Document Detail


NGF/TrkA-mediated Kidins220/ARMS signaling activated in the allergic airway challenge in mice.
MedLine Citation:
PMID:  20934630     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
BACKGROUND: Nerve growth factor (NGF), combined with its high-affinity receptor tyrosine kinase receptor A (TrkA), has been reported to be involved in the pathogenesis of asthma.
OBJECTIVE: To investigate whether the downstream protein ankyrin-rich membrane spanning (ARMS), a novel transmembrane substrate of protein kinase D (Kidins220), is activated in the pathogenesis of asthma.
METHODS: The asthmatic model was established by the inhalation of ovalbumin in BALB/c mice. The effects of NGF and TrkA on Kidins220/ARMS in an allergic airway challenge were assessed by administering anti-NGF or anti-TrkA antibody to the mice. Pathologic changes in the bronchi and lung tissues were examined by means of hematoxylin and eosin staining; the inflammatory cells in the bronchoalveolar lavage fluid (BALF) were counted; and co-expression of ARMS and TrkA in BALF cells was observed by means of immunofluorescence. In addition, Kidins220/ARMS, CrkL, NGF, TrkA protein, and Kidins220 messenger RNA levels were determined using Western blot or quantitative reverse transcription-polymerase chain reaction.
RESULTS: Using fluorescence microscopy, we found that Kidins220 and TrkA were co-expressed on the membranes of the BALF cells of asthmatic mice. Compared with expression in control animals, Kidins220/ARMS, CrkL, NGF, and TrkA were overexpressed in the lungs after allergen challenge. Moreover, after the mice were treated with anti-NGF or anti-TrkA, the Kidins220/ARMS levels and allergen-induced airway inflammation decreased.
CONCLUSIONS: These results suggest that Kidins220/ARMS partly participates in the pathogenesis of asthma through the NGF-TrkA signaling pathway, possibly representing a new mechanism in asthma.
Authors:
Xiuqin Ni; Xing Li; Xiubin Fang; Ning Li; Wanpeng Cui; Baohui Zhang
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology     Volume:  105     ISSN:  1081-1206     ISO Abbreviation:  Ann. Allergy Asthma Immunol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9503580     Medline TA:  Ann Allergy Asthma Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  299-306     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Affiliation:
Department of Neurobiology, Institute of Respiratory Diseases, China Medical University, Shenyang, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Infants with low immunoglobulin levels: Isolated low IgA level vs other immunoglobulin abnormalities...
Next Document:  Association analysis of UBE3C polymorphisms in Korean aspirin-intolerant asthmatic patients.