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Am J Physiol Lung Cell Mol Physiol (December 27, 2002). doi:10.1152/ajplung.00117.2002
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Submitted on April 19, 2002
Accepted on December 18, 2002

Cell-specific and Developmental Expression of Phospholipase C{gamma}(PLC{gamma}) and Diacylglycerol in Fetal Lung

Sujatha M. Ramadurai1*, Wu-Yuan Chen1, George B. Yerozolimsky1, Michelle Zagami1, Christiane EL Dammann1, and Heber C. Nielsen1

1 Department of Pediatrics, Tufts-New England Medical Center, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sramadurai{at}lifespan.org.

EGF Receptor (EGF-R) regulates the development of cell-cell communication in fetal lung, but the signal transduction mechanisms involved are unknown. We hypothesized that in late gestation fetal rat lung, PLC{gamma} expression and activation by EGF is cell-specific and developmentally regulated. PLC{gamma} immunolocalized to cuboidal epithelium and mesenchymal clusters underlying developing saccules. PLC{gamma} protein increased from d17 to d19 then decreased. In cultured fetal lung fibroblasts, EGF stimulated PLC{gamma} phosphorylation, 2.6-fold (d17), 10.8-fold (d19), and 4.2-fold (d21). EGF stimulated 3H-DAG production in fibroblasts (beginning at d18 in females and d19 in males) but not in type II cells of any gestation. EGFR blockade abrogated the observed stimulation of PLC{gamma} phosphorylation by EGF. In conclusion, PLC{gamma} expression and activation by EGF in fetal lung is cell-specific corresponding to the development of EGF-R expression. EGF induces DAG production in a cell- and gestation-specific manner. PLC{gamma} activation by EGF-R in fetal lung fibroblasts may be involved in EGF control of lung development.




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