mice overexpressing beta1-AR were not protected by the presence of dominant-negative p38-alpha, even though they exhibited increased p38-alpha expression. This study indicates that p38-alpha has an important role downstream of beta2-AR, but not beta1-AR, in development of heart disease. Other signaling molecules must therefore be activated downstream of beta1-AR, and the authors suggest that targeting the signaling molecules downstream of beta-ARs might provide a new approach to treating individuals with heart failure.

TITLE: Inhibition of p38-alpha MAPK rescues cardiomyopathy induced by overexpressed beta2-adrenergic receptor, but not beta1-adrenergic receptor

AUTHOR CONTACT:

Dorothy E. Vatner
University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA
Phone: (973) 972-8920; Fax: (973) 972-7489; E-mail: vatnerdo@umdnj.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=29576

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AUTOIMMUNITY

Autoantibodies help T cells "see" their target

Autoimmune diseases such as type I diabetes and rheumatoid arthritis are caused by the immune system attacking the bodys own tissues. Determining the factors that trigger the immune system to attack is an area of intensive research. In a new study appearing online on April 19, in advance of publication in the May print issue of the Journal of Clinical Investigation, Raphael Clynes and colleagues from Columbia University show that autoantibodies are required to induce disease in a mouse model of autoimmune diabetes mediated by immune cells known as T cells. When CD8+ T cells that recognize ovalbumin were transplanted into mice expressing ovalbumin in the pancreas (the organ targeted by the immune system in type I diabetes) they caused diabetes only if the mice were also transplanted
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
19-Apr-2007

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