Document Detail


Hypoxia-induced mitogenic factor modulates surfactant protein B and C expression in mouse lung.
MedLine Citation:
PMID:  16166744     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have demonstrated a robust pulmonary expression of hypoxia-induced mitogenic factor (HIMF) during the perinatal period, when surfactant protein (SP) synthesis begins. We hypothesized that HIMF modulates SP expression and participates in lung development and maturation. The temporal-spatial expression of HIMF, SP-B, and SP-C in developing mouse lungs was examined by immunohistochemical staining, Western blot, and RT-PCR. The expression and localization of SP-B and SP-C were investigated in mouse lungs after intratracheal instillation of HIMF in adult mice. The effects of HIMF on SP-B and SP-C transcription activity, and on mRNA degradation, were investigated in mouse lung epithelial (MLE)-12 and C10 cells using the promoter-luciferase reporter assay and actinomycin D incubation. The activation of Akt, extracellular signal-regulated kinase (ERK)1/2, and p38 mitogen-activated protein kinase was explored by Western blot. Intratracheal instillation of HIMF resulted in significant increases of SP-B and SP-C production, predominantly localized to alveolar type II cells. In MLE-12 and C10 cells, HIMF enhanced SP-B and SP-C mRNA levels in a dose-dependent manner. Meanwhile, HIMF increased transcription activity and prevented actinomycin D-facilitated SP-B and SP-C mRNA degradation in MLE-12 cells. Incubation of cells with LY294002, PD098059, or U0126 abolished HIMF-induced Akt and ERK1/2 phosphorylation and suppressed HIMF-induced SP-B and SP-C production, whereas SB203580 had no effect. These results indicate that HIMF induces SP-B and SP-C production in mouse lungs and alveolar type II-like cell lines via activations of phosphatidylinositol 3-kinase/Akt and ERK1/2 mitogen-activated protein kinase, suggesting that HIMF plays critical roles in lung development and maturation.
Authors:
Qiangsong Tong; Liduan Zheng; Jeffrey Dodd-o; John Langer; Danming Wang; Dechun Li
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2005-09-15
Journal Detail:
Title:  American journal of respiratory cell and molecular biology     Volume:  34     ISSN:  1044-1549     ISO Abbreviation:  Am. J. Respir. Cell Mol. Biol.     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2005-12-15     Completed Date:  2006-02-07     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  28-38     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Embryo, Mammalian / anatomy & histology
Epithelial Cells / cytology,  metabolism
Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors,  metabolism
Intercellular Signaling Peptides and Proteins
Lung / cytology,  growth & development,  metabolism*
Male
Mice
Mice, Inbred C57BL
Nerve Growth Factor / genetics,  metabolism
Phosphatidylinositol 3-Kinases / antagonists & inhibitors,  metabolism
Proteins / genetics,  metabolism*
Proto-Oncogene Proteins c-akt / metabolism
Pulmonary Surfactant-Associated Protein B / genetics,  metabolism*
Pulmonary Surfactant-Associated Protein C / genetics,  metabolism*
RNA Stability
Transcription, Genetic
Grant Support
ID/Acronym/Agency:
HL075755/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Intercellular Signaling Peptides and Proteins; 0/Proteins; 0/Pulmonary Surfactant-Associated Protein B; 0/Pulmonary Surfactant-Associated Protein C; 0/Retnla protein, mouse; 9061-61-4/Nerve Growth Factor; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases
Comments/Corrections

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