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J. Biol. Chem., Vol. 279, Issue 24, 25574-25581, June 11, 2004

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Cell Type-specific Occurrence of Caveolin-1 and -1 in the Lung Caused by Expression of Distinct mRNAs^*

Hiroshi Kogo, Toshisada Aiba, and Toyoshi Fujimoto

From the Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan

Two isoforms of caveolin-1, and , had been thought to be generated by alternative translation initiation of an mRNA (FL mRNA), but we showed previously that a variant mRNA (5'V mRNA) encodes the isoform specifically (Kogo, H., and Fujimoto, T. (2000) FEBS Lett. 465, 119–123). In the present study, we demonstrated strong correlation between the expression of the caveolin-1 protein isoforms and mRNA variants in culture cells and the developing mouse lung. The isoform protein and FL mRNA were expressed constantly during the lung development, whereas expression of the isoform protein and 5'V mRNA was negligible in the fetal lung before 17.5 days post-coitum, and markedly increased simultaneously at 18.5 days post coitum, when the alveolar type I cells started to differentiate. Immunohistochemical analysis revealed the cell type-specific expression of the two isoforms; the alveolar type I cell expresses the isoform predominantly, while the endothelium harbors the isoform chiefly. The mutually exclusive expression of caveolin-1 isoforms was verified by Western blotting of the selective plasma membrane preparation obtained from the endothelial and alveolar epithelial cells. The present result indicates that the two caveolin-1 isoforms are generated from distinct mRNAs in vivo and that their production is regulated independently at the transcriptional level. The result also suggests that the and isoforms of caveolin-1 may have unique physiological functions.

Received for publication, October 1, 2003 , and in revised form, March 10, 2004.

^* This work was supported by grants-in-aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of the Japanese Government, a research grant from Nagoya University, and a research grant from Narishige Zoological Science Award. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Division of Molecular Genetics, Inst. for Comprehensive Medical Science, Fujita Health University, Dengakugakubo 1-98, Kutsukake-cho, Toyoake-shi, Aichi 470-1192, Japan. Tel.: 81-562-93-9392; Fax: 81-562-93-8831; E-mail: hkogo{at}fujita-hu.ac.jp.

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