Pulmonary dysfunction in neonatal SP-B-deficient mice

Keisuke Tokieda, Jeffrey A. Whitsett, Jean C. Clark, Timothy E. Weaver, Kazushige Ikeda, Keith B. McConnell, Alan H. Jobe, Machiko Ikegami, Harriet S. Iwamoto

研究成果: Article査読

110 被引用数 (Scopus)


Pulmonary function was assessed in newborn wild-type and homozygous and heterozygous surfactant protein B (SP-B)-deficient mice after birth. SP-B +/+ and SP-B+/- mice became well oxygenated and survived postnatally. Although lung compliance was decreased slightly in the SP-B+/- mice, lung volumes and compliances were decreased markedly in homozygous SP-B-/- mice. They died rapidly after birth, failing to inflate their lungs or oxygenate. SP-B proprotein was absent in the SP-B-/- mice and was reduced in the SP-B+/- mice, as assessed by Western analysis. Surfactant protein A, surfactant proprotein C, surfactant protein D, and surfactant phospholipid content in lungs from SP-B+/- and SP-B-/- mice were not altered. Lung saturated phosphatidylcholine and precursor incorporation into saturated phosphatidylcholine were not influenced by SP-B genotype. Intratracheal administration of perfluorocarbon resulted in lung expansion, oxygenation, and prolonged survival of SP-B-/- mice and in reduced lung compliance in SP- B+/+ and SP-B+/- mice. Lack of SP-B caused respiratory failure at birth, and decreased SP-B protein was associated with reduced lung compliance. These findings demonstrate the critical role of SP-B in perinatal adaptation to air breathing.

ジャーナルAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
4 17-4
出版ステータスPublished - 1997

ASJC Scopus subject areas

  • 生理学
  • 呼吸器内科
  • 生理学(医学)
  • 細胞生物学


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