Notch1 Contributes to Scar Tissue in the Lungs
A group led by Dr. Sem Phan at the University of Michigan, Ann Arbor identified Notch1 as a mediator of lung fibrosis. They present their data in the May 2009 issue of The American Journal of Pathology.
Scar tissue, or fibrosis, can accumulate in the lungs, restricting the flow of oxygen and leading to end-stage lung disease, respiratory failure, and eventually death. An increase in the number of a special type of cells, myofibroblasts, strongly contributes to lung fibrosis.
FIZZ1, a protein found in the lungs, increases the number of myofibroblasts in the lungs. Liu et al hypothesized that Notch1, which regulates cell fate in numerous cell types, plays a role in FIZZ1-mediated myofibroblast differentiation. They found that Notch1 led to an increase of myofibroblasts in the lungs, and that mice that lacked Notch1 had decreased responses to FIZZ1 and lower levels of lung fibrosis.
Taken together, these data suggest that "Notch1 signaling in response to FIZZ1 may play a significant role in myofibroblast differentiation during lung fibrosis." Therefore, Notch1 may provide a novel target for treatment of scar tissue in the lungs.
Liu T, Hu B, Choi YY, Chung MJ, Ullenbruch M, Yu H, Lowe JB, Phan SH: Notch1 signaling in FIZZ1 induction of myofibroblast differentiation. Am J Pathol 2009, 174: 1745-1755
Suppressor of Cytokine Signaling (SOCS)-1 Inhibits Prostate Cancer Growth
Zoran Culig and colleagues at the Innsbruck Medical University, Austria discovered that SOCS-1 negatively regulates prostate cancer proliferation. This report can be found in the May 2009 issue of The American Journal of Pathology.
SOCS family members are expressed in a variety of cancers, including chronic myeloid leukemia, melanoma, and prostate cancer. The role of the various SOCS family members in carcinogenesis, howev
|Contact: Angela Colmone|
American Journal of Pathology