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Microarray Analysis of Gene Expression in the Embryonic Lung*

Sui Lin, PhD; John M. Shannon, PhD
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*From the Division of Pulmonary Biology, Children’s Hospital Medical Center, Cincinnati, OH.

Correspondence to: John M. Shannon, PhD, Professor of Pediatrics, 3333 Burnet Ave, Cincinnati, OH 45229-3039; e-mail: john.shannon@chmcc.org



Chest. 2002;121(3_suppl):80S-81S. doi:10.1378/chest.121.3_suppl.80S-a
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The embryonic lung and trachea are closely related, both arising as the result of interactions between the pharyngeal endoderm and its subtending splanchnic mesenchyme. Tissue recombination studies have shown that eventual respiratory epithelial phenotype is specified by inductive signals emanating from the mesenchyme. We have used oligonucleotide microarray analysis to identify differentially expressed genes in the embryonic mouse lung and tracheas. Total RNA from 1,200 E11.5 embryonic lungs and tracheas were isolated for microchip hybridizations, which screened 38,018 known genes and expressed sequence tags. From these, we identified 110 genes that were lung specific and 94 genes that were up-regulated in the lung, as well as 162 genes that were trachea specific and 169 genes that were up-regulated in the trachea. Among the lung-specific group, a gene called melanoma inhibitory activity (MIA) was highly differentially expressed. Whole-mount in situ hybridization of E10 through E13.5 lung/trachea complexes confirmed that MIA was expressed in the lung but not the trachea, and was restricted to the distal lung epithelium. Beginning on E14.5, MIA signal was also observed in tracheal cartilage. Quantitative real-time polymerase chain reaction showed that MIA was up-regulated eightfold in the E11.5 lung vs the trachea, which gave a barely detectable signal. Interestingly, MIA is also known as cartilage-derived retinoic acid (RA)-sensitive protein, because its expression in cultured chondrocytes is down-regulated by RA. These RA-regulated characteristics, along with the known morphogenetic effects of RA in the developing lung, suggested that MIA/cartilage-derived RA-sensitive protein might play a role in early lung development. To test this hypothesis, whole lungs were cultured in the presence and absence of RA. The results clearly showed that MIA, like surfactant protein C, was down-regulated by RA. Furthermore, we used mesenchyme-free culture to demonstrate that MIA is induced in tracheal epithelium under conditions that also induce expression of surfactant protein C and other markers of the distal lung phenotype, suggesting that MIA may play a role in lung epithelial differentiation. How MIA may affect early lung development is under investigation.

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