PMID- 22513464
OWN - NLM
STAT- MEDLINE
DCOM- 20130530
LR  - 20131121
IS  - 0371-0874 (Print)
IS  - 0371-0874 (Linking)
VI  - 64
IP  - 2
DP  - 2012 Apr 25
TI  - [Inhibitory effect of caveolin-1 on endoplasmic reticulum stress-induced 
      apoptosis in macrophages via p38 MAPK pathway].
PG  - 149-54
AB  - Endoplasmic reticulum (ER) stress occurs in macrophage-rich areas of advanced 
      atherosclerotic lesions and contributes to macrophage apoptosis and subsequent 
      plaque necrosis. The purpose of the present study was to investigate the effects 
      of caveolin-1 (Cav-1) on ER stress-induced apoptosis in cultured macrophages and 
      the underlying mechanisms. RAW264.7 cells were incubated with thapsigargin (TG) 
      to establish ER stress model. And Cav-1 expression was detected by Western blot. 
      After being pretreated with filipin(III), a caveolae inhibitor, RAW264.7 cells 
      were assayed with flow cytometry and confocal laser scanning microscopy to detect 
      cell apoptosis. Moreover, p38 mitogen-activated protein kinase (MAPK) 
      phosphorylation and C/EBP homologous protein (CHOP) expression were detected with 
      Western blot. The results showed that Cav-1 expression was markedly increased at 
      early stage of TG treatment (P < 0.05) and then decreased with prolonged or high 
      dose TG treatments. The increasing of Cav-1 expression induced by TG in RAW264.7 
      cells was abolished under inhibition of caveolae by filipin(III) (P < 0.05). The 
      effect of TG on apoptosis of RAW264.7 cells was further augmented after 
      pretreatment with filipin(III) (P < 0.05). Western blotting showed that MAPK 
      phosphorylation induced by TG was inhibited by filipin(III) in RAW264.7 cells (P 
      < 0.05), whereas CHOP remained unchanged (P > 0.05). These results suggest that 
      Cav-1 may play a critical role in suppressing ER stress-induced macrophages 
      apoptosis in vitro, and one of the mechanisms may be correlated with the 
      activation of p38 MAPK prosurvival pathway.
FAU - Yue, Wen
AU  - Yue W
AD  - Pathophysiology Department, Taishan Medical College, Taian, China.
FAU - Yao, Shu-Tong
AU  - Yao ST
FAU - Zhou, Xiao
AU  - Zhou X
FAU - Si, Yan-Hong
AU  - Si YH
FAU - Sang, Hui
AU  - Sang H
FAU - Wang, Jia-Fu
AU  - Wang JF
FAU - Shang, Zhan-Ping
AU  - Shang ZP
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Sheng Li Xue Bao
JT  - Sheng li xue bao : [Acta physiologica Sinica]
JID - 20730130R
RN  - 0 (Caveolin 1)
RN  - 0 (Ddit3 protein, rat)
RN  - 147336-12-7 (Transcription Factor CHOP)
RN  - 67526-95-8 (Thapsigargin)
RN  - 87Z59R7D14 (Filipin)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Caveolin 1/genetics/*metabolism
MH  - Cell Line
MH  - Endoplasmic Reticulum Stress/*physiology
MH  - Filipin/pharmacology
MH  - MAP Kinase Signaling System
MH  - Macrophages/*cytology/drug effects
MH  - Mice
MH  - Thapsigargin/pharmacology
MH  - Transcription Factor CHOP/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2012/04/20 06:00
MHDA- 2013/06/01 06:00
CRDT- 2012/04/20 06:00
PHST- 2012/04/20 06:00 [entrez]
PHST- 2012/04/20 06:00 [pubmed]
PHST- 2013/06/01 06:00 [medline]
PST - ppublish
SO  - Sheng Li Xue Bao. 2012 Apr 25;64(2):149-54.