2009年7月
Essential role of the TRIC-B channel in Ca2+ handling of alveolar epithelial cells and in perinatal lung maturation
DEVELOPMENT
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- 巻
- 136
- 号
- 14
- 開始ページ
- 2355
- 終了ページ
- 2361
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1242/dev.036798
- 出版者・発行元
- COMPANY OF BIOLOGISTS LTD
TRIC channels function as monovalent cation-specific channels that mediate counter ion movements coupled with ryanodine receptor-mediated Ca2+ release from intracellular stores in muscle cells. Mammalian tissues differentially contain two TRIC channel subtypes: TRIC-A is abundantly expressed in excitable cells, whereas TRIC-B is ubiquitously expressed throughout tissues. Here, we report the physiological role of TRIC-B channels in mouse perinatal development. TRIC-B-knockout neonates were cyanotic owing to respiratory failure and died shortly after birth. In the mutant neonates, the deflated lungs exhibited severe histological defects, and alveolar type II epithelial cells displayed ultrastructural abnormalities. The metabolic conversion of glycogen into phospholipids was severely interrupted in the mutant type II cells, and surfactant phospholipids secreted into the alveolar space were insufficient in the mutant neonates. Moreover, the mutant type II cells were compromised for Ca2+ release mediated by inositol-trisphosphate receptors, despite Ca2+ overloading in intracellular stores. Our results indicate that TRIC-B channels take an active part in Ca2+ signalling to establish specialised functions in type II cells and are thus essential for perinatal lung maturation.
- リンク情報
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- DOI
- https://doi.org/10.1242/dev.036798
- J-GLOBAL
- https://jglobal.jst.go.jp/detail?JGLOBAL_ID=200902226525628981
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/19515693
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000267218500006&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1242/dev.036798
- ISSN : 0950-1991
- J-Global ID : 200902226525628981
- PubMed ID : 19515693
- Web of Science ID : WOS:000267218500006