PMID- 32569018
OWN - NLM
STAT- MEDLINE
DCOM- 20210629
LR  - 20210629
IS  - 1533-4023 (Electronic)
IS  - 0160-2446 (Linking)
VI  - 76
IP  - 3
DP  - 2020 Sep
TI  - CEACAM1 Inhibited IkappaB-alpha/NF-kappaB Signal Pathway Via Targeting MMP-9/TIMP-1 Axis in 
      Diabetic Atherosclerosis.
PG  - 329-336
LID - 10.1097/FJC.0000000000000868 [doi]
AB  - Atherosclerosis (AS) is the most common and serious complication in type 2 
      diabetes mellitus (T2DM). Recent studies have emphasized that inflammation is the 
      main cause of atherosclerosis. Studies have shown that carcinoembryonic 
      antigen-related cellular adhesion molecule 1 (CEACAM1) regulates the expression 
      of matrix metallopeptidase 9 (MMP-9) after ischemic stroke to reduce 
      inflammation. The aim of this study was to elucidate potential molecular 
      mechanism of CEACAM1 on the inflammatory response in atherosclerosis. The serum 
      levels of CEACAM1, MMP-9, and tissue inhibitors of metalloproteinase 1 (TIMP-1) 
      in T2DM patients and healthy control was detected. The results showed that the 
      levels of CEACAM1 and TIMP-1 were significantly decreased, and the levels of 
      MMP-9 were significantly higher than those in the control group. Moreover, we 
      also observed the effect of CEACAM1 on atherosclerosis in T2DM rats. Hematoxylin 
      & eosin (HE) staining and oil red staining showed that CEACAM1 recombinant 
      protein reduced intima-media thickness and the area of atherosclerotic plaques. 
      To further explore the molecular mechanism of CEACAM1 regulating MMP-9/TIMP-1, we 
      conducted experiments in rat aorta vascular endothelial cells and rat aorta 
      smooth muscle cells. The result showed that CEACAM1 inhibits inflammatory 
      response via MMP-9/TIMP-1 axis. Taken together, CEACAM1 attenuates diabetic 
      atherosclerosis by inhibition of IkappaB/NF-kappaB signal pathway via MMP-9/TIMP-1 axis, 
      which indicate that CEACAM1 is potentially amenable to therapeutic manipulation 
      for clinical application in atherosclerosis in T2DM.
FAU - Yu, Jie
AU  - Yu J
AD  - Department of Thoracocardiac Surgery, 920th Hospital of Joint Logistics Support 
      Force, Kunming, Yunnan, China.
FAU - Sun, Guihu
AU  - Sun G
AD  - Laboratory of Molecular Cardiology, Department of Cardiology, The First 
      Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
FAU - Chen, Yu
AU  - Chen Y
AD  - Department of Thoracocardiac Surgery, 920th Hospital of Joint Logistics Support 
      Force, Kunming, Yunnan, China.
FAU - Li, Lin
AU  - Li L
AD  - Department of Cardiovascular, The First Hospital of Kunming, Kunming, Yunnan, 
      China.
FAU - Wang, Huawei
AU  - Wang H
AD  - Laboratory of Molecular Cardiology, Department of Cardiology, The First 
      Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
FAU - Tu, Dong
AU  - Tu D
AD  - Department of Thoracocardiac Surgery, 920th Hospital of Joint Logistics Support 
      Force, Kunming, Yunnan, China.
FAU - Li, Longjun
AU  - Li L
AD  - Laboratory of Molecular Cardiology, Department of Cardiology, The First 
      Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
FAU - Meng, Zhaohui
AU  - Meng Z
AD  - Laboratory of Molecular Cardiology, Department of Cardiology, The First 
      Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
FAU - Wang, Yan
AU  - Wang Y
AD  - Laboratory of Molecular Cardiology, Department of Cardiology, The First 
      Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antigens, CD)
RN  - 0 (CD66 antigens)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (TIMP1 protein, human)
RN  - 0 (TIMP1 protein, rat)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - EC 3.4.24.35 (MMP9 protein, human)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - EC 3.4.24.35 (Mmp9 protein, rat)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antigens, CD/metabolism/*pharmacology
MH  - Arteries/*drug effects/enzymology/pathology
MH  - Atherosclerosis/enzymology/etiology/pathology/*prevention & control
MH  - Case-Control Studies
MH  - Cell Adhesion Molecules/metabolism/*pharmacology
MH  - Diabetes Mellitus, Experimental/complications/*drug therapy/enzymology
MH  - Diabetes Mellitus, Type 2/complications/*drug therapy/enzymology
MH  - Diabetic Angiopathies/enzymology/etiology/pathology/*prevention & control
MH  - Female
MH  - Humans
MH  - I-kappa B Proteins/*metabolism
MH  - Male
MH  - Matrix Metalloproteinase 9/*metabolism
MH  - Middle Aged
MH  - NF-kappa B/*metabolism
MH  - Plaque, Atherosclerotic
MH  - Rats, Wistar
MH  - Signal Transduction
MH  - Tissue Inhibitor of Metalloproteinase-1/*metabolism
EDAT- 2020/06/23 06:00
MHDA- 2021/06/30 06:00
CRDT- 2020/06/23 06:00
PHST- 2020/06/23 06:00 [pubmed]
PHST- 2021/06/30 06:00 [medline]
PHST- 2020/06/23 06:00 [entrez]
AID - 10.1097/FJC.0000000000000868 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2020 Sep;76(3):329-336. doi: 
      10.1097/FJC.0000000000000868.