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JCI early table of contents for Nov. 26, 2012
Date:11/26/2012

>A sticky situation: researchers identify mucus-producing pathway in human airway cells

Inflammatory airway diseases such as asthma, COPD, and cystic fibrosis are associated with increased mucus production, but the molecular mechanisms that are responsible for mucus production in these diseases have not been determined. In this issue of the Journal of Clinical Investigation, researchers led by Michael Holtzman at Washington University of St. Louis defined a cell signaling pathway that enhances mucus production in the cells that line the human airway. The pathway, which involves the protein MAPK13, was also activated in human COPD patients. By inhibiting the activity of MAPK13, Holtzman and colleagues were able to reduce mucus production in human airway epithelial cells, suggesting that therapeutics targeting this pathway might be useful for the treatment of mucus production in humans.

TITLE:
IL-13-induced airway mucus production is blocked by MAPK13 inhibition

AUTHOR CONTACT:
Michael Holtzman
Washington University School of Medicine, St. Louis, MO, USA
Phone: 314-362-8970; Fax: 314-362-9002; E-mail: holtzmanm@wustl.edu

View this article at: http://www.jci.org/articles/view/64896?key=33af0229095ae19f52d5

Too much of a good thing: extra VEGF signaling slows tumor growth

Angiogenesis is the formation of new blood vessels. Establishment of a blood supply promotes tumor growth by providing access to oxygen and nutrients. Blood vessel development is largely mediated by a growth factor known as VEGF, which is targeted by anti-angiogenic therapies. In this issue of the Journal of Clinical Investigation, researchers led by Hong Chen at the University of Oklahoma identified two new proteins, epsin1 and epsin2, as important regulators of VEGF-sti
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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