MONDAY, Jan. 14 (HealthDay News) -- The Pin1 protein contributes to lung fibrosis and airway remodeling in chronic asthma by regulating activated eosinophils' production of transforming growth factor-beta-1 (TGF-β1), according to research published online Jan. 10 in the Journal of Clinical Investigation.
Zhong-Jian Shen, Ph.D., and colleagues from the University of Wisconsin-Madison, investigated factors regulating TGF-β1 in pulmonary eosinophils responsible for remodeling in chronic asthma.
The researchers found that the peptidyl-prolyl-isomerase Pin1 promoted the stability of the TGF-β1 messenger RNA and regulated cytokine production in activated eosinophils. Blocking Pin1 activity in a rat asthma model reduced expression of TGF-β1 and collagen, as well as eosinophilic pulmonary inflammation and airway remodeling. Mice lacking the Pin1 gene that are chronically exposed to allergens had reduced peribronchiolar collagen deposition.
"These data suggest that pharmacologic suppression of Pin1 may be a novel therapeutic option to prevent airway fibrosis in individuals with chronic asthma," Shen and colleagues conclude.
Abstract
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