Biochimica et biophysica acta
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Biochim. Biophys. Acta · Nov 2011
Influence of aging and hemorrhage injury on Sirt1 expression: possible role of myc-Sirt1 regulation in mitochondrial function.
Trauma-hemorrhage (T-H) causes hypoxia and organ dysfunction. Mitochondrial dysfunction is a major factor for cellular injury due to T-H. Aging also has been known to cause progressive mitochondrial dysfunction. ⋯ Additionally, expression of mitochondrial biogenesis regulating transcription factors Foxo1 and Nrf-1 was also decreased with T-H and aging. Based upon these observations we conclude that Sirt1 expression is negatively modulated by T-H causing downregulation of mitochondrial biogenesis. Thus, induction of Sirt1 is likely to produce salutary effects following T-H induced injury and hence, Sirt1 may be a potential molecular target for translational research in injury resolution.
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Biochim. Biophys. Acta · Nov 2011
ReviewEmerging pathways in asthma: innate and adaptive interactions.
Allergic asthma is a complex and chronic airway inflammatory disorder, and the prevalence of asthma has increased. Adaptive antigen-dependent immunity is a classical pathway of asthmatic pathology. Recent studies have focused on innate antigen-independent immunity in asthma. ⋯ Finding specific mechanisms of innate and/or adaptive immunity in asthma are timely goals for further research. Integration of bioinformatics and systems biology tools, particularly in relation to microbiome analysis, may be helpful in providing an understanding to allergic immune responses. This article is part of a Special Issue entitled Biochemistry of Asthma.
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Biochim. Biophys. Acta · Nov 2011
F508del-CFTR increases intracellular Ca(2+) signaling that causes enhanced calcium-dependent Cl(-) conductance in cystic fibrosis.
In many cells, increase in intracellular calcium ([Ca(2+)](i)) activates a Ca(2+)-dependent chloride (Cl(-)) conductance (CaCC). CaCC is enhanced in cystic fibrosis (CF) epithelial cells lacking Cl(-) transport by the CF transmembrane conductance regulator (CFTR). Here, we show that in freshly isolated nasal epithelial cells of F508del-homozygous CF patients, expression of TMEM16A and bestrophin 1 was unchanged. ⋯ This was confirmed by expression of the double mutant F508del/G551D-CFTR, which remained in the ER but had no effects on [Ca(2+)](i). Moreover, F508del-CFTR could serve as a scavenger for inositol-1,4,5-trisphosphate [IP3] receptor binding protein released with IP(3) (IRBIT). Our data may explain how ER-localized F508del-CFTR controls intracellular Ca(2+) signaling.