PMID- 22890916
OWN - NLM
STAT- MEDLINE
DCOM- 20130517
LR  - 20211021
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 371
IP  - 1-2
DP  - 2012 Dec
TI  - Atorvastatin suppresses oxidized LDL-induced dendritic cell-like differentiation 
      of RAW264.7 cells regulated by the p38 MAPK pathway.
PG  - 105-13
LID - 10.1007/s11010-012-1427-3 [doi]
AB  - Dendritic cells (DCs) are the most potent professional antigen-presenting cells 
      and are involved in the initiation and progression of atherosclerosis. Recent 
      data suggest that mature macrophages differentiate into dendritic-like cells when 
      exposed to oxidized low-density lipoprotein (oxLDL). The purpose of the present 
      study was to determine the effect of atorvastatin on the differentiation of 
      macrophages to DCs and the molecular mechanisms of this transition. Mouse 
      macrophage-like RAW264.7 cell was differentiated into a dendritic-like phenotype 
      by incubation with oxLDL in the absence or presence of atorvastatin. The results 
      showed that atorvastatin suppressed DC-like morphologic changes in vitro as 
      assessed by decreased expression of DC maturation markers (CD83, CD11c, CD86, 
      major histocompatibility complex class II, and CD1d). Atorvastatin also inhibited 
      other oxLDL-induced functional changes including endocytic activity, ability to 
      induce T cell proliferation, and cytokine secretion. Western blot analysis showed 
      that oxLDL treatment of RAW264.7 cells induced phosphorylation of p38 
      mitogen-activated protein kinase (MAPK). However, blocking p38 MAPK with SB203580 
      significantly downregulated the expression of DC maturation markers, accompanied 
      by decreased cytokine secretion. The findings of the present work demonstrate 
      that that atorvastatin suppresses the oxLDL-induced DC-like differentiation of 
      RAW264.7 cells by inactivating the p38 MAPK signaling pathway.
FAU - Hu, Liu-Hua
AU  - Hu LH
AD  - Department of Cardiology, Renji Hospital, Shanghai Jiaotong University School of 
      Medicine, Shanghai 200127, China.
FAU - Zhang, Tuo
AU  - Zhang T
FAU - Shao, Qin
AU  - Shao Q
FAU - Li, Dan-Dan
AU  - Li DD
FAU - Jin, Shu-Xuan
AU  - Jin SX
FAU - Nie, Peng
AU  - Nie P
FAU - Yi, Jing
AU  - Yi J
FAU - He, Ben
AU  - He B
FAU - Shen, Ling-Hong
AU  - Shen LH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120814
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (Antigens, CD1d)
RN  - 0 (B7-2 Antigen)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Heptanoic Acids)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Pyrroles)
RN  - 0 (oxidized low density lipoprotein)
RN  - A0JWA85V8F (Atorvastatin)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Antigens, CD1d/genetics/metabolism
MH  - Atorvastatin
MH  - B7-2 Antigen/genetics/metabolism
MH  - Cell Differentiation/drug effects
MH  - Cell Proliferation
MH  - Dendritic Cells/cytology/*drug effects/metabolism
MH  - Down-Regulation
MH  - Heptanoic Acids/*pharmacology
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology
MH  - Lipoproteins, LDL/*antagonists & inhibitors/metabolism
MH  - Macrophages/cytology/*drug effects/metabolism
MH  - Mice
MH  - Pyrroles/*pharmacology
MH  - Signal Transduction
MH  - Time Factors
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2012/08/15 06:00
MHDA- 2013/05/18 06:00
CRDT- 2012/08/15 06:00
PHST- 2012/04/20 00:00 [received]
PHST- 2012/08/03 00:00 [accepted]
PHST- 2012/08/15 06:00 [entrez]
PHST- 2012/08/15 06:00 [pubmed]
PHST- 2013/05/18 06:00 [medline]
AID - 10.1007/s11010-012-1427-3 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2012 Dec;371(1-2):105-13. doi: 10.1007/s11010-012-1427-3. Epub 
      2012 Aug 14.