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Nuclear factor-kappa B (NFκB) signal is essential for neuronal survival and its activation may protect neuron against various stimuli. Since purinergic signals activate NFκB through the P2X7 receptor, we investigated the distinct pattern of NF-κB phosphorylation in neurons by P2X7 receptor activation following status epilepticus (SE) in an effort to understand the role of P2X7 receptor in epileptogenic insult. In non-SE animals, 2′(3′)- O-(4-benzoyl)benzoyl adenosine 5′-triphosphate (BzATP, a P2X7R agonist) treatment increased only p52-Ser869 NF-κB phosphorylation in neuron. Following SE, p52-Ser865, p52-Ser869, p65-Ser276, p65-Ser311, p65-Ser468, and p65-Ser529 NF-κB phosphorylation was significantly decreased in CA1 and CA3 neurons. However, BzATP treatment prevented reductions in p65-Ser276, p65-Ser311, p65-Ser529, and p52-Ser869 NF-κB phosphorylations in CA1 and/or CA3 neurons induced by SE. Furthermore, BzATP treatment reduced SE-induced p65-Ser311, p65-Ser468, p65-Ser536, and p52-Ser869 NF-κB phosphorylations in astrocytes. These findings indicate that P2X7 functions may be involved in the regulation of SE-induced reactive astrocytes and neuronal degeneration via NF-κB phosphorylations in response to pilocarpine-induced SE in the rat hippocampus. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Bone adapts to its environment. Osteoblasts and osteocytes are subject to mechanical load in vivo. It has been shown that osteoblasts alter cytokine expression in response to mechanical loading. However, signal transduction pathways that mediate bone cell response to mechanical stimuli have not been elucidated. In this study, we report an increase in proinflammatory gene expression in response to fluid shear stress (FSS) in human mesenchymal stem cells (hMSCs) and mouse preosteoblasts. Fluid shear stress (FSS)-induced effect was blocked by the inhibition of the calcineurin–NFATc1 axis, thus implicating a role for nuclear factor of activated T cells (NFAT) signaling in mechanotransduction. [ABSTRACT FROM AUTHOR]