| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA; Department of Developmental Biology, China Medical University, Shenyang, Liaoning, China
2 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA
3 Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA
4 Department of Developmental Biology, China Medical University, Shenyang, Liaoning, China
5 Developmental Biology Program, The Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, CA, USA; Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: wshi{at}chla.usc.edu.
BMP4 plays very important roles in regulating developmental processes of many organs, including lung. Smad1 is one of the BMP receptor downstream signaling
proteins that transduce BMP4 ligand signaling from cell surface to nucleus. The dynamic expression patterns of Smad1 in embryonic mouse lungs were examined
using immunohistochemistry. Smad1 protein was predominantly detected in peripheral airway epithelial cells of early embryonic lung tissue (E12.5), while
Smad1 protein expression in mesenchymal cells increased during mid-late gestation. Many Smad1-positive mesenchymal cells were localized adjacent to large airway
epithelial cells and endothelial cells of blood vessels, which colocalized with a molecular marker of smooth muscle cells (
-smooth muscle actin). The biological
function of Smad1 in early lung branching morphogenesis was then studied in our established E11.5 lung explant culture model. Reduction of endogenous Smad1
expression was achieved by adding a Smad1-specific antisense DNA oligonucleotide, causing about 20% reduction of lung epithelial branching. Furthermore, airway
epithelial cell proliferation and differentiation were also inhibited when endogenous Smad1 expression was knocked down. Therefore, these data indicate that Smad1,
acting as an intracellular BMP signaling pathway component, positively regulates early mouse embryonic lung branching morphogenesis.
This article has been cited by other articles:
|
|
 |
|
  Y. Maeda, V. Dave, and J. A. Whitsett Transcriptional Control of Lung Morphogenesis Physiol Rev, January 1, 2007; 87(1): 219 - 244. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. V. Cardoso and J. Lu Regulation of early lung morphogenesis: questions, facts and controversies Development, May 1, 2006; 133(9): 1611 - 1624. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
