PMID- 28300760
OWN - NLM
STAT- MEDLINE
DCOM- 20170420
LR  - 20220331
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 18
IP  - 3
DP  - 2017 Mar 16
TI  - The Essential Role of Pin1 via NF-kappaB Signaling in Vascular Inflammation and 
      Atherosclerosis in ApoE(-/-) Mice.
LID - 10.3390/ijms18030644 [doi]
LID - 644
AB  - Atherosclerosis, as a chronic inflammatory disease, is the major underlying cause 
      of death worldwide. However, the mechanisms that underlie the inflammatory 
      process are not completely understood. Prolyl-isomerase-1 (Pin1), as a unique 
      peptidyl-prolyl isomerase, plays an important role in inflammation and 
      endothelial dysfunction. Herein, we investigate whether Pin1 regulates vascular 
      inflammation and atherosclerosis, and clarify its mechanisms in these processes. 
      ApoE(-/-) mice were randomly given either juglone (0.3, 1 mg/kg, two times per 
      week) or vehicle i.p. for 4 weeks. Compared with ApoE(-/-) mice, treatment by 
      juglone resulted not only in markedly attenuated macrophage infiltration and 
      atherosclerotic lesion area in a lipid-independent manner, but also in decreased 
      expression of Pin1, vascular cell adhesion molecule-1 (VCAM-1), monocyte 
      chemoattractant protein-1 (MCP-1), and NF-kappaB activity in aorta. Then, EA.hy926 
      cells were pretreated with juglone (6 mumol/L), Pin1 siRNA, NF-kappaB inhibitor, or 
      vehicle prior to exposure to ox-LDL (50 mug/mL). It was observed that treatment 
      with juglone or Pin1 siRNA suppressed expression of VCAM-1 in oxLDL-incubated 
      EA.hy926 cells and decreased THP-1 cell adhesion to oxLDL-stimulated endothelial 
      cells through the NF-kappaB signal pathway. Our findings indicate that Pin1 plays a 
      vital role on the development of vascular inflammation and atherosclerosis.
FAU - Liu, Ming
AU  - Liu M
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. lmingw0559@163.com.
FAU - Yu, Peng
AU  - Yu P
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. ypbaggio@163.com.
FAU - Jiang, Hong
AU  - Jiang H
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. jiang.hong@zs-hospital.sh.cn.
FAU - Yang, Xue
AU  - Yang X
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. sherrina_1010@126.com.
FAU - Zhao, Ji
AU  - Zhao J
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. zhao.ji@zs-hospital.sh.cn.
FAU - Zou, Yunzeng
AU  - Zou Y
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. zou.yunzeng@zs-hospital.sh.cn.
FAU - Ge, Junbo
AU  - Ge J
AD  - Shanghai Institute of Cardiovascular Diseases, Institute of Clinical Science, 
      Zhongshan Hospital, Shanghai Medical College, Fudan University, 180 Fenglin Road, 
      Shanghai 200032, China. jbge@zs-hospital.sh.cn.
LA  - eng
PT  - Journal Article
DEP - 20170316
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Apolipoproteins E)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (NIMA-Interacting Peptidylprolyl Isomerase)
RN  - 0 (Naphthoquinones)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - W6Q80SK9L6 (juglone)
SB  - IM
MH  - Animals
MH  - Aorta/metabolism/pathology
MH  - Apolipoproteins E/deficiency/*genetics
MH  - Atherosclerosis/*metabolism
MH  - Cell Line
MH  - Chemokine CCL2/genetics/metabolism
MH  - Endothelium, Vascular/drug effects/*metabolism
MH  - Humans
MH  - Macrophages/drug effects
MH  - Male
MH  - Mice
MH  - NF-kappa B/genetics/*metabolism
MH  - NIMA-Interacting Peptidylprolyl Isomerase/genetics/*metabolism
MH  - Naphthoquinones/pharmacology
MH  - *Signal Transduction
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
PMC - PMC5372656
OTO - NOTNLM
OT  - NF-kappaB
OT  - Pin1
OT  - atherosclerosis
OT  - inflammation
COIS- The authors declare no conflict of interest.
EDAT- 2017/03/17 06:00
MHDA- 2017/04/21 06:00
PMCR- 2017/03/01
CRDT- 2017/03/17 06:00
PHST- 2017/02/21 00:00 [received]
PHST- 2017/03/10 00:00 [revised]
PHST- 2017/03/13 00:00 [accepted]
PHST- 2017/03/17 06:00 [entrez]
PHST- 2017/03/17 06:00 [pubmed]
PHST- 2017/04/21 06:00 [medline]
PHST- 2017/03/01 00:00 [pmc-release]
AID - ijms18030644 [pii]
AID - ijms-18-00644 [pii]
AID - 10.3390/ijms18030644 [doi]
PST - epublish
SO  - Int J Mol Sci. 2017 Mar 16;18(3):644. doi: 10.3390/ijms18030644.