Linked Life Data

14636948

Source:http://linkedlifedata.com/resource/pubmed/id/14636948

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-11-25
pubmed:abstractText
Changes in brain water and cerebral volume can lead to brain edema that may be one of the underlying causes of death in many neurological diseases. Cerebral water content is regulated by aquaporin 4 (AQ4) present in astrocytic end feet and around blood vessels. In systemic lupus erythematosus (SLE), magnetic resonance imaging (MRI) studies of the brain have demonstrated lesions with the prominent appearance of edema. Activation of complement may play a significant role in the pathogenesis of lupus cerebritis by causing inflammation that can lead to edema. In this study, the well-established MRL/lpr lupus mouse model was used to evaluate the role of complement in lupus cerebritis. IgG and C1q colocalized in perivascular deposits indicating that the blood-brain barrier was compromised. Both RNA and protein expressions of AQ4 were significantly increased in brains of MRL/lpr mice. Chronic administration of the soluble complement inhibitor, Crry-Ig, reduced inflammation as measured by decreased accumulation of IgG. In contrast to control MRL/lpr mice, AQ4 expression in complement inhibited MRL/lpr mice was not changed relative to untreated congenic controls. These results illustrate that complement activation in brains of lupus mice leads to enhanced AQ4 expression and inflammation. It is conceivable that increased AQ4 expression results in cerebral edema and hence complement inhibition may provide a new therapeutic option in inflammatory cerebral disorders such as lupus cerebritis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
1639
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
169-76
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:14636948-Animals, pubmed-meshheading:14636948-Aquaporin 4, pubmed-meshheading:14636948-Aquaporins, pubmed-meshheading:14636948-Astrocytes, pubmed-meshheading:14636948-Base Sequence, pubmed-meshheading:14636948-Blood-Brain Barrier, pubmed-meshheading:14636948-Brain, pubmed-meshheading:14636948-Complement Inactivator Proteins, pubmed-meshheading:14636948-DNA Primers, pubmed-meshheading:14636948-Disease Models, Animal, pubmed-meshheading:14636948-Gene Expression Regulation, pubmed-meshheading:14636948-Immunoglobulin G, pubmed-meshheading:14636948-Inflammation, pubmed-meshheading:14636948-Lupus Vasculitis, Central Nervous System, pubmed-meshheading:14636948-Magnetic Resonance Imaging, pubmed-meshheading:14636948-Male, pubmed-meshheading:14636948-Mice, pubmed-meshheading:14636948-Mice, Inbred MRL lpr, pubmed-meshheading:14636948-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:14636948-Oligonucleotide Probes, pubmed-meshheading:14636948-Receptors, Complement, pubmed-meshheading:14636948-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2003
pubmed:articleTitle
Administration of the soluble complement inhibitor, Crry-Ig, reduces inflammation and aquaporin 4 expression in lupus cerebritis.
pubmed:affiliation
Department of Medicine, Section of Nephrology, University of Chicago, Chicago, IL 60637, USA. jalexand@medicine.uchicago.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.