Microglia RAGE exacerbates the progression of neurodegeneration within the SOD1(G93A) murine model of amyotrophic lateral sclerosis in a sex-dependent manner.
These findings provide novel insight into the role of RAGE-mediated oxidative stress macrophage activation and the pathogenesis of lung disease due to cigarette smoke exposure.
data demonstrate that under the diabetic condition DRG neurons are directly affected by elevated levels of glucose independent of vascular or glial signals and dependent on RAGE expression.
Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 messenger RNA in enriched hippocampal microglia and robust and persistent upregulation of RAGE messenger RNA. CUS increased surface expression of RAGE protein on hippocampal microglia and anhedonic behavior. RAGE knockout mice were resilient to stress-induced anhedonia.
Receptor for AGE expression and reactive oxygen species production were upregulated in db/db mouse livers together with impaired proteolytic antioxidant and mitochondrial respiratory activities. In parallel acute exposure of HepG2 cells to glycated albumin also elicited intracellular free radical formation
Data indicate that chronic hypoxia is associated with downregulation of pulmonary receptor for advanced glycation end products (RAGE) protein levels but a relative increase in sRAGE.
RAGE-mediated N(epsilon)-(carboxymethyl)lysine (CML) accumulation in adipose tissue and the activation of the CML-RAGE axis are important mechanisms involved in the dysregulation of adipokines in obesity.
Mouse spatial cognitive impairment caused by ribose-derived AGEs is correlated with activation of an astrocyte-mediated RAGE-dependent inflammatory response.
Conditional over-expression of RAGE by embryonic alveolar epithelium compromises the respiratory membrane and impairs endothelial cell differentiation.
findings suggest the physiological importance of RAGE and its soluble forms in supporting the respiratory mechanics in which RAGE trans interactions and the influence on elastin expression might play an important role
RAGE expression in keratinocytes is critically involved in the perpetuation of acute inflammation and support the central role of RAGE in paracrine communication between keratinocytes and stromal immune cells.
These results demonstrate for the first time that changes in the redox profile and expression of tissue-specific proteins of organs such as heart lungs and brain are observed in early stages of S. mansoni infection.
RAGE is inducibly expressed on lung endothelium and one functional consequence of RBC transfusion is increased RAGE expression and endothelial activation.
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