Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells

Diabetic nephropathy (DN) is accompanied by characteristic changes in the glomerulus, but little is known about the effect of diabetes on parietal epithelial cells (PECs). In this study, a descriptive analysis of PECs was undertaken in diabetic db/db mice and in diabetic patients. PEC hypertrophy was significantly more prominent in diabetic mice than in nondiabetic mice, and this was evident even at the early stage. Additionally, the number of vacuoles in PECs was markedly increased in diabetic mice, suggesting the presence of cellular injury in PECs in DN. Although rare, binuclear cells were observed in mice with early diabetes. In cultured PECs, a high glucose condition, compared with normal glucose condition, induced cellular hypertrophy and apoptosis. Flow cytometry showed that some PECs in the G0 phase reentered the cell cycle but got arrested in the S phase. Finally, in human diabetic subjects, hypertrophy and vacuolization were observed in the PECs. Our data showed that PECs undergo substantial changes in DN and may participate in rearrangement for differentiation into podocytes

Involvement of Heat-Shock Proteins During Periodontal Ligament Remodeling

Mechanical stress induces various molecules such as heat-shock protein (HSP), which causes structural changes in the proteins in periodontal ligament (PDL). We carried out an experiment to induce traumatic occlusion in mouse PDL and analyzed the expression of HSPs. HSPs investigated acts differently depending on the time of expression. HSPs are constitutively expressed in the PDL and defend cells from stress and maintain homeostasis under normal conditions. During bone addition to the PDL on the tension side, HSP27 and HSP47, HSP70 also acts as molecular chaperone, which assists the maturation of bone morphogenetic proteins and aids osteoblast activation. In HSP 70 and HSP 47, mechanical stress is applied to the PDL on the tension side for a short period of time for alveolar bone repairing, and when abnormality occurs in the collagen structure fibroblasts of PDL, it functions at the injured site, whereby extracellular that promotes abnormal collagen secretion and stores the modified protein in the endoplasmic reticulum, there by controlling the decalcification of PDL. In other words, HSP47 and HSP70 are expressed in PDL fibroblasts on the pressure side damaged by application of mechanical stress and contribute to the repair of collagen tissue by activating PDL fibroblasts, supporting recovery from cell damage

Cytokine profiles in children with primary Epstein-Barr virus infection

Primary Epstein-Barr virus (EBV) infection causes infectious mononucleosis and hemophagocytic lymphohistiocytosis (HLH) in children, where EBV infects B and CD8+ T cells, respectively. We measured pro-inflammatory and anti-inflammatory cytokines in both diseases. Significantly higher concentrations of various mediators, including interferon-γ, neopterin, interleukin (IL)-6, IL-10, IL-18, and heme oxygenase-1, were observed in EBV-HLH. Because of their similarity to the profile of familial HLH, this profile was likely a consequence of HLH, but not ectopic infection. TNF-α levels were elevated in both diseases. Elevation of those mediators may contribute to the disease pathogenesis of EBV-HLH by activating and inhibiting host immune responses. © 2013 Wiley Periodicals, Inc

Chapter 3 : Involvement of heat-shock proteins during periodontal logament remondeling.

Mechanical stress induces various molecules such as heat-shock protein (HSP), which causes structural changes in the proteins in periodontal ligament (PDL). We carried out an experiment to induce traumatic occlusion in mouse PDL and analyzed the expression of HSPs. HSPs investigated acts diff erently depending on the time of expression. HSPs are constitutively expressed in the PDL and defend cells from stress and maintain homeostasis under normal conditions. During bone addition to the PDL on the tension side, HSP27 and HSP47, HSP70 also acts as molecular chaperone, which assists the matu-ration of bone morphogenetic proteins and aids osteoblast activation. In HSP 70 and HSP 47, mechanical stress is applied to the PDL on the tension side for a short period of time for alveolar bone repairing, and when abnormality occurs in the collagen structure fi broblasts of PDL, it functions at the injured site, whereby extracellular that promotes abnormal collagen secretion and stores the modifi ed protein in the endoplasmic reticulum, there by controlling the decalcifi cation of PDL. In other words, HSP47 and HSP70 are expressed in PDL fi broblasts on the pressure side damaged by application of mechanical stress and contribute to the repair of collagen tissue by activating PDL fi broblasts, supporting recovery from cell damage.Edited by Jane Manakil,282p,illus. : London : IntechOpen, 2019

A Consideration on the Role of HSP70 Appearing in the Periodontal Tissues due to Experimental Orthodontic Force

実験的歯科矯正力によりマウス歯根膜組織に誘導されるHSP70 とp-HSP70 の初期における発現状況の変化を免疫組織化学的に検討した。その結果、対照群歯根膜線維芽細胞はその歯根膜の全周にわたるHSP70 とp-HSP70 の活性が低い状態で保たれていた。実験群では、HSP70 は時間の経過とともに陽性反応が増強していた。p-HSP70は、HSP70の発現より若干遅れて陽性反応の増強を示していた。これらの実験結果はHSP70がホメオスタシスの維持や傷害を受けた細胞の修復、またそのリン酸化したp-HSP70として、牽引側歯根膜組織における骨芽細胞活性化による同部への骨添加傾向へのシフトが正常に行われるよう分子シャペロンとして働いていることを示唆した。We examined immunohistochemical expressions of HSP70 and p-HSP70 in the orthodontic periodontal tissues. In the control group, the HSP70 and p-HSP70 expression was observed in the periodontal ligament fibroblasts and that was kept in low levels. In the experimental group, the strong expression of HSP70 was detected according to over time. However, p-HSP70 expression was a bit delayed. The data suggests thatHSP70 has been closely involved in the repair of tissue to maintain homeostasis of the periodontal tissues by the activation of periodontal ligament fibroblasts. Farthermore, the data also suggests that HSP70 act as a molecular chaperone of osteogenesis through an activation of osteoblasts