Transduction of phosphatase and tensin homolog deleted on chromosome 10 into eosinophils attenuates survival, chemotaxis, and airway inflammation.

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is part of a complex signaling system that affects a variety of important cell functions. PTEN antagonizes the action of PI3K by dephosphorylating the signaling lipid phosphatidylinositol 3,4,5-triphosphate. In the present study, we used a TAT fusion protein transduction system to elucidate the role of PTEN in eosinophils and airway inflammation.

The role of platelet-derived growth factor receptor in eotaxin signaling of eosinophils.

Background: Receptor tyrosine kinases (RTKs) such as epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFR) are capable of eliciting kinase activity after ligand binding. In several cells, RTKs are activated via the G-protein-coupled receptor independent of the ligand-RTK interaction. We have previously found that EGFR is transactivated via CC chemokine receptor 3 in bronchial epithelial cells and that this pathway is important for mitogen-activated protein (MAP) kinase activation and cytokine production.

[Reye syndrome and drug induced encephalopathy].

Reye syndrome, characterized by acute encephalopathy, selective liver damages, a fatty degeneration in visceral organs and miserable prognosis, is probably caused by various drugs, especially antipyretic such as acetylsalicylate. The incidence of the disease has been decreased by prohibition of administration of aspirin for children with high fever, especially caused by influenza infection in western countries, also in Japan. The pathophysiology of the disease has extensively studied, however, still being unknown to be dissolved.

Analysis of the comprehensive effects of polyunsaturated fatty acid on mRNA expression using a gene chip.

To investigate the comprehensive effects of polyunsaturated fatty acids (PUFA) on gene expression, we analyzed changes of mRNA expression in PUFA-treated HepG2 cells using a DNA micro array. We incubated HepG2 cells for 24 h with or without 0.25 mM oleic acid (OA), arachidonic acid (AA), eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), and then compared the expression profiles of thousands of genes using a GeneChip.