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JCI online early table of contents: March 9, 2009
Date:3/9/2009

s deleted or inhibited, HSPC proliferation was increased, but the ability of these cells to home and adhere to the bone marrow microenvironment was inhibited. Furthermore, the authors show that MuPAR is inactivated by plasmin, which triggers HSPC mobilization. Finally, loss of the gene encoding MuPAR impaired the ability of the HSPCs to repopulate the bone marrow in recipient mice. The authors conclude from these results that MuPAR and plasmin play key roles in regulating HSPC maintenance, homing, engraftment, and mobilization in the bone marrow.

TITLE: Membrane-anchored uPAR regulates the proliferation, marrow pool size, engraftment, and mobilization of mouse hematopoietic stem/progenitor cells

AUTHOR CONTACT:
Peter Carmeliet
Katholieke Universiteit Leuven, Campus Gasthuisberg, Leuven, Belgium.
Phone: 32-16-34-57-72; Fax: 32-16-34-59-90; E-mail: peter.carmeliet@med.kuleuven.be

View the PDF of this article at: https://www.the-jci.org/article.php?id=36010


CARDIOVASCULAR DISEASE: Insulin resistance in liver cells reduces atherosclerosis

Individuals with type 2 diabetes have an increased risk of developing a disease known as atherosclerosis (or hardening of the arteries), which is a leading cause of heart attack and stroke. One characteristic of type 2 diabetes, altered levels of certain fats in the blood (a condition known as dyslipidemia), is thought to be a fundamental reason for the increased risk of developing atherosclerosis. However, the contribution to atherosclerosis risk of another characteristic of type 2 diabetes, the inability of cells to respond to the hormone insulin (a condition known as insulin resistance), has not been definitively determined. Seongah Han and colleagues at Columbia University, New York, have now found, surprisingly, that mice lacking
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Contact: Brooke Grindlinger
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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