Feb 9, 2000

Targeted disruption of NDST-1 gene leads to pulmonary hypoplasia and neonatal respiratory distress in mice

FEBS Letters
G FanGengxi Hu

Abstract

In order to address the biological function of GlcNAc N-deacetylase/N-sulfotransferase-1 (NDST-1), we disrupted the NDST-1 gene by homologous recombination in mouse embryonic stem cells. The NDST-1 null mice developed respiratory distress and atelectasis that subsequently caused neonatal death. Morphological examination revealed type II pneumocyte immaturity, which was characterized by an increased glycogen content and a reduced number of lamellar bodies and microvilli. Biochemical analysis further indicated that both total phospholipids and disaturated phosphatidylcholine were reduced in the mutant lung. Our data revealed that NDST-1 was essential for the maturation of type II pneumocytes and its inactivation led to a neonatal respiratory distress syndrome.

  • References9
  • Citations83

Citations

Mentioned in this Paper

Lung
Cessation of Life
Gene Deletion
Pulmonary Surfactants
Sulfotransferase
Respiratory Distress Syndrome, Newborn
Cell Differentiation Process
Phosphatidylcholines
NDST1 protein, human
Electron Microscopy

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