PMID- 15010288
OWN - NLM
STAT- MEDLINE
DCOM- 20040428
LR  - 20071115
IS  - 0014-4800 (Print)
IS  - 0014-4800 (Linking)
VI  - 76
IP  - 2
DP  - 2004 Apr
TI  - Hemodynamic forces regulate mural macrophage infiltration in experimental aortic 
      aneurysms.
PG  - 108-16
AB  - Blood flow (BF) and wall shear stress (WSS) influence reactive oxygen species 
      production and oxidative stress in abdominal aortic aneurysm (AAA) disease. To 
      gain further insight into the mechanisms of hemodynamic influences on AAA 
      inflammation, we examined aneurysm macrophage density, chemotaxis and survival 
      under varying aortic flow conditions. Rat AAAs were created via porcine 
      pancreatic elastase (PPE) infusion. In selected cohorts, AAA flow was increased 
      via left common femoral arteriovenous fistula (AVF) creation (HF-AAA) or 
      decreased by left common iliac ligation (LF-AAA). WSS was highest in HF-AAA (10.4 
      +/- 2.3 dyn/cm(2) vs. 2.4 +/- 0.4 and 0.5 +/- 0.2 for NF- and LF-AAA, 
      respectively, P < 0.001) 7 days after PPE infusion, with reduced medial 
      macrophage density and increased apoptosis. Adventitial macrophage density was 
      not significantly influenced by flow. Monocyte chemoattractant protein-1 (MCP-1) 
      and granulocyte-macrophage colony-stimulating factor (GM-CSF) gene expression 
      correlated with observed macrophage densities in the media and adventitia. 
      Luminal flow conditions regulate AAA inflammation in part via influences on 
      medial macrophage density. Hemodynamic forces may modulate AAA inflammation and 
      diameter enlargement via direct regulation of intimal macrophage adhesion, 
      transmural migration or survival.
FAU - Sho, Eiketsu
AU  - Sho E
AD  - Division of Vascular Surgery, Stanford University, Palo Alto, CA 94304, USA.
FAU - Sho, Mien
AU  - Sho M
FAU - Hoshina, Katsuyuki
AU  - Hoshina K
FAU - Kimura, Hideo
AU  - Kimura H
FAU - Nakahashi, Takeshi Ken
AU  - Nakahashi TK
FAU - Dalman, Ronald L
AU  - Dalman RL
LA  - eng
GR  - 1 R01 HL46338/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Exp Mol Pathol
JT  - Experimental and molecular pathology
JID - 0370711
RN  - 0 (Chemokine CCL2)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 3.4.21.36 (Pancreatic Elastase)
SB  - IM
MH  - Animals
MH  - Aortic Aneurysm, Abdominal/chemically induced/pathology/*physiopathology
MH  - Apoptosis/physiology
MH  - Cell Movement
MH  - Chemokine CCL2/metabolism
MH  - Gene Expression
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Hemodynamics
MH  - Hemorheology
MH  - Immunohistochemistry
MH  - Macrophages/*physiology
MH  - Male
MH  - Pancreatic Elastase/toxicity
MH  - Rats
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Shear Strength
EDAT- 2004/03/11 05:00
MHDA- 2004/04/29 05:00
CRDT- 2004/03/11 05:00
PHST- 2003/10/21 00:00 [received]
PHST- 2004/03/11 05:00 [pubmed]
PHST- 2004/04/29 05:00 [medline]
PHST- 2004/03/11 05:00 [entrez]
AID - S0014480003001400 [pii]
AID - 10.1016/j.yexmp.2003.11.003 [doi]
PST - ppublish
SO  - Exp Mol Pathol. 2004 Apr;76(2):108-16. doi: 10.1016/j.yexmp.2003.11.003.