Document Detail


Hypoxia-induced mitogenic factor has antiapoptotic action and is upregulated in the developing lung: coexpression with hypoxia-inducible factor-2alpha.
MedLine Citation:
PMID:  15117738     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypoxia-induced mitogenic factor (HIMF), also called FIZZ1 or RELMalpha, was a newly found cytokine. Hypoxia caused robust HIMF induction in the lung, and HIMF has potent pulmonary vasoconstrictive, proliferative, and angiogenic properties. To investigate the role of HIMF in lung development, we determined its spatial and temporal expression. From embryonic day (E)16 to postnatal day (P)28, HIMF was strongly expressed in the cytoplasm of bronchial epithelial cells, type II cells, endothelial cells, and primitive mesenchymal cells. Treatment with HIMF resulted in a significant reduction of apoptosis in cultured embryonic lung, thus revealing a previously unknown function of HIMF. Because HIMF gene is upregulated by hypoxia and contains a hypoxia-inducible transcription factor (HIF) binding site, we subsequently investigated whether HIMF was coexpressed with HIF-2alpha or HIF-1alpha. HIF-1alpha expression was temporally distinct from HIMF expression. In contrast, HIF-2alpha was present in endothelial cells, bronchial epithelial cells, and type II cells from E18 to P28. Thus, HIMF and HIF-2alpha were temporally and spatially coexpressed in the developing lung. These results indicate a role for HIMF in lung development, possibly under the control of HIF-2, and suggest that HIMF regulates apoptosis and may participate in lung alveolarization and maturation.
Authors:
Klaus F Wagner; Ann-Katrin Hellberg; Susan Balenger; Reinhard Depping; Jeffrey Dodd-O; Roger A Johns; Dechun Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-04-29
Journal Detail:
Title:  American journal of respiratory cell and molecular biology     Volume:  31     ISSN:  1044-1549     ISO Abbreviation:  Am. J. Respir. Cell Mol. Biol.     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-08-19     Completed Date:  2004-10-05     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  276-82     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland 21287, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Apoptosis / drug effects,  genetics,  physiology*
Basic Helix-Loop-Helix Transcription Factors
Cells, Cultured
Endothelium, Vascular / cytology,  metabolism
Fetus
Gene Expression Regulation, Developmental / genetics
Hypoxia-Inducible Factor 1, alpha Subunit
Immunohistochemistry
Intercellular Signaling Peptides and Proteins
Lung / blood supply,  cytology,  embryology*
Mesoderm / cytology,  metabolism
Mice
Mice, Inbred C57BL
Neovascularization, Physiologic / genetics,  physiology*
Nerve Growth Factor / genetics*,  metabolism*,  pharmacology
Proteins*
Respiratory Mucosa / cytology,  metabolism
Trans-Activators / genetics,  metabolism
Transcription Factors / genetics,  metabolism
Up-Regulation / drug effects,  genetics,  physiology*
Grant Support
ID/Acronym/Agency:
HL 39706/HL/NHLBI NIH HHS; HL75755/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Basic Helix-Loop-Helix Transcription Factors; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Intercellular Signaling Peptides and Proteins; 0/Proteins; 0/Retnla protein, mouse; 0/Trans-Activators; 0/Transcription Factors; 0/endothelial PAS domain-containing protein 1; 9061-61-4/Nerve Growth Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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