Cells within the bone marrow (progenitor cells) that express a protein called CD34 have been shown to leave the marrow and travel to sites of tissue injury to mediate repair. Once the cells arrive at the site of injury it has been demonstrated that they can turn into a variety of different cell types, including blood vessel cells, muscle cells, nerve cells, and blood cells, which enhances wound healing. However, the mechanisms responsible for recruiting these CD34-positive progenitor cells from the bone marrow and to the site of tissue damage are unclear. Now, in a study appearing online on February 23 in advance of print publication in the March issue of the Journal of Clinical Investigation, Judy Varner and colleagues from the University of California, San Diego show that a protein called alpha4-beta1 integrin (or VLA-4) promotes the homing of these progenitor cells to VLA-4binding molecules called VCAM and fibronectin found on both actively healing and tumor-associated blood vessels. The researchers found that progenitor cells were drawn to sites of active blood vessel formation in tumors, but not to normal tissues, due to the presence of VLA-4 in the tumor vessels. In addition, the authors found that blocking VLA-4 with an antibody prevented the progenitor cells from sticking to blood vessels, from migrating to newly formed vessels, and from changing into different cell types. Together these studies support a potent role of VLA-4 in the regulation of bone marrowderived progenitor cells in wound repair and migration. The authors suggest that inhibiting this homing process could be useful in suppressing new blood vessel formation in tumors.

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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
23-Feb-2006

Page: 1
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