An exon 5-less splice variant of the extracellular calcium-sensing receptor rescues absence of the full-length receptor in the developing mouse lung
| Autor: | Stacey Louise Bailey, William J. Wilkinson, Daniela Riccardi, Brenda A. Finney, Paul J. Kemp, Lydia Searchfield, Martin Cole |
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| Rok vydání: | 2011 |
| Předmět: |
Pulmonary and Respiratory Medicine
Clinical Biochemistry Cell Growth Processes Biology Mice Exon Organ Culture Techniques Fetal Organ Maturity Extracellular Animals Secretion Calcium Signaling Receptor Lung Molecular Biology Mice Knockout Cell growth Alternative splicing Exons Molecular biology Phenotype Mice Inbred C57BL Calcium Calcium-sensing receptor Receptors Calcium-Sensing |
| Zdroj: | Experimental Lung Research. 37:269-278 |
| ISSN: | 1521-0499 0190-2148 |
| DOI: | 10.3109/01902148.2010.545471 |
| Popis: | The authors have recently demonstrated that, in the developing mouse lung, fetal plasma Ca(2+) suppresses branching morphogenesis and cell proliferation while promoting fluid secretion via activation of the extracellular Ca(2+)-sensing receptor (CaSR). The aim of the current study was to further elucidate the role of Ca(2+) in lung development by studying the effects of extracellular Ca(2+) on fetal lung development in mice lacking the CaSR. These mice were produced by exon 5 deletion in the CaSR gene. Since such a maneuver has been known to induce the expression of an exon 5-less splice variant of the CaSR in some tissues, the molecular and functional expression of this splice variant in the developing mouse lung was also investigated. Whereas there was a mild in vivo phenotype observed in these mice, in vitro sensitivity of Casr(-/-) lung explants to specific activators of the CaSR was unaffected. These results imply that compensatory expression of an exon 5-less splice variant rescues CaSR function in this mouse model and therefore a lung-specific, complete CaSR knockout model must be developed to fully appreciate the role for this receptor in lung development and the contribution of its ablation to postnatal respiratory disease. |
| Databáze: | OpenAIRE |
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