NDLI: Deletion of STK40 protein in mice causes respiratory failure and death at birth.

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Deletion of STK40 protein in mice causes respiratory failure and death at birth.

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Deletion of STK40 protein in mice causes respiratory failure and death at birth.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yu, Hongyao Ning, Wen He, Ke Sun, Lei Tang, Fan Li, Lingjie Li, Ruizhen Jin, Ying
Description	Author Affiliation: Yu H ( Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai JiaoTong University School of Medicine, 225 South Chongqing Road, Shanghai 200025, China.)
Abstract	STK40 is a putative serine/threonine kinase and was shown to induce extraembryonic endoderm differentiation from mouse embryonic stem cells. However, little is known about its physiological function in vivo. Here, we generate Stk40 knock-out mice and demonstrate that loss of the Stk40 gene causes neonatal lethality at birth. Further examination reveals that the respiratory distress and atelectasis occur in the homozygous mutants. The maturation of lung and alveolar epithelium is delayed in the mutant, as indicated by narrowed air spaces, thickened interstitial septa, and increased glycogen content in the lungs of Stk40(-/-) mice. The reduction in levels of T1- , SP-B, and SP-C indicates delayed maturation of both type I and type II respiratory epithelial cells in Stk40(-/-) lungs. Moreover, Stk40 is found to be most highly expressed in lungs of both fetal and adult mice among all organs tested. Mechanistically, a genome-wide RNA microarray analysis reveals significantly altered expression of multiple genes known to participate in lung development. The expression of some genes involved in lipid metabolism, immune response, and glycogen metabolism is also disrupted in the lung of Stk40(-/-) mice. Protein affinity purification identifies RCN2, an activator of ERK/MAPK signaling, as an STK40-associated protein. Consistently, Stk40 deficiency attenuates the ERK/MAPK activation, and inhibition of ERK/MAPK activities reduces surfactant protein gene expression in lung epithelial cells. Collectively, this study uncovers an important role of STK40 for lung maturation and neonatal survival. STK40 may associate with RCN2 to activate ERK/MAPK signaling and control the expression of multiple key regulators of lung development.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	8
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-02-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Gene Expression Regulation, Developmental Lung Physiology Protein-Serine-Threonine Kinases Genetics Respiratory Insufficiency Animals Epithelium Metabolism Extracellular Signal-Regulated MAP Kinases Fibroblasts Cytology Gene Deletion Genome-Wide Association Study Genotype Glutathione Transferase Embryology Mice Mice, Transgenic Oligonucleotide Array Sequence Analysis Pulmonary Alveoli Pulmonary Surfactants Mortality Time Factors Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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