Abstract |
The potential for bone marrow-derived progenitor cells ( BMDPC) to regenerate myocardial tissue following infarction depends on homing, migration, nourishment, and spatially appropriate growth of BMDPC. Requisite to these objectives is the expression of adhesion molecules (ICAM-1) and chemoattractant cytokines (MCP-1), matrix metalloproteinase ( MMP) activity, a neovasculature, and fibrillar collagen scaffolding. We found that enhanced ICAM-l and MCP-1, as well as MMP activity on day 3 and 7 postMI, are present to facilitate the homing, chemotaxis, and migration of circulating cells into the infarct site. The vascular network formed at the infarct site contains a ratio of conduit to exchange vessels that is greater than that for control tissue and therefore its ability to nourish BMDPC for their growth appears to be tenuous. These findings, together with the dense formation of a fibrillar collagen scar beyond week 2, suggest the optimal time to rebuild myocardium from BMDPC resides within 2 week postMI.
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Authors | Li Lu, John Q Zhang, Felix J Ramires, Yao Sun |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 320
Issue 3
Pg. 907-13
(Jul 30 2004)
ISSN: 0006-291X [Print] United States |
PMID | 15240134
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Chemokine CCL2
- Tissue Inhibitor of Metalloproteinase-1
- Intercellular Adhesion Molecule-1
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Topics |
- Animals
- Cardiac Surgical Procedures
(methods)
- Chemokine CCL2
(metabolism)
- Enzyme Activation
- Extracellular Matrix
(metabolism)
- Hematopoietic Stem Cell Transplantation
(methods)
- Intercellular Adhesion Molecule-1
(metabolism)
- Male
- Myocardial Infarction
(metabolism, pathology, surgery)
- Myocardium
(metabolism, pathology)
- Rats
- Rats, Sprague-Dawley
- Regeneration
(physiology)
- Tissue Distribution
- Tissue Inhibitor of Metalloproteinase-1
(metabolism)
- Wound Healing
(physiology)
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