|  Help  |  About  |  Contact Us

Publication : Dexamethasone enhances ras-recision gene expression in cultured murine fetal lungs: role in development.

First Author  Chinoy MR Year  2000
Journal  Am J Physiol Lung Cell Mol Physiol Volume  279
Issue  2 Pages  L312-8
PubMed ID  10926554 Mgi Jnum  J:63985
Mgi Id  MGI:1888570 Doi  10.1152/ajplung.2000.279.2.L312
Citation  Chinoy MR, et al. (2000) Dexamethasone enhances ras-recision gene expression in cultured murine fetal lungs: role in development. Am J Physiol Lung Cell Mol Physiol 279(2):L312-8
abstractText  We have shown that dexamethasone (Dex) accelerates maturation and differentiation of cultured fetal murine lungs (Cilley RE, Zgleszewski SE, Krummel TM, and Chinoy MR. Surg Forum 47: 692-695, 1996). We now demonstrate that although Dex inhibits thinning of acinar walls and secondary septa formation, it does, however, promote lung growth. CD-1 murine fetal lungs were cultured for 7 days in the presence and absence of 10 nM Dex. Dex-modulated genes were investigated and identified by differential display of mRNAs performed with specific anchor primer H-T(11)G and 24 arbitrary primers. Thirty-five differentially expressed cDNAs were isolated, subcloned, sequenced, and identified through BLAST searches. One of these cDNAs, termed Dex2, with enhanced expression in Dex-treated lungs, had 100% similarity with ras-recision gene (rrg), also known as the lysyl oxidase (LOX) gene that encodes lysyl oxidase. LOX gene is very highly conserved, with significant sequence similarity among mouse, rat, and human. Two other cDNAs, termed Dex1 and Dex4, were also identified as rrg, with 92 and 97% sequence similarity with the existing data bank sequence of rrg. LOX enzyme is known to downregulate p21(ras) protein and play a central role in the maturation of collagen and elastin in the extracellular matrix as well as modulate the cytoskeletal elements. Thus LOX may be important in lung developmental processes involving epithelial-mesenchymal interactions.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression