NMDA receptor stimulation in the absence of extracellular Ca2+ potentiates Ca2+ influx-dependent cell death system.

The meaning of Ca2+ influx in the time course of glutamate stimulation of neuronal cells was addressed. We demonstrated that Ca2+ influx did not work straightforward in the determination of the fate of neuronal cells. There appears to be a critical period for Ca2+ influx to work efficiently in glutamate-induced neuronal cell death.

Mechanical stress induces production of angiogenic regulators in cultured human gingival and periodontal ligament fibroblasts.

Background: As periodontal tissues are constantly exposed to mechanical stress during mastication, the relationship between mechanical stimulation and biochemical phenomena has been extensively investigated.

Objectives: The aim of the present study was to assess the change in the production of angiogenic regulators produced by human gingival fibroblasts (HGF) and periodontal ligament fibroblasts (HPLF), cultured on a flexible substrate, before and after application of cyclic tensile stretching.

Materials And Methods: Both cell types were stretched in a Flexercell Strain Unit to 7, 14 and 21% elongation, at a frequency of 12 cycles/min.

Development of a liquid culture system for megakaryocyte terminal differentiation: fibrinogen promotes megakaryocytopoiesis but not thrombopoiesis.

Megakaryocyte differentiation is composed of three distinct stages: formation of erythromegakaryocytic progenitor cells, maturation of megakaryocytes and production of platelets. We have developed a liquid culture system for megakaryocyte terminal differentiation from haematopoietic stem cells into proplatelets. In this system, CD34+ cells isolated from human cord blood, differentiated to CD41+ cells, were classified either as propidium iodide (PI)+ cells (large) or PI- cells (small) by fluorescence-activated cell sorting analysis on the late-stage CD41+ cells.

Oxidative neuronal death caused by glutamate uptake inhibition in cultured hippocampal neurons.

Glutamate transporters are coupled with cystine/glutamate antiporters to supply cystine as a component of glutathione, an important antioxidant. We sought evidence that L-trans-pyrrolidine-2,4-dicarboxylate (PDC) enhances glutamate-induced neuronal damage not only via the N-methyl-D-aspartate (NMDA) receptor mediated pathway, but also through induction of oxidative stress. Cultured hippocampal cells were exposed to glutamate (100 microM) for 5 min, washed and incubated for 18 hr with PDC (200 microM).

Inhibitory Effects of Antioxidants on NF-KappaB Activation in Bovine Carotid Artery Endothelial Cells.

NF-Kappa B is one of important transcription factor, which plays an important role in many immune and inflammatory responses. A large variety of stimulus can induce the degradation of IKappa B-alpha, an inhibitor of NF-KappaB, leading to the activation and translocation of NF-KappaB into nuclei. In the present study, the effects of antioxidants on TNF-alpha-induced NF-KappaB activation were tested by using cultured bovine carotid artery endothelial cells.

4,4'-diisothiocyano-2 ,2'-stilbenedisulfonate protects cultured cerebellar granule neurons from death.

We examined the effects of 4,4'-diisothiocyano-2,2'-stilbenedisulfonate (DIDS), an inhibitor of the chloride-bicarbonate exchangers and chloride channels, on death in cultured cerebellar granule neurons. Various stimuli, such as reduction of extracellular K+ concentration, removal of growth factors, and staurosporine treatment, induced cell death. This death was blocked by DIDS in a dose dependent manner.

Induction of KDR expression in bovine arterial endothelial cells by thrombin: involvement of nitric oxide.

Thrombin, a multifunctional serine protease, is generated at the site with vascular injuries. It not only participates in the coagulation cascade, but also can induce a lot of events related to cell mitogenesis and migration. In this study, we investigated the effect of thrombin on endothelial cell proliferation induced by vascular endothelial growth factor (VEGF).