidized low density lipoprotein)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Animals
MH  - CCAAT-Enhancer-Binding Protein-beta/analysis/*physiology
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cyclic AMP/*physiology
MH  - Cyclic AMP-Dependent Protein Kinases/*physiology
MH  - Humans
MH  - Lipoproteins, LDL/*antagonists & inhibitors/pharmacology
MH  - Mice
MH  - Peptides/*pharmacology
MH  - Signal Transduction/*physiology
PMC - PMC4852680
EDAT- 2016/04/22 06:00
MHDA- 2017/03/08 06:00
PMCR- 2016/05/05
CRDT- 2016/04/22 06:00
PHST- 2016/04/22 06:00 [entrez]
PHST- 2016/04/22 06:00 [pubmed]
PHST- 2017/03/08 06:00 [medline]
PHST- 2016/05/05 00:00 [pmc-release]
AID - ChinMedJ_2016_129_9_1108_180519 [pii]
AID - CMJ-129-1108 [pii]
AID - 10.4103/0366-6999.180519 [doi]
PST - ppublish
SO  - Chin Med J (Engl). 2016 May 5;129(9):1108-12. doi: 10.4103/0366-6999.180519.