Results

RDF/XMLNTriplesTurtleShow queryShare ▶
SubjectPredicateObject
http://purl.uniprot.org/citations/21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21251247http://www.w3.org/2000/01/rdf-schema#comment"

Background

Abnormal proliferation, apoptosis, migration and contraction of airway smooth muscle (ASM) cells in airway remodeling in asthma are basically excessive repair responses to a network of inflammatory mediators such as PDGF, but the mechanisms of such responses remain unclear. Nogo-B, a member of the reticulum family 4(RTN4), is known to play a key role in arteriogenesis and tissue repair. Further studies are needed to elucidate the role of Nogo-B in airway smooth muscle abnormalities.

Methods

A mouse model of chronic asthma was established by repeated OVA inhalation and subjected to Nogo-B expression analysis using immunohistochemistry and Western Blotting. Then, primary human bronchial smooth muscle cells (HBSMCs) were cultured in vitro and a siRNA interference was performed to knockdown the expression of Nogo-B in the cells. The effects of Nogo-B inhibition on PDGF-induced HBSMCs proliferation, migration and contraction were evaluated. Finally, a proteomic analysis was conducted to unveil the underlying mechanisms responsible for the function of Nogo-B.

Results

Total Nogo-B expression was approximately 3.08-fold lower in chronic asthmatic mice compared to naïve mice, which was obvious in the smooth muscle layer of the airways. Interference of Nogo-B expression by siRNA resulted nearly 96% reduction in mRNA in cultured HBSMCs. In addition, knockdown of Nogo-B using specific siRNA significantly decreased PDGF-induced migration of HBSMCs by 2.3-fold, and increased the cellular contraction by 16% compared to negative controls, but had limited effects on PDGF-induced proliferation. Furthermore, using proteomic analysis, we demonstrate that the expression of actin related protein 2/3 complex subunit 5 (ARPC 2/3) decreased and, myosin regulatory light chain 9 isoform a (MYL-9) increased after Nogo-B knockdown.

Conclusions

These data define a novel role for Nogo-B in airway remodeling in chronic asthma. Endogenous Nogo-B, which may exert its effects through ARPC 2/3 and MYL-9, is necessary for the migration and contraction of airway smooth muscle cells."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.org/dc/terms/identifier"doi:10.1186/1465-9921-12-14"xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Cai Z."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Li Q."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Hong W."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Xu W."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Shao Y."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/author"Ning Y."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/name"Respir Res"xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/pages"14"xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/title"Nogo-B regulates migration and contraction of airway smooth muscle cells by decreasing ARPC 2/3 and increasing MYL-9 expression."xsd:string
http://purl.uniprot.org/citations/21251247http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/21251247http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21251247
http://purl.uniprot.org/citations/21251247http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21251247
http://purl.uniprot.org/uniprot/#_A0A384NY64-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_A6XGP7-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_B4DM63-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_B2R4D5-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_B4DZ44-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_O15144-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_O15145-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_G5E9J0-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
http://purl.uniprot.org/uniprot/#_G5E9S7-mappedCitation-21251247http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21251247
▶