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1 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA
2 Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA
3 Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA; Developmental Biology Division, China Medical University, Shenyang, Liaoning, China
4 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA
5 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA; Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: wshi{at}chla.usc.edu.
Transforming growth factor-
(TGF-) signaling plays an important regulatory role during lung development and remodeling. Smad3 is a major downstream signal transducer in the TGF- pathway from the cell membrane to the nucleus. In Smad3 null mutant mice, we have
observed retarded lung alveolarization from postnatal day 7 to day 28, and subsequently centrilobular emphysema starting from day 28, as determined by morphometric analysis. In addition to the morphological changes, peripheral lung cell proliferation in Smad3 knockout
mice was reduced as compared to the wild-type control between postnatal days 7-28. Expression of tropoelastin at the mRNA level was also dramatically decreased in Smad3 knockout lungs from postnatal day 28 through adulthood. Furthermore, increased MMP9 protein expression and
activity were detected in the Smad3 knockout mouse lung tissue and the bronchoalveolar lavage fluid at postnatal day 28, when the centrilobular emphysema pathology was just beginning to appear. Therefore, these results indicate that Smad3 has not only a positive regulatory impact on
neonatal lung alveolarization, but also potentially plays a protective role against the occurrence of centrilobular emphysema later on in life.
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