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Preview of articles to be published Jan. 3, 2012
Date:1/3/2012

Research identifies how time heals all wounds

Wound healing requires complex interactions between cells resident at the damaged site and infiltrating immune cells. As healing progresses, the growth of new blood vessels is critical to provide nutrients and oxygen. Endothelial progenitor cells (EPCs) are cells that come from the bone marrow and are key to the production of new vessels, but the signals that direct their emigration from the bone marrow are unknown. In this paper, Toshikazu Kondo and colleagues at Wakayama Medical University, in Wakayama, Japan, demonstrate that the chemokine CCL5 helps to direct the recruitment of EPCs to sites of wounding by acting on the chemokine receptor CCR5. Mice that don't express CCR5 display delayed wound healing. These findings suggest that humans who carry mutations in CCR5 may also experience problems with wound healing, and identify the CCR5/CCL5 as a potential clinical target to promote healing.

TITLE: Pivotal role of the CCL5/CCR5 interaction for recruitment of endothelial progenitor cells in mouse wound healing

AUTHOR CONTACT:
Toshikazu Kondo
Dept Forensic Med Wakayama Med Univ, Wakayama, JPN
Phone: +81-73-441-0641; Fax: +81-73-441-0641; E-mail: kondot@wakayama-med.ac.jp
View this article at: http://www.jci.org/articles/view/43027?key=c20fc207be9b9c2d8fa1


ONCOLOGY

Cbx7 suppresses tumor growth

The unregulated cell growth that occurs in cancer is in part related to changes in the expression of genes that control the cell cycle. CBX7 is a gene known to be involved in a repressor complex that is capable of altering the proteins around which DNA is wrapped such that genes cannot be expressed. Previous research has implicated the loss of CBX7 in cancer progression; its loss is correlated with malign
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Contact: Karen Honey
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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