Niigata University

About: Niigata University is a education organization based out in Niigata, Japan. It is known for research contribution in the topics: Population & Transplantation. The organization has 18847 authors who have published 35135 publications receiving 819766 citations. The organization is also known as: Niigata daigaku.

LPS induces NK1.1+ alpha beta T cells with potent cytotoxicity in the liver of mice via production of IL-12 from Kupffer cells.

Abstract: We recently reported that systemic administration of IL-12 into mice activates NK11+ alpha beta T cells with intermediate TCR (NK1+TCRint) and induces strong MHC-unrestricted cytotoxicity in C57BL/6 mice In the present report, we examined the effect of LPS on Kupffer cells and NK1+TCRint, cells in C57BL/6 mice Administration of LPS, as well as synthetic lipid A analogue (ONO-4007), but not detoxified LPS, induces the increase of NK1 expression of NK1+TCRint cells (NKlhighTCRint) and the acquisition of strong MHC-unrestricted cytotoxicity of these cells against NK-sensitive and NK-resistant targets as does IL-12 administration LPS as well as ONO-4007 induced IL-12 mRNA in hepatic mononuclear cells, mainly in plastic-adherent Kupffer cells LPS-induced cytotoxicity of hepatic mononuclear cells was greatly reduced by in vivo injections of anti-IL-12 Ab, to a lesser extent by anti-IFN-gamma Ab, but not by anti-IL-1 nor anti-TNF-alpha Ab Pretreatment of mice with LPS induced inhibition of hepatic metastases of iv injected EL4 cells in C57BL/6 euthymic and athymic mice and this antimetastasis was inhibited by injection of anti-IL-12 Ab This antimetastatic effect of LPS in the liver was also observed in different strains of mice and tumors, In contrast to IL-12, however, LPS was not so effective when administered after tumor inoculation These results revealed that LPS (lipid A) stimulates NK1+TCRint cells through IL-12 production from Kupffer cells and suggest that bacterial components, probably including those from intestine, are activators of Kupffer cells and NK1+TCRint, cells in the liver It is also suggested that the host condition as well as LPS-induced cytokines other than IL-12 may affect antitumor effect induced by LPS in the liver

Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury

Abstract: Podocytes in the renal glomerulus express unusual intermediate filament (IF) proteins for epithelial cells. To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. An upregulation of IF proteins may increase the mechanical stability of cells, thus enabling podocytes to undergo morphological changes on the tensile glomerular capillary wall.

Tissue response to titanium implants in the rat maxilla: ultrastructural and histochemical observations of the bone-titanium interface.

Abstract: Background: The detailed mechanism of osseointegration, the most appropriate implant-bone interface, remains unclear in jaw tissues at the ultrastructural level in contrast to the many reports using long bones. The present study reports on tissue response to titanium-implantation on an animal model using rat maxilla. Methods: Animals were sacrificed at 1 to 28 days postimplantation and prepared tissue specimens, freed from implants by a cryofracture technique, were processed for transmission electron microscopy and histochemistry for tartrate resistant acid phosphatase activity (TRAPase). Results: Different patterns in bone formation were recognized between lateral and base areas of implant cavities. In the lateral area with narrow gaps, bone deposition took place from the pre-existing bone towards the implant after active bone resorption by osteoclasts reactive to TRAPase. However, no distinct bone formation appeared in the lateral area where the implant had been installed close to the osteotomy margin. ...

Ubiquitylation of p62/sequestosome1 activates its autophagy receptor function and controls selective autophagy upon ubiquitin stress

Abstract: Alterations in cellular ubiquitin (Ub) homeostasis, known as Ub stress, feature and affect cellular responses in multiple conditions, yet the underlying mechanisms are incompletely understood. Here we report that autophagy receptor p62/sequestosome-1 interacts with E2 Ub conjugating enzymes, UBE2D2 and UBE2D3. Endogenous p62 undergoes E2-dependent ubiquitylation during upregulation of Ub homeostasis, a condition termed as Ub+ stress, that is intrinsic to Ub overexpression, heat shock or prolonged proteasomal inhibition by bortezomib, a chemotherapeutic drug. Ubiquitylation of p62 disrupts dimerization of the UBA domain of p62, liberating its ability to recognize polyubiquitylated cargoes for selective autophagy. We further demonstrate that this mechanism might be critical for autophagy activation upon Ub+ stress conditions. Delineation of the mechanism and regulatory roles of p62 in sensing Ub stress and controlling selective autophagy could help to understand and modulate cellular responses to a variety of endogenous and environmental challenges, potentially opening a new avenue for the development of therapeutic strategies against autophagy-related maladies.