In mice models, TGF-beta is enhanced in lungs and it’s inhibition can reverse the ill affects.



Researchers found that the activity of transforming growth factor-beta (TGF-beta) is elevated in the lungs of a mice model of bronchopulmonary dysplasia (BDP). Additionally, treatment with an antibody to TGF-beta decreased the growth factor’s activity and improved lung development.


To test TGF-beta affect on BDP, a group of pregnant mice received injections of either an antibody against TGF-beta or a control substance a few days before giving birth. Their offspring were housed in either normal air or 85% oxygen, a concentration known to cause BPD in mice, for 10 days after birth.


The investigators from Massachusetts General Hospital and Genzyme saw that the newborn mice exposed to high oxygen levels without the neutralizing antibody treatment had elevated TGF-beta activity. Their alveoli were also incompletely developed, a deficit typically seen in BPD.


The mice that received the TGF-beta-neutralizing antibody showed significantly lower levels of growth factor activity and more normal lung development. Moreover, the improved lung development of these mice was also associated with improved body growth, at a rate of which was virtually identical to that of the animals in normal air.


This study will appear in the American Journal of Physiology—Lung Cellular and Molecular Physiology.








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