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

ter a heart attack. They found that CaMKII inhibition substantially reduced the expression of inflammatory proteins that are usually upregulated following a heart attack. They report that the expression of one such protein, complement factor B (CFB), is triggered by CaMKII activation during heart attack or exposure to a bacterial endotoxin, and that mice lacking the Cfb gene were partially protected from the adverse consequences of a heart attack. The data suggest that CaMKII is important in regulating inflammatory gene expression following a heart attack.

TITLE: Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart

AUTHOR CONTACT:
Madhu V. Singh
Carver College of Medicine, University of Iowa, Iowa, City, Iowa, USA.
Phone: (319) 335-8954; Fax: (319) 353-5552; E-mail: madhu-singh@uiowa.edu

Mark E. Anderson
Carver College of Medicine, University of Iowa, Iowa, City, Iowa, USA.
Phone: (319) 353-7101; Fax: (319) 353-6343; E-mail: mark-e-anderson@uiowa.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=35814


STEM CELLS: The protein MuPAR regulates the proliferation and mobilization of blood stem cells

The mechanisms underlying the adhesion and mobilization of hematopoietic stem/progenitor cells (HSPCs), cells that give rise to all other blood cell types, have been poorly understood. Using wild-type and genetically manipulated mice, Peter Carmeliet and his colleagues at Katholieke Universiteit Leuvan, Belgium, reveal in a new study that a membrane-anchored form of the urokinase receptor known as MuPAR is present on a subset of HSPCs and helps maintain this cell population in the bone marrow.

When MuPAR wa
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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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