PMID- 10969035
OWN - NLM
STAT- MEDLINE
DCOM- 20000927
LR  - 20190706
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 87
IP  - 5
DP  - 2000 Sep 1
TI  - Contribution of monocytes/macrophages to compensatory neovascularization: the 
      drilling of metalloelastase-positive tunnels in ischemic myocardium.
PG  - 378-84
AB  - In a transgenic model of ischemic cardiomyopathy in which monocytes are attracted 
      to the myocardium by the targeted overexpression of monocyte chemoattractant 
      protein-1 (MCP-1), we have observed the presence of endothelial NO synthase and 
      platelet endothelial cell adhesion molecule-1-negative tunnels, occasionally 
      containing blood-derived cells, that probe the cardiac tissue. 
      Immunohistochemical data show that monocytes/macrophages (MCs/Mphs) drill tunnels 
      using the broad-spectrum mouse macrophage metalloelastase. 
      5-Bromo-2'-deoxyuridine incorporation and neo-endothelial markers present in the 
      microvasculature of MCP-1 mouse hearts suggest an active angiogenic process. 
      Further studies will be required to establish that the MC-/Mph-drilled tunnels 
      evolve to become capillaries, connected to the existing vessels and colonized by 
      circulating endothelial cell progenitors. This possibility is supported by the 
      availability of these cells, which is demonstrated by cell tagging with 
      beta-galactosidase placed under an active endothelial Tie-2 promoter. This 
      phenomenon might represent another mechanism, in addition to the secretion of the 
      angiogenic factors, by which MCs/MPhs may participate in the elaboration of new 
      blood vessels in adult tissues.
FAU - Moldovan, N I
AU  - Moldovan NI
AD  - Heart and Lung Institute and the Division of Cardiology, Department of Internal 
      Medicine, College of Medicine and Public Health, Ohio State University, Columbus, 
      Ohio 43210, USA. moldovan-1@medctr.osu.edu
FAU - Goldschmidt-Clermont, P J
AU  - Goldschmidt-Clermont PJ
FAU - Parker-Thornburg, J
AU  - Parker-Thornburg J
FAU - Shapiro, S D
AU  - Shapiro SD
FAU - Kolattukudy, P E
AU  - Kolattukudy PE
LA  - eng
GR  - GM53236/GM/NIGMS NIH HHS/United States
GR  - HL48916/HL/NHLBI NIH HHS/United States
GR  - HL52315/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Chemokine CCL2)
RN  - 0 (Thy-1 Antigens)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, mouse)
RN  - EC 3.4.24.- (Metalloendopeptidases)
SB  - IM
CIN - Circ Res. 2000 Sep 1;87(5):341-3. PMID: 10969028
MH  - Animals
MH  - Capillaries/physiopathology
MH  - Chemokine CCL2/analysis/*biosynthesis
MH  - Heart/*physiopathology
MH  - Immunohistochemistry
MH  - Macrophages/enzymology/*physiology
MH  - Metalloendopeptidases/analysis
MH  - Mice
MH  - Mice, Transgenic
MH  - Monocytes/enzymology/*physiology
MH  - Myocardial Ischemia/blood/*metabolism/physiopathology
MH  - Myocardium/enzymology/pathology/ultrastructure
MH  - Neovascularization, Physiologic/*physiology
MH  - Nitric Oxide Synthase/analysis
MH  - Nitric Oxide Synthase Type II
MH  - Nitric Oxide Synthase Type III
MH  - Staining and Labeling
MH  - Thy-1 Antigens/analysis
EDAT- 2000/09/02 00:00
MHDA- 2000/09/30 00:00
CRDT- 2000/09/02 00:00
PHST- 2000/09/02 00:00 [pubmed]
PHST- 2000/09/30 00:00 [medline]
PHST- 2000/09/02 00:00 [entrez]
AID - 10.1161/01.res.87.5.378 [doi]
PST - ppublish
SO  - Circ Res. 2000 Sep 1;87(5):378-84. doi: 10.1161/01.res.87.5.378.