Linked Life Data

21482734

Source:http://linkedlifedata.com/resource/pubmed/id/21482734

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2011-5-4
pubmed:abstractText
Close apposition of nerve and mast cells is viewed as a functional unit of neuro-immune mechanisms, and it is sustained by trans-homophilic binding of cell adhesion molecule-1 (CADM1), an Ig superfamily member. Cerebral nerve-mast cell interaction might be developmentally modulated, because the alternative splicing pattern of four (a-d) types of CADM1 transcripts drastically changed during development of the mouse cerebrum: developing cerebrums expressed CADM1b and CADM1c exclusively, while mature cerebrums expressed CADM1d additionally and predominantly. To probe how individual isoforms are involved in nerve-mast cell interaction, Neuro2a neuroblastoma cells that express CADM1c endogenously were modified to express additionally either CADM1b (Neuro2a-CADM1b) or CADM1d (Neuro2a-CADM1d), and they were cocultured with mouse bone marrow-derived mast cells (BMMCs) and BMMC-derived cell line IC-2 cells, both of which expressed CADM1c. BMMCs were found to adhere to Neuro2a-CADM1d neurites more firmly than to Neuro2a-CADM1b neurites when the adhesive strengths were estimated from the femtosecond laser-induced impulsive forces minimally required for detaching BMMCs. GFP-tagging and crosslinking experiments revealed that the firmer adhesion site consisted of an assembly of CADM1d cis-homodimers. When Neuro2a cells were specifically activated by histamine, intracellular Ca(2+) concentration was increased in 63 and 38% of CADM1c-expressing IC-2 cells that attached to the CADM1d assembly site and elsewhere, respectively. These results indicate that CADM1d is a specific neuronal isoform that enhances nerve-mast cell interaction, and they suggest that nerve-mast cell interaction may be reinforced as the brain grows mature because CADM1d becomes predominant.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5983-92
pubmed:dateRevised
2011-8-23
pubmed:meshHeading
pubmed-meshheading:21482734-Alternative Splicing, pubmed-meshheading:21482734-Animals, pubmed-meshheading:21482734-Calcium, pubmed-meshheading:21482734-Cell Adhesion, pubmed-meshheading:21482734-Cell Adhesion Molecules, pubmed-meshheading:21482734-Cell Communication, pubmed-meshheading:21482734-Cell Line, Tumor, pubmed-meshheading:21482734-Cells, Cultured, pubmed-meshheading:21482734-Cerebrum, pubmed-meshheading:21482734-Coculture Techniques, pubmed-meshheading:21482734-Histamine, pubmed-meshheading:21482734-Immunoglobulins, pubmed-meshheading:21482734-Mast Cells, pubmed-meshheading:21482734-Mice, pubmed-meshheading:21482734-Mice, Inbred C57BL, pubmed-meshheading:21482734-Mice, Inbred ICR, pubmed-meshheading:21482734-Mice, Knockout, pubmed-meshheading:21482734-Neurites, pubmed-meshheading:21482734-Neurons, pubmed-meshheading:21482734-Polymerase Chain Reaction, pubmed-meshheading:21482734-Protein Isoforms
pubmed:year
2011
pubmed:articleTitle
Enhanced nerve-mast cell interaction by a neuronal short isoform of cell adhesion molecule-1.
pubmed:affiliation
Division of Molecular Pathology, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't