PMID- 25967876
OWN - NLM
STAT- MEDLINE
DCOM- 20160208
LR  - 20211203
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 35
IP  - 6
DP  - 2015
TI  - Angiotensin-(1-7) Attenuates Angiotensin II-Induced ICAM-1, VCAM-1, and MCP-1 
      Expression via the MAS Receptor Through Suppression of P38 and NF-kappaB Pathways in 
      HUVECs.
PG  - 2472-82
LID - 10.1159/000374047 [doi]
AB  - BACKGROUND/AIMS: Atherosclerosis is a chronic inflammatory disease. Intracellular 
      adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and 
      monocyte chemoattractant protein-1 (MCP-1) play important roles in inflammatory 
      processes. P38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB 
      signaling regulate ICAM-1, VCAM-1, and MCP-1 expression. Angiotensin (Ang) II 
      upregulates ICAM-1, VCAM-1, and MCP-1 expression through the P38 MAPK and NF-kappaB 
      pathways. Ang-(1-7) may oppose the actions of Ang II. We investigated whether 
      Ang-(1-7) prevents Ang II-induced ICAM-1, VCAM-1, and MCP-1 expression in human 
      umbilical vein endothelial cells (HUVECs). METHODS: ICAM-1, VCAM-1, and MCP-1 
      expression was estimated by real-time polymerase chain reaction (PCR) and 
      enzyme-linked immunosorbent assay (ELISA); P38, NF-kappaB, and p-IkappaB-alpha expression was 
      estimated by western blotting. RESULTS: Ang-(1-7) inhibited Ang II-induced 
      ICAM-1, VCAM-1, and MCP-1 expression and secretion in HUVECs. Ang II sharply 
      increased P38 MAPK phosphorylation, which was inhibited by pretreatment with 
      Ang-(1-7). Moreover, Ang-(1-7) significantly inhibited Ang II-induced IkappaB-alpha 
      phosphorylation and NF-kappaB P65 nuclear translocation. The MAS receptor antagonist 
      A-779 abolished the suppressive effects of Ang-(1-7). CONCLUSION: Ang-(1-7) 
      attenuates Ang II-induced ICAM-1, VCAM-1, and MCP-1 expression via the MAs 
      receptor by suppressing the P38 and NF-kappaB pathways in HUVECs. Ang-(1-7) might 
      delay the progression of inflammatory diseases, including atherosclerosis.
CI  - (c) 2015 S. Karger AG, Basel.
FAU - Liang, Bin
AU  - Liang B
AD  - Department of Cardiology, The Second Hospital of Shanxi Medical University, 
      Taiyuan, China.
FAU - Wang, Xin
AU  - Wang X
FAU - Zhang, Nana
AU  - Zhang N
FAU - Yang, Huiyu
AU  - Yang H
FAU - Bai, Rui
AU  - Bai R
FAU - Liu, Ming
AU  - Liu M
FAU - Bian, Yunfei
AU  - Bian Y
FAU - Xiao, Chuanshi
AU  - Xiao C
FAU - Yang, Zhiming
AU  - Yang Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150424
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (NFKBIA protein, human)
RN  - 0 (Peptide Fragments)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 11128-99-7 (Angiotensin II)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 9041-90-1 (Angiotensin I)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - IJ3FUK8MOF (angiotensin I (1-7))
SB  - IM
MH  - Angiotensin I/*pharmacology
MH  - Angiotensin II/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/drug effects/metabolism
MH  - Humans
MH  - I-kappa B Proteins/metabolism
MH  - Intercellular Adhesion Molecule-1/*metabolism
MH  - NF-KappaB Inhibitor alpha
MH  - NF-kappa B/*metabolism
MH  - Peptide Fragments/*pharmacology
MH  - Phosphorylation/drug effects
MH  - Proto-Oncogene Mas
MH  - Proto-Oncogene Proteins/*metabolism
MH  - Receptors, G-Protein-Coupled/*metabolism
MH  - Signal Transduction/drug effects
MH  - Vascular Cell Adhesion Molecule-1/*metabolism
MH  - p38 Mitogen-Activated Protein Kinases/*metabolism
EDAT- 2015/05/15 06:00
MHDA- 2016/02/09 06:00
CRDT- 2015/05/14 06:00
PHST- 2015/03/06 00:00 [accepted]
PHST- 2015/05/14 06:00 [entrez]
PHST- 2015/05/15 06:00 [pubmed]
PHST- 2016/02/09 06:00 [medline]
AID - 000374047 [pii]
AID - 10.1159/000374047 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2015;35(6):2472-82. doi: 10.1159/000374047. Epub 2015 Apr 
      24.