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Biotech / Medical : Indications -- scarring, fibrosis, adhesions, keloids
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From: scaram(o)uche10/26/2011 12:34:21 AM
   of 32
 
Am J Respir Cell Mol Biol. 2011 Oct 20. [Epub ahead of print]

MEK-ERK pathway modulation ameliorates pulmonary fibrosis associated with epidermal growth factor receptor activation.

Madala SK, Schmidt S, Davidson C, Ikegami M, Wert S, Hardie WD.

Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States.

Pulmonary fibrosis remains a significant public health burden with no proven therapies. The MAPK/MEK/ERK signaling cascade is a major pathway controlling cellular processes associated with fibrogenesis including growth, proliferation and survival. Activation of the MAPK/ERK pathway is detected in the lungs of human fibrosis samples; however the effect of modulating the pathway in vivo is unknown. Overexpression of transforming growth factor alpha (TGFa) in the lung epithelium of transgenic mice causes a progressive pulmonary fibrosis associated with increased MEK/ERK activation localized primarily in mesenchymal cells. To determine the role of MEK pathway in the induction of TGFa-induced lung fibrosis, TGFa was overexpressed for four weeks while mice were simultaneously treated with the specific MEK inhibitor ARRY-142886 (ARRY). Treatment with ARRY prevented increases in lung cell proliferation and total lung collagen, attenuated production of extracellular matrix genes and protected mice from changes in lung function. ARRY administered as a rescue treatment after fibrosis was already established inhibited fibrosis progression as assessed by lung histology, changes in body weights, extracellular matrix gene expression and lung mechanics. These findings demonstrate MEK inhibition prevents progression of established fibrosis in the TGFa model and provides proof-of-concept of targeting the MEK pathway in fibrotic lung disease.
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