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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00380.2001
Submitted on September 24, 2001
Accepted on February 15, 2002
1 Pediatrics/Obstetrics and Gynecology, Harbor-UCLA Research & Education Institute, Torrance, CA, USA
* To whom correspondence should be addressed. E-mail: jtorday{at}gcrc.rei.edu.
Intrauterine lung development, culminating in physiologic pulmonary surfactant production by epithelial type II (TII) cells, is driven by fluid distension through unknown mechanisms. Differentiation of alveolar epithelial and mesenchymal cells is mediated by soluble factors like Parathyroid Hormone-related Protein (PTHrP), a stretch-sensitive TII cell product; PTHrP stimulates pulmonary surfactant production by a paracrine feed-back loop mediated by leptin, a soluble product of the mature lipofibroblast (LF). When LFs and TIIs are stretched in co-culture, there is a 5-fold increase in surfactant phospholipid synthesis, which can be "neutralized" by inhibitors of PTHrP or leptin, implicating a paracrine feed-back loop in this mechanism. Stretching lipofibroblasts stimulates PTHrP binding (2.5-fold) and down-stream stimulation of triglyceride uptake quantitatively (15-25%), due to up-regulation of Adipocyte Differentiation Related Protein expression. Stretching TII cells increases leptin stimulation of their surfactant phospholipid synthesis by 3-fold, suggesting that retrograde signaling by leptin to TII cells is also stretch-sensitive. We conclude that the effect of stretch on alveolar LF and TII differentiation is coordinated by PTHrP, leptin, and their receptors.
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