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Extracellular CIRP (eCIRP) and inflammation
The current review focuses on the pathobiology of eCIRP by emphasizing on signal transduction machineries, leading to discovering novel therapeutic interventions targeting eC IRP in various inflammatory diseases.
Microarray Analyses of Peripheral Blood Cells Identifies Unique Gene Expression Signature in Psoriatic Arthritis
PBC gene expression profiling identified a gene expression signature that differentiated PsA from RA, andPsA from controls, and several novel genes were differentially expressed and may prove to be diagnostic biomarkers or serve as new targets for the development of therapies.
CXCL10 and its receptor CXCR3 regulate synovial fibroblast invasion in rheumatoid arthritis.
- T. Laragione, M. Brenner, B. Sherry, P. Gulko
- Biology, MedicineArthritis and rheumatism
- 1 November 2011
It is suggested that the CXCL10/CXCR3 axis is a potential new target for therapies aimed at reducing FLS invasion and its associated joint damage and pannus invasion and destruction in RA.
Whole-Genome Sequences of DA and F344 Rats with Different Susceptibilities to Arthritis, Autoimmunity, Inflammation and Cancer
Genetic differences between DA, F344, and BN, including high-impact SNPs and short insertions and deletions affecting >2500 genes, are likely to account for most of the phenotypic variation between these strains.
A resource for the simultaneous high-resolution mapping of multiple quantitative trait loci in rats: the NIH heterogeneous stock.
It is shown how one obstacle to progress, the fine-mapping of quantitative trait loci (QTL), can be overcome by using an outbred population of rats to map a locus contributing to variation in a fear-related measure to a region on chromosome 5 containing nine genes.
The Arthritis Severity Quantitative Trait Loci Cia4 and Cia6 Regulate Neutrophil Migration into Inflammatory Sites and Levels of TNF-α and Nitric Oxide1
This is the first time that non-MHC autoimmune arthritis loci are found to regulate three central components of the innate immune response implicated in disease pathogenesis, namely neutrophil migration into an inflammatory site, as well as exudate levels of TNF-α and NO.
Buprenorphine Markedly Elevates a Panel of Surrogate Markers in a Murine Model of Sepsis
Repeated administration of buprenorphine is strongly recommended not to repetitively administer to eliminate its potential complication to animal sepsis models, which may adversely jeopardize the ability to use the CLP model to reliably simulate human sepsi, and to understand the complex mechanism underlying the pathogenesis of lethal sepsIS.
Release mechanisms of major DAMPs
The shared and DAMP-specific mechanisms reported in the literature for high mobility group box 1, ATP, extracellular cold-inducible RNA-binding protein, histones, heat shock proteins, extacellular RNAs and cell-free DNA are reviewed.
The non-major histocompatibility complex quantitative trait locus Cia10 contains a major arthritis gene and regulates disease severity, pannus formation, and joint damage.
This study determined that Cia10 harbors a major autoimmune arthritis-regulatory gene that regulates clinical disease severity, histologic damage, and the levels of at least two central proinflammatory cytokines in rats with pristane-induced arthritis.
Cold-inducible RNA-binding protein (CIRP) causes sepsis-associated acute lung injury via induction of endoplasmic reticulum stress
- M. Khan, Weng-Lang Yang, M. Brenner, A. Bolognese, Ping Wang
- Biology, MedicineScientific reports
- 27 January 2017
CIRP induces lung ER stress and downstream responses to cause sepsis-associated ALI and this suggests CIRP directly induces ER stress via TLR4 activation.