PMID- 21411099
OWN - NLM
STAT- MEDLINE
DCOM- 20111014
LR  - 20171116
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 216
IP  - 2
DP  - 2011 Jun
TI  - Hepatocyte growth factor promotes an anti-inflammatory cytokine profile in human 
      abdominal aortic aneurysm tissue.
PG  - 307-12
LID - 10.1016/j.atherosclerosis.2011.02.025 [doi]
AB  - Abdominal aortic aneurysm (AAA) is characterized by the destruction of tissue 
      architecture due to chronic inflammation of unknown etiology. Recent studies have 
      indicated that control of inflammation is a promising therapeutic strategy; 
      however, no established pharmacological intervention is currently available for 
      AAA. We found that hepatocyte growth factor (HGF) was expressed in aneurysmal 
      tissue, and colocalized with von Willebrand factor, the endothelial cell marker, 
      in the most damaged part of the aneurysmal walls. In ex vivo cultures of human 
      AAA tissue, exogenously added HGF in the presence of tumor necrosis factor-alpha 
      (TNF-alpha) enhanced the secretion of anti-inflammatory cytokine interleukin-10 
      (IL-10) and suppressed the secretion of proinflammatory monocyte/macrophage 
      chemotactic protein-1 (MCP-1). The angiotensin converting enzyme (ACE) 
      inhibitors, imidaprilat and perindoprilat, enhanced the secretion of endogenous 
      HGF, augmented the TNF-alpha-induced IL-10 secretion and suppressed MCP-1 secretion 
      from AAA tissue. The ACE inhibitors also augmented the expression of HGF in the 
      presence of bradykinin in human aortic endothelial cells in culture (HAECs). In 
      contrast, HGF secretion was not affected by either an angiotensin II type 1 
      receptor (AT1) antagonist or angiotensin II in AAA tissue or in HAECs. These 
      results suggested that angiotensin converting enzyme inhibitors may be useful in 
      controlling chronic inflammation in AAA, partly due to their enhancement of HGF 
      secretion.
CI  - Copyright (c) 2011 Elsevier Ireland Ltd. All rights reserved.
FAU - Shintani, Yusuke
AU  - Shintani Y
AD  - Department of Surgery, Kurume University School of Medicine, Japan.
FAU - Aoki, Hiroki
AU  - Aoki H
FAU - Nishihara, Michihide
AU  - Nishihara M
FAU - Ohno, Satoko
AU  - Ohno S
FAU - Furusho, Aya
AU  - Furusho A
FAU - Hiromatsu, Shin-ichi
AU  - Hiromatsu S
FAU - Akashi, Hidetoshi
AU  - Akashi H
FAU - Imaizumi, Tsutomu
AU  - Imaizumi T
FAU - Aoyagi, Shigeaki
AU  - Aoyagi S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110224
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Imidazolidines)
RN  - 0 (Indoles)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 2UV6ZNQ92K (perindoprilat)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - WUU07Y30IA (imidaprilat)
SB  - IM
MH  - Angiotensin-Converting Enzyme Inhibitors/pharmacology
MH  - Anti-Inflammatory Agents/metabolism/*pharmacology
MH  - Aorta/pathology
MH  - Aortic Aneurysm, Abdominal/*metabolism
MH  - Cytokines/*biosynthesis/metabolism
MH  - Endothelial Cells/cytology
MH  - Hepatocyte Growth Factor/*metabolism
MH  - Humans
MH  - Imidazolidines/pharmacology
MH  - Indoles/pharmacology
MH  - Interleukin-10/metabolism
MH  - Renin-Angiotensin System
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/blood
EDAT- 2011/03/18 06:00
MHDA- 2011/10/15 06:00
CRDT- 2011/03/18 06:00
PHST- 2010/08/23 00:00 [received]
PHST- 2011/02/04 00:00 [revised]
PHST- 2011/02/15 00:00 [accepted]
PHST- 2011/03/18 06:00 [entrez]
PHST- 2011/03/18 06:00 [pubmed]
PHST- 2011/10/15 06:00 [medline]
AID - S0021-9150(11)00186-9 [pii]
AID - 10.1016/j.atherosclerosis.2011.02.025 [doi]
PST - ppublish
SO  - Atherosclerosis. 2011 Jun;216(2):307-12. doi: 
      10.1016/j.atherosclerosis.2011.02.025. Epub 2011 Feb 24.