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Biomedical subjects

I Kihara

Publications and source records attributed to I Kihara.

At least 37 records · Page 2Linked to original sources
PubMed1997

Characterization of cytokine and iNOS mRNA expression in situ during the course of experimental autoimmune myocarditis in rats.

Ribonuclease protection assay was used to demonstrate mRNA expression of several cytokines as well as inducible NO synthase (iNOS), constitutive endothelial NO synthase (cNOS) and perforin in the myocardium during the course of experimental autoimmune myocarditis (EAM) in rats. Interleukin 2 (IL-2) appeared in the initial inflammatory phase (day 14), subsided in the maximum inflammatory phase (day 19) and disappeared by the recovery phase (day 25). mRNA of IL-3 beta, interferon gamma INF-gamma and tumor necrosis factor alpha (TNF-alpha) were detected only in the maximum inflammatory phase and iNOS also appeared for several days at this time. In contrast. IL-10 mRNA was detected after the maximum inflammatory stage and persisted into the recovery phase (days 25-36). Although transforming growth factor beta 1 (TGF-beta 1) could be detected in all phases, the expression was markedly enhanced in the maximum inflammatory phase and gradually diminished (around day 36) to basal levels. Perforin mRNA was not detected at any point in the disease. Besides macrophages and CD4 T cells, a number of neutrophils were found in the myocardium especially at peak inflammatory stage. We suggest that antigen (Ag) primed Ag presenting cells or macrophages interact with T cells (Th1) to produce IL-2 and subsequent IFN-gamma, which further activates macrophages in the myocardium. Consequently, TNF-alpha and iNOS may inflict tissue damage to myocardium. It is also suggested that TGF-beta) and one representative Th2 cytokine, IL-10, help inhibit inflammation. These findings suggest that Th1 and Th2 cytokines are produced at different stages of EAM and modulate the inflammation and the course of EAM.

Animals↗
PubMed1997

Juxtaglomerular cell tumor of the kidney: report of a non-functioning variant.

A case of a juxtaglomerular cell tumor (JCT) in a 46-year-old man is reported. The tumor, 2.4 cm at its greatest dimension, was incidentally detected by ultrasonography. Although histological, immunohistochemical, and electron microscopic examinations revealed typical features of a JCT, the patient had no history of hypertension or hypokalemia. This is the first report of a non-functioning JCT in the literature.

Biomarkers↗
PubMed1997

Expression of AQP family in rat kidneys during development and maturation.

The mRNA expression and localization of the aquaporin (AQP) family in rat kidney were examined by ribonuclease protection assay and immunohistochemistry. AQP1, AQP2, AQP3, and AQP4 mRNA were hardly detectable in 16-day gestation fetuses. AQP1 mRNA was explosively expressed at 1 wk, keeping the level throughout life. AQP2 mRNA expression was apparently noticed in 18-day fetuses and was enhanced gradually with age to reach a plateau at 4 wk. AQP3 and AQP4 mRNA expression was significantly found at birth but was not changed remarkably thereafter. AQP2 protein appeared first at the apical side of collecting duct cells in 18-day fetuses. The staining intensity at the site increased with age, and basolateral staining was added in adult rats. AQP3 was distinctly demonstrated at the basolateral side of collecting duct cells after birth, and the staining intensity was almost stable throughout life. The progressive induction of AQP2 expression in the first 4 wk after birth is presumed to contribute to the maturation of urinary concentrating capacity during the kidney development.

Aging↗
PubMed1997

Suppression of anti-glomerular basement membrane nephritis by administration of anti-monocyte chemoattractant protein-1 antibody in WKY rats.

Anti-glomerular basement membrane (GBM) nephritis in WKY rats is characterized by an accumulation of CD8-positive lymphocytes (CD8+ lym) and monocytes/macrophages (Mo/M psi) in the glomeruli and crescent formation. In the study presented here, the involvement of a chemokine for Mo/M psi, monocyte chemoattractant protein-1 (MCP-1), was examined in this model. An intense induction of mRNA for MCP-1 in the glomeruli and a suppressive effect of anti-MCP-1 antibody administration on the glomerular Mo/M psi accumulation and proteinuria were found. MCP-1 mRNA was expressed intensely in the glomeruli 4 d after the anti-GBM antibody injection. When MCP-1 was neutralized with anti-MCP-1 antibody administration, the number of Mo/M psi infiltrating in the glomeruli decreased by 34.7% (19.6 +/- 7.1 versus 30.0 +/- 6.0 per glomerular cross-section, P < 0.01) and proteinuria by 66.2% (15.6 +/- 9.3 versus 46.1 +/- 15.1 mg/d, P < 0.01) at day 4. In contrast, the number of CD8+ lym accumulating in the glomeruli was not affected significantly (6.6 +/- 2.7 versus 6.0 +/- 3.0 per glomerular cross-section, P > 0.05). However, the treatment with the anti-MCP-1 antibody did not reduce Mo/M psi infiltration, urinary protein excretion, and crescent formation at day 8. These data suggest that MCP-1 plays a role in the glomerular accumulation of Mo/M psi, and that the infiltrating Mo/M psi cause glomerular injury and increased excretion of protein in the urine.

Animals↗
PubMed1997

Podocyte detachment and epithelial cell reaction in focal segmental glomerulosclerosis with cellular variants.

In primary focal segmental glomerulosclerosis with cellular variants the type of epithelial cells that segmentally or globally increased and their relation to sites where podocytes detached from the capillary wall, remain unclear. Two renal samples containing glomeruli with cellular variants were serially examined using transmission electron microscopy. A total of 10 lesions, including 2 collapsing glomerulopathy, 7 cellular lesions, and 1 sclerosis, were examined. Disappearance of the dense basal band of microfilaments from portions of podocytes was followed by detachment from the capillary basement membrane, resulting in segmental denudation of the capillary wall. The defects were not covered by other portions of epithelial cells, when the defects occurred in more central regions of the glomerulus. When detachment of podocytes occurred in the peripheral areas of the glomerulus, the defects were covered with new basement membrane and by other epithelial cells. These epithelial cells were characterized by the formation of intercellular junctional complexes of zonula adherens and desmosomes between each other and with the parietal epithelial cells (PECs), by showing occasional cilia, apoptotic nuclei, and mitosis. Thus, repair is achieved as the defect is covered by the participation of PECs; synechia and glomerular sclerosis result, depending upon the extent of the original podocyte injury.

Apoptosis↗
PubMed1996

Perinuclear distribution of plectin characterizes visceral epithelial cells of rat glomeruli.

Plectin is an intermediate-filament-associated protein identified over a wide range of tissue and cell types. The distribution of this protein in glomerular visceral epithelial cells (VECs) during the differentiation and growth of rat kidneys was studied in comparison with that of vimentin. By immunofluorescence microscopy, preferential localization of these two cytomatrix elements was different, although both were observed in the cell body and primary processes of VECs. Strong staining of plectin was always found in the perinuclear region of the VEC body in kidneys of young and adult rat, but vimentin stained distinctly only in the primary processes of young rats yet in both cell bodies and primary processes of the adults. This perinuclear staining was unique to VECs, that is, was absent from other cells. In the neonatal kidney, plectin staining during differentiation of VECs changed from weak and diffuse throughout the cytoplasm in the S-shaped body to prominently perinuclear in the maturing stage. However, after the differentiation of VECs, the staining intensity of plectin did not change further. In contrast, that of vimentin increased conspicuously in parallel with the growth of VECs rather than at differentiation. After a long period of culture and during aminonucleoside nephrosis, situations when VECs lose differentiated phenotypes, most of the cells had no perinuclear plectin. These findings indicate that the perinuclear distribution of plectin may play an important role in the differentiation of VECs.

Animals↗
PubMed1995

Transient expression of type I collagen in glomeruli with anti-Thy-1 antibody-induced mesangial proliferative lesions.

Glomerular expression of extracellular matrices at the protein and mRNA levels was examined in rats with mesangial proliferative glomerulonephritis induced by the intravenous administration of a monoclonal anti-rat Thy-1 antibody. In close association with the mesangial proliferative lesion, type I collagen was immunostained at day 8 but not demonstrated at day 28 in the glomeruli of the kidneys. Type I collagen mRNA expression prominently increased in the nephritic glomeruli at day 4, prior to the appearance of type I collagen protein. In addition, fibronectin expression was also elevated in the diseased glomeruli at both the protein and mRNA levels. These results indicated that glomerular, probably mesangial cells, change their phenotypes during this disease, to synthesize abnormal extracellular matrices that lead to the progression of glomerular sclerosis.

Animals↗
PubMed1995

Limitations of podocyte adaptation for glomerular injury in puromycin aminonucleoside nephrosis.

Glomerular synechiae that occurred in nephrotic rats with a single intraperitoneal injection of puromycin aminonucleoside were analyzed by immunohistochemistry, radiolabeled thymidine ([3H]-thymidine) autoradiography, as well as light, electron and immunoelectron microscopy. To discriminate podocytes from parietal epithelial cells (PEC) and monocytes, monoclonal antibodies (mAb) against podocalyxin and ED1 were used. The cell kinetics of glomerular epithelial cells were autoradiographically assessed with isotope labeling procedures before and during nephrosis (co-labeled), and a mAb against proliferating cell nuclear antigen (PCNA). All the cell types except the podocyte of normal kidneys were labelled with [3H]-thymidine at different rates. Detachment of degenerated podocytes from the outside of the glomerular basement membrane (GBM) is the first step of synechia, and detached sites are confronted by PEC that were hypertrophied and frequently radiolabeled. Evidence that podocytes in glomeruli of nephrotic rats can proliferate was shown by the presence of mitoses, [3H]-thymidine uptake in the co-labeled experiment, and by PCNA staining, but re-epithelialization over bare segments of the GBM with proliferated podocytes is doubtful. It was concluded that glomerular synechia resulted from the limits of podocyte adaptation to glomerular injuries.

Animals↗
PubMed1995

Vasopressin increases AQP-CD water channel in apical membrane of collecting duct cells in Brattleboro rats.

The effect of vasopressin on subcellular localization of AQP-CD and AQP3 water channels was examined in thirsted Brattleboro rats by immunohistochemistry and immunoelectron microscopy. AQP-CD was mainly present in the cytoplasm of the collecting duct cells in association with cytoplasmic vesicles but was sparse in the apical membrane in control vehicle-injected rats. In rats given vasopressin 15 min before death, the number of immunogold particles for AQP-CD in the apical membrane increased significantly (P < 0.002) from 1.8 +/- 0.2 to 10.0 +/- 0.4/microns with a significant decrease (P < 0.05) of cytoplasmic labeling from 32.6 +/- 6.4 to 24.6 +/- 5.6/microns 2, indicating that AQP-CD is the vasopressin-regulated water channel predicted by the "shuttle" hypothesis. In contrast, AQP3 was restricted to the basolateral membrane of the collecting duct cells, and the labeling density of AQP3 was unchanged by vasopressin treatment, indicating that AQP3 is constitutively expressed and may maintain high water permeability of the basolateral membrane.

Amino Acid Sequence↗
PubMed1995

Urinary excretion of podocalyxin indicates glomerular epithelial cell injuries in glomerulonephritis.

Immunofluorescent study of urine sediments was performed to detect glomerular epithelial cell injuries using specific monoclonal antibody against podocalyxin, a glycoprotein that is prominently expressed on glomerular epithelial cells. Three kinds of structures (casts, granules and cells) were stained in urine sediments from various glomerular diseases. The presence of podocalyxin in urines was confirmed by absorption test, immunoelectron microscopy and Western blotting. Podocalyxin was detected in the urinary sediments of patients with various forms of glomerulonephritis, particularly those with acute onset. The amount of their urinary excretion apparently indicates the degree of the glomerular epithelial cell injuries in glomerular diseases.

Adolescent↗
PubMed1995

Visceral epithelial cells in rat glomerular cell culture.

The purpose of this study was to identify and characterize visceral epithelial cells (VECs) of renal glomeruli in culture. Such cells have been described variably as regular, polygonal cells showing a high rate of replication and a cobblestone-like appearance at confluence and also as irregular, arborized and often multinucleated cells showing a very limited proliferative capacity. We examined early outgrowths from the glomeruli by immunofluorescence microscopy using antibodies specific for VECs (anti-podocalyxin(1A), anti-pp44 and 5-1-6), for endothelial cells (anti-von Willebrand factor (vWF) and RECA-1) and for mesangial cells (anti-Thy-1). 1A and anti-pp44 reacted with several types of irregular, arborized cells, but never with regular, polygonal cells. 5-1-6 did not react with any of the cells. Neither the 1A- nor anti-pp44-positive cells (1A/pp44(+) cells) stained with anti-vWF, RECA-1 or anti-Thy-1. However, all the 1A/pp44(+) cells expressed desmin and vimentin but not cytokeratin. These results show that the 1A/pp44(+) cells are derived from VECs, supporting the idea that most polygonal cells in glomerular cultures are of parietal epithelial origin.

Animals↗
PubMed1994

Expression of mRNA for natriuretic peptide receptor subtypes in bovine kidney.

The localization of mRNA for atrial natriuretic peptide (ANP) receptor subtypes (A, B, C) in the kidney was examined. Quantitative analysis of the ribonuclease protection assay showed that the numbers of type A receptor (ANPRA) mRNA were 6.9 x 10(7) in the glomeruli and 10.4 x 10(7) molecules/micrograms of total RNA in the inner medulla, and that of type C receptor (ANPRC) mRNA was 21.7 x 10(7) molecules/micrograms of total RNA in the glomeruli. The type B receptor (ANPRB) mRNA was present in smaller numbers (4.5-4.9 x 10(6) molecules/micrograms of total RNA) evenly throughout the kidney fractions. In situ hybridization demonstrated both ANPRA and ANPRC mRNA selectively in the glomerular epithelial cells and ANPRA mRNA in the collecting duct cells of the inner medulla. ANPRC was also localized on the foot processes of glomerular epithelial cells by immunohistochemistry using a specific antibody against the receptor. These results indicate that ANPRA is the major biologically active receptor for the ANP family of hormones in the kidney and is present selectively on the glomerular epithelial cells and inner medullary collecting duct cells. These cells are presumed to play a role in the regulation of glomerular filtration rate and sodium excretion induced by the family of ANP.

Animals↗