0000000000072803
AUTHOR
Triantafyllos Chavakis
P0926 : Representation of human non-alcoholic fatty liver disease in murine models
COX-2 enhances insulin signaling. Finally, the relationship between COX-2 and the miRNAs was confirmed in NAS. Conclusions: COX-2 represses the expression of miRNAs implicated in the insulin signaling pathway via a PI3K/p300-dependent upregulation of DDX5, and by modulating the activity of the Drosha complex. Our study proposes a novel miRNA-dependent mechanism through which COX-2 promotes insulin signaling in liver cells.
Binding of Escherichia coli hemolysin and activation of the target cells is not receptor-dependent.
Abstract Production of a single cysteine substitution mutant, S177C, allowed Escherichia coli hemolysin (HlyA) to be radioactively labeled with tritiated N-ethylmaleimide without affecting biological activity. It thus became possible to study the binding characteristics of HlyA as well as of toxin mutants in which one or both acylation sites were deleted. All toxins bound to erythrocytes and granulocytes in a nonsaturable manner. Only wild-type toxin and the lytic monoacylated mutant stimulated production of superoxide anions in granulocytes. An oxidative burst coincided with elevation of intracellular Ca2+, which was likely because of passive influx of Ca2+ through the toxin pores. Competi…
Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells
Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells.…