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10.3389/fncel.2015.00458 http://scihub22266oqcxt.onion/10.3389/fncel.2015.00458 C4672043!4672043 !26696823     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26696823 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Cell+Neurosci 2015 ; 9 (ä): 458 Nephropedia Template TP {{tp|p=26696823 |t=2015. The Role of Stefin B in Neuro-inflammation |pdf=|usr=}}{{26696823 }} gab.com Text The Role of Stefin B in Neuro-inflammation JO: Front Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26696823 #FOAvip Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibitor localized in the cytosol, mitochondria and nucleus. Its expression is upregulated upon macrophage activation and cellular stress. Mutations in the gene of stefin B are associated with the neurodegenerative disease known as Unverricht-Lundborg disease (EPM1). It was reported that early microglial activation precedes neuronal loss in the brain of the stefin B-deficient mice, implying a role of the inhibitor at the cross-talk between microglia and cerebellar cells. Detailed analysis of microglial activation in stefin B-deficient microglia showed a significantly higher proportion of both pro-inflammatory M1 and anti-inflammatory M2 microglia in stefin B-deficient mouse brain compared with control mice. In our recent work, we demonstrated that stefin B-deficient mice were significantly more sensitive to the lethal lipopolysaccharide (LPS)-induced sepsis, due to increased caspase-11 expression and secreted higher amounts of pro-inflammatory cytokines IL-1? and IL-18. Upon LPS stimulation, stefin B was targeted into the mitochondria, and the lack of stefin B resulted in the increased destabilization of the mitochondrial membrane potential and mitochondrial superoxide generation. The increased caspase-11 gene expression and better pro- inflammatory caspase-1 and -11 activation determined in stefin B deficient bone marrow-derived macrophages resulted in enhanced non-canonical inflammasome activation. Since signaling pathways in macrophages could be compared to the ones in microglia we propose that inflammasome activation could play an important role in the pathogenesis of EPM1. Twit Text FOAVip The Role of Stefin B in Neuro-inflammation ????Front Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26696823 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26696823 #FOAvip English Wikipedia <ref>{{Cite pmid|26696823 }}</ref> The Role of Stefin B in Neuro-inflammation #MMPMID26696823 Kopitar-Jerala N Front Cell Neurosci 2015[]; 9 (ä): 458 PMID26696823 show ga Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibitor localized in the cytosol, mitochondria and nucleus. Its expression is upregulated upon macrophage activation and cellular stress. Mutations in the gene of stefin B are associated with the neurodegenerative disease known as Unverricht-Lundborg disease (EPM1). It was reported that early microglial activation precedes neuronal loss in the brain of the stefin B-deficient mice, implying a role of the inhibitor at the cross-talk between microglia and cerebellar cells. Detailed analysis of microglial activation in stefin B-deficient microglia showed a significantly higher proportion of both pro-inflammatory M1 and anti-inflammatory M2 microglia in stefin B-deficient mouse brain compared with control mice. In our recent work, we demonstrated that stefin B-deficient mice were significantly more sensitive to the lethal lipopolysaccharide (LPS)-induced sepsis, due to increased caspase-11 expression and secreted higher amounts of pro-inflammatory cytokines IL-1? and IL-18. Upon LPS stimulation, stefin B was targeted into the mitochondria, and the lack of stefin B resulted in the increased destabilization of the mitochondrial membrane potential and mitochondrial superoxide generation. The increased caspase-11 gene expression and better pro- inflammatory caspase-1 and -11 activation determined in stefin B deficient bone marrow-derived macrophages resulted in enhanced non-canonical inflammasome activation. Since signaling pathways in macrophages could be compared to the ones in microglia we propose that inflammasome activation could play an important role in the pathogenesis of EPM1. äThe Role of Stefin B in Neuro-inflammation (epmc).pdf DeepDyve Pubget Overpricing