Cell and Tissue Research

, Volume 306, Issue 1, pp 57–63

Mice lacking CCAAT/enhancer-binding protein-α show hyperproliferation of alveolar type II cells and increased surfactant protein mRNAs

  • Kazuhiro Sugahara
  • Ken-Ichi Iyama
  • Tatsuya Kimura
  • Kimihiko Sano
  • Gretchen J. Darlington
  • Tsuguno Akiba
  • Masaki Takiguchi
Regular Article

DOI: 10.1007/s004410100420

Cite this article as:
Sugahara, K., Iyama, KI., Kimura, T. et al. Cell Tissue Res (2001) 306: 57. doi:10.1007/s004410100420

Abstract.

The lung-specific surfactant proteins (SP) are essential for normal respiratory function. Transcription factors may play an important role in the regulation of surfactant proteins. The CCAAT/enhancer-binding protein (C/EBP) family consists of transcription factors that can stimulate expression of genes in lipid-metabolizing epithelial cells. C/EBPα-deficient mice have been shown to exhibit abnormal pulmonary histopathology. Recently, we demonstrated that C/EBP family members are differentially expressed in alveolar type II cell proliferation and in pulmonary fibrosis. In the present study, to investigate whether the C/EBP family would be involved in the regulation of surfactant proteins, we examined the protein expression of SP-A, and SP-C, and mRNA expression of SP-A, SP-B, and SP-C in the lungs from newborn C/EBPα-deficient mice. Using immunohistochemistry, we demonstrated that positive cells for SP-C, specific to alveolar type II cells, in the lungs were more abundant in the newborn C/EBPα-deficient mice than in control mice, which suggests the hyperproliferation of alveolar type II cells in the lungs of the C/EBPα-deficient mice. In situ hybridization analysis revealed that expression of SP-A, SP-B, and SP-C mRNAs were increased in the lungs of newborn C/EBPα-deficient mice. Northern blot analysis revealed that surfactant protein mRNAs were also increased. Thus, these results suggest that C/EBPα may play a key role in the proliferation of alveolar type II cells and the regulation of genes of surfactant protein.

Alveolar type II cells Gene regulation In situ hybridization Lung injury Wound healing Mutant mice (C/EBPα-deficient) 

Copyright information

© Springer-Verlag 2001

Authors and Affiliations

  • Kazuhiro Sugahara
    • 1
  • Ken-Ichi Iyama
    • 2
  • Tatsuya Kimura
    • 3
  • Kimihiko Sano
    • 4
  • Gretchen J. Darlington
    • 6
  • Tsuguno Akiba
    • 5
  • Masaki Takiguchi
    • 5
  1. 1.Department of Anesthesiology, University of the Ryukyus Faculty of Medicine, 207 Uehara, Nishihara, Okinawa 903-0215, Japan
  2. 2.Department of Surgical Pathology, Kumamoto University School of Medicine, Kumamoto 860-8556, Japan
  3. 3.Department of Molecular Genetics, Kumamoto University School of Medicine, Kumamoto 860-8556, Japan
  4. 4.Department of Pediatrics, Kobe University School of Medicine, Kobe 650-0017, Japan
  5. 5.Department of Biochemistry, Chiba University School of Medicine, Chiba 260-8670, Japan
  6. 6.Department of Pathology and Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA

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