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6. Supplementary Material for: Proteinuria and Glomerular Damage in Rab3A Knockout Mice Chronically Fed a High-Glucose Diet

Author

Armelloni, S., Calvaresi, N., Ikehata, M., Corbelli, A., Mattinzoli, D., Giardino, L.A., Li, M., Messa, P., and Rastaldi, M.P.

Abstract

Background/Aims: The relative contribution of genetic factors and dietary patterns to glomerular damage in healthy individuals and prediabetic conditions is currently unclear. All Rab3A knockout (KO) mice spontaneously develop macroalbuminuria, but only male mice exhibit a glucose-intolerant phenotype, thus making the model suitable to examine the impact of a diet on preexisting podocyte damage. Methods: Male and female Rab3A KO and wild-type (WT) mice were chronically fed a high-glucose diet (HGD). Biochemical tests, histology and immunohistochemistry were periodically performed whilst primary podocytes served for in vitro analyses. Results: Chronic administration of an HGD did not induce de novo alterations in WT kidneys but caused progressive worsening of podocyte and glomerular damage in both male and female Rab3A KO. Though glomerular lesions, reminiscent of human diabetic nephropathy, were more severe in male mice, overt proteinuria and renal damage were also evident in female mice. The in vitro analysis of Rab3A WT and KO podocytes revealed diminished actin plasticity in the cell processes of KO podocytes. Furthermore, a modest increase in glucose concentration induced profound cytoskeletal changes only in Rab3A KO cells. Conclusions: Our data show that chronic administration of an HGD to Rab3A KO mice that have a genetic defect that impairs podocyte actin plasticity results in increased podocyte damage and leads to overt proteinuria. If the same diet is given to male Rab3A KO animals, with additionally altered glucose homeostasis, this results in renal lesions similar to those of human diabetic nephropathy.

Published
2017
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11. Common noncoding UMOD promoter variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression

Author

TRUDU M, JANAS S, LANZANI C, DEBAIX H, SCHAEFFER C, IKEHATA M, CITTERIO L, DEMARETZ S, TREVISANI F, RISTAGNO G, GLAUDEMANS B, LAGHMANIK, DELL’ANTONIO G, the Swiss Kidney Project on Genes in Hypertension team 11, LOFFING J, RASTALDI MG, MANUNTA , PAOLO, DEVUYST O, RAMPOLLI L., RAMPOLDI, LUCA, Trudu, M, Janas, S, Lanzani, C, Debaix, H, Schaeffer, C, Ikehata, M, Citterio, L, Demaretz, S, Trevisani, F, Ristagno, G, Glaudemans, B, Laghmanik, Dell’Antonio, G, the Swiss Kidney Project on Genes in Hypertension team, 11, Loffing, J, Rastaldi, Mg, Manunta, Paolo, Devuyst, O, Rampolli, L., and Rampoldi, Luca

Published
2013

12. Reconstruction of Inclusions for the Inverse Boundary Value Problem with Mixed Type Boundary Condition

Author

Daido, Y., Ikehata, M., and Nakamura, G.

Subjects
Inverse boundary value problem, Conductiviy equation, Probe method, Mixed type boundary condition
Abstract

We consider an inverse boundary value problem for identifying the inclusion inside a known anisotropic conductive medium. We give a reconstruction procedure for identifying the in­clusion from the Dirichlet-Neumann map or the Neumann-Dirichlet map associated with the mixed type boundary condition.

Published
2003

13. Characterization of MPO-ANCA reactivity in patients with Churg-Strauss syndrome (CSS)

Author

Radice, A, Bianchi, L, Bredi, E, Maggiore, U, Gregorini, G, Ikehata, M, Wieslander, J, Farina, L, Romelli, P, SINICO, RENATO ALBERTO, Radice, A, Bianchi, L, Bredi, E, Maggiore, U, Gregorini, G, Ikehata, M, Wieslander, J, Farina, L, Romelli, P, and Sinico, R

Subjects
ANCA, anti-MPO, Churg-Strauss syndrome, epitope
Published
2009

14. RENAL HISTOPATHOLOGY. IMMUNOTACTOID GLOMEROLUPATHY: A CASE OF MONOCLONAL GAMMAPATHY OF RENAL SIGNIFICANCE

Author

Volgina, G., Gadzhikulieva, M., Uyshuk, N., Kawamura, E., Hisano, S., Nakashima, H., Saito, T., Boor, P., Babi kova, J., Martin, I. V., Bucher, E. B., Eriksson, U., Van Roeyen, C. R. C., Eitner, F., Floege, J., Peutz Kootstra, C. J., Ostendorf, T., Leh, S., Leh, F., Bjanes, T. K., Ohldieck, C., Svarstad, E., Han, B. G., Kim, J. S., Yang, J. W., Choi, S. O., Lollinga, W., Rahbar, A., De Wit, R. H., Riezebos Brilman, A., Soderberg Naucler, C., Van Son, W. J., Sanders, J. S., Smit, M. J., Van Den Born, J., Koike, K., Tsuboi, N., Ikezumi, Y., Go, K., Ogura, M., Saitoh, A., Yokoo, T., Yamaguchi, T., Nokiba, H., Hara, M., Morito, T., Kakihana, K., Ohashi, K., Ando, M., Kimura, T., Yagisawa, T., Nanmoku, K., Kurosawa, A., Sakuma, Y., Miki, A., Nukui, A., Alfieri, C. M., Regalia, A., Simonini, P., Ikehata, M., Chatziantoniou, C., Moroni, G., Rastaldi, M. P., Messa, P., Bockmeyer, C., Sauber lich, K., Zell, S., Zeuschner, P., Agustian, P. A., Wittig, J., Becker, J. U., Peters, B., Andersson, Y., Hadimeri, H., Stegmayr, B., Molne, J., Li, T., He, Y., Chen, H., Chen, J., Kobayashi, A., Mitome, J., Yamamoto, I., Mafune, A., Yamakawa, T., Nakada, Y., Tanno, Y., Ohkido, I., Yamamoto, H., Yokoyama, K., Dervishi, E., Buti, E., Nozzoli, C., Caldini, L. A., Giannakakis, Konstantinos, Minetti, E. E., Cirami, L., Bergesio, F., Ryuge, A., Nomura, A., Shimizu, H., Fujita, Y., Nishi, S., Goto, S., Nakai, K., Ito, J., Fujii, H., Hara, S., Mori, G., Ligabue, G., Cappelli, G., Pinho, A., Moreno, F., Dias, R., Vizcaino, R., Ossareh, S., Asgari, M., Abdi, E., Ataipour, Y., Malakoutian, T., Saddadi, F., and Rayatnia, M.

Published
2014

16. Common noncoding UMOD gene variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression

Author

Trudu, M., Janas, S., Lanzani, C., Debaix, H., Schaeffer, C., Ikehata, M., Citterio, L., Demaretz, S., Trevisani, F., Ristagno, G., Glaudemans, B., Laghmani, K., Dell'antonio, G., Bochud, M., Burnier, M., Devuyst, O., Martin, P.Y., Mohaupt, M., Paccaud, F., Pechère-Bertschi, A., Vogt, B., Ackermann, D., Ehret, G., Guessous, I., Ponte, B., Pruijm, M., Loffing, J., Rastaldi, M.P., Manunta, P., Rampoldi, L., Swiss Kidney Project on Genes in Hypertension (SKIPOGH) team, Bochud, M., Burnier, M., Devuyst, O., Martin, PY., Mohaupt, M., Paccaud, F., Pechère-Bertschi, A., Vogt, B., Ackermann, D., Ehret, G., Guessous, I., Ponte, B., and Pruijm, M.

Subjects
Male, Tamm–Horsfall protein, Hypertension/chemically induced/genetics, Genome-wide association study, 030204 cardiovascular system & hematology, Mice, 0302 clinical medicine, Promoter Regions, Genetic, ddc:616, 0303 health sciences, Kidney, education.field_of_study, biology, General Medicine, Middle Aged, 3. Good health, Up-Regulation, medicine.anatomical_structure, Hypertension, Female, Sodium, Dietary/adverse effects/pharmacokinetics, Adult, medicine.medical_specialty, Population, Renal function, Mice, Transgenic, Renal Insufficiency, Chronic/genetics, Polymorphism, Single Nucleotide, General Biochemistry, Genetics and Molecular Biology, Uromodulin/genetics, 03 medical and health sciences, Young Adult, Internal medicine, Uromodulin, medicine, Genetic predisposition, Animals, Humans, Genetic Predisposition to Disease, Renal Insufficiency, Chronic, education, 030304 developmental biology, ddc:613, Aged, Sodium, Dietary, medicine.disease, Promoter Regions, Genetic/genetics, Endocrinology, Blood pressure, Gene Expression Regulation, biology.protein, Kidney disease, Genome-Wide Association Study
Abstract

Hypertension and chronic kidney disease (CKD) are complex traits representing major global health problems. Multiple genome-wide association studies have identified common variants in the promoter of the UMOD gene, which encodes uromodulin, the major protein secreted in normal urine, that cause independent susceptibility to CKD and hypertension. Despite compelling genetic evidence for the association between UMOD risk variants and disease susceptibility in the general population, the underlying biological mechanism is not understood. Here, we demonstrate that UMOD risk variants increased UMOD expression in vitro and in vivo. Uromodulin overexpression in transgenic mice led to salt-sensitive hypertension and to the presence of age-dependent renal lesions similar to those observed in elderly individuals homozygous for UMOD promoter risk variants. The link between uromodulin and hypertension is due to activation of the renal sodium cotransporter NKCC2. We demonstrated the relevance of this mechanism in humans by showing that pharmacological inhibition of NKCC2 was more effective in lowering blood pressure in hypertensive patients who are homozygous for UMOD promoter risk variants than in other hypertensive patients. Our findings link genetic susceptibility to hypertension and CKD to the level of uromodulin expression and uromodulin's effect on salt reabsorption in the kidney. These findings point to uromodulin as a therapeutic target for lowering blood pressure and preserving renal function.

Published
2013

21. Proteinuria and hyperglycemia induce endoplasmic reticulum stress

Author

Lindenmeyer, M T, Rastaldi, M P, Ikehata, M, Neusser, M A, Kretzler, M, Cohen, C D, Schlöndorff, D, and University of Zurich

Subjects
2727 Nephrology, 10076 Center for Integrative Human Physiology, 570 Life sciences, biology, 610 Medicine & health, 10035 Clinic for Nephrology, 10052 Institute of Physiology
Published
2008
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22. RENAL HISTOPATHOLOGY

Author

Volgina, G., primary, Gadzhikulieva, M., additional, Uyshuk, N., additional, Kawamura, E., additional, Hisano, S., additional, Nakashima, H., additional, Saito, T., additional, Boor, P., additional, Babi kova, J., additional, Martin, I. V., additional, Bucher, E. B., additional, Eriksson, U., additional, Van Roeyen, C. R. C., additional, Eitner, F., additional, Floege, J., additional, Peutz-Kootstra, C. J., additional, Ostendorf, T., additional, Leh, S., additional, Leh, F., additional, Bjanes, T. K., additional, Ohldieck, C., additional, Svarstad, E., additional, Han, B. G., additional, Kim, J. S., additional, Yang, J. W., additional, Choi, S. O., additional, Lollinga, W., additional, Rahbar, A., additional, De Wit, R. H., additional, Riezebos-Brilman, A., additional, Soderberg-Naucler, C., additional, Van Son, W. J., additional, Sanders, J.-S., additional, Smit, M. J., additional, Van Den Born, J., additional, Koike, K., additional, Tsuboi, N., additional, Ikezumi, Y., additional, Go, K., additional, Ogura, M., additional, Saitoh, A., additional, Yokoo, T., additional, Yamaguchi, T., additional, Nokiba, H., additional, Hara, M., additional, Morito, T., additional, Kakihana, K., additional, Ohashi, K., additional, Ando, M., additional, Kimura, T., additional, Yagisawa, T., additional, Nanmoku, K., additional, Kurosawa, A., additional, Sakuma, Y., additional, Miki, A., additional, Nukui, A., additional, Alfieri, C. M., additional, Regalia, A., additional, Simonini, P., additional, Ikehata, M., additional, Chatziantoniou, C., additional, Moroni, G., additional, Rastaldi, M. P., additional, Messa, P., additional, Bockmeyer, C., additional, Sauberlich, K., additional, Zell, S., additional, Zeuschner, P., additional, Agustian, P. A., additional, Wittig, J., additional, Becker, J. U., additional, Peters, B., additional, Andersson, Y., additional, Hadimeri, H., additional, Stegmayr, B., additional, Molne, J., additional, Li, T., additional, He, Y., additional, Chen, H., additional, Chen, J., additional, Kobayashi, A., additional, Mitome, J., additional, Yamamoto, I., additional, Mafune, A., additional, Yamakawa, T., additional, Nakada, Y., additional, Tanno, Y., additional, Ohkido, I., additional, Yamamoto, H., additional, Yokoyama, K., additional, Dervishi, E., additional, Buti, E., additional, Nozzoli, C., additional, Caldini, L. A., additional, Giannakakis, C., additional, Minetti, E. E., additional, Cirami, L., additional, Bergesio, F., additional, Ryuge, A., additional, Nomura, A., additional, Shimizu, H., additional, Fujita, Y., additional, Nishi, S., additional, Goto, S., additional, Nakai, K., additional, Ito, J., additional, Fujii, H., additional, Hara, S., additional, Mori, G., additional, Ligabue, G., additional, Cappelli, G., additional, Pinho, A., additional, Moreno, F., additional, Dias, R., additional, Vizcaino, R., additional, Ossareh, S., additional, Asgari, M., additional, Abdi, E., additional, Ataipour, Y., additional, Malakoutian, T., additional, Saddadi, F., additional, and Rayatnia, M., additional

Published
2014
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23. Subtyping of cytomegalovirus strains obtained from immunocompetent children

Author

Kei Numazaki, Ikehata, M., and Chiba, S.

Subjects
Genotype, Viral Envelope Proteins, Cytomegalovirus Infections, DNA, Viral, Cytomegalovirus, Humans, Infant, DNA-Directed DNA Polymerase, Genes, Immediate-Early, Immunocompetence, Polymerase Chain Reaction, Polymorphism, Restriction Fragment Length
Abstract

We analyzed 33 clinical isolates of cytomegalovirus (CMV) obtained from immunocompetent Japanese children. DNA was extracted from infected MRC-5 cells and we amplified CMV glycoprotein-B (gB), major IE (MIE), DNA polymerase and glycoprotein-H (gH) genes using PCR. Among the 33 clinical isolates, 24 were identified as gB group 1, one as group 2, 6 as group 3, and 2 as simultaneous infections with group 1 and group 3 strains. Clinical isolates of CMV have also been classified into 18 MIE, 8 DNA polymerase and 15 gH genotype patterns by restriction fragment length polymorphism (RFLP). RFLP analysis is useful in molecular epidemiological studies of CMV infection in immunocompetent individuals.

Published
2001

25. Anti-C1q autoantibodies in lupus nephritis: Prevalence and clinical significance

Author

Sinico, R, Radice, A, Ikehata, M, Giammarresi, G, Corace, C, Arrigo, G, Bollini, B, Li Vecchi, M, SINICO, RENATO ALBERTO, Li Vecchi, M., Sinico, R, Radice, A, Ikehata, M, Giammarresi, G, Corace, C, Arrigo, G, Bollini, B, Li Vecchi, M, SINICO, RENATO ALBERTO, and Li Vecchi, M.

Abstract

Recently, anti-C1q autoantibodies have been proposed as a useful marker in systemic lupus erythematosus (SLE) since their occurrence correlates with renal involvement and, possibly, with nephritic activity. We aimed to evaluate the prevalence of anti-C1q antibodies in patients with SLE, with and without renal involvement, and to correlate these markers' presence and levels with the activity of the disease and nephropathy. We studied 61 patients with SLE, 40 of whom had biopsy-proven lupus nephritis; 35 patients with other connective tissue diseases; and 54 healthy controls. In addition, 18 lupus nephritis patients were followed up during the disease time course. Anti-C1q antibodies were measured using "homemade" ELISA with high salt concentration (1 M sodium chloride). High anti-C1q antibody titers (> 55 AU) were present in 27 of 61 (44%) SLE patients and in 4% and 0% of normal blood donors and pathologic controls, respectively. Anti-C1q antibodies were found in 60% of patients with lupus nephritis compared with only 14% of SLE patients without nephropathy (P < 0.05). Moreover, patients who were positive for anti-C1q antibodies had a higher European Consensus Lupus Activity Measurement (ECLAM) score (4.35 vs. 2.2); 89% of patients with active lupus nephritis showed high titers of anti-C1q antibodies compared with 0% of patients with inactive nephritis. Anti-C1q and anti-dsDNA antibodies agreed in 79% of cases. Our results confirm that anti-C1q antibodies are present in a significant percentage of SLE patients, and that their presence and levels correlate with disease activity-in particular, during renal flare-ups. © 2005 New York Academy of Sciences

Published
2005

26. A novel model of in vitro osteocytogenesis

Author

Mattinzoli⁎, D., primary, Messa, P., additional, Corbelli, A., additional, Ikehata, M., additional, Zennaro, C., additional, Armelloni, S., additional, Li, M., additional, Giardino, L., additional, and Rastaldi, M.P., additional

Published
2012
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49. Public Health on Electromagnetic Fields and Magnetic Shield of Linearmotorcar EDS Maglev.

Author

Ueno, Shoogo, Nakagawa, M., Ikehata, M., and Koana, T.

Abstract

As a legal term, the Labor Safety and Hygiene Law (LSHL; enforced October, 1972) uses it with a denotation of laborious disaster prevention. Activities for disaster prevention of workplace are divided into safety management and hygienic management by a narrow sense. Here, we think that it is prevention of an emergent danger with a task of "safety" of a narrow sense concerning LSHL, and we are allowed to think it is prevention of a health impairment that occurs chronically with an issue of "hygiene". We state about "safety" related to magnetic field or electromagnetic field. Safety issues about a case of MRI taking a superconducting magnet (SCM) as an example, are as follows; 1. a strong magnetic field attracts an iron-made oxygen bomb and a stretcher (simple bed with wheels that carries a patient prostrate) or causes a hammer and operative instruments to fly. injuring personnel nearby; 2. danger of an asphyxia for a personnel nearby, when a SCM is quenched under insutFicient ventilation; and 3. when dB / dt change in magnetic field of super-high-speed MRI equipinent is large, induced currents stimulate nerves, muscles and directly act on the heart. [ABSTRACT FROM AUTHOR]

Published
1996
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50. Inhibition of UV-induced G1 arrest by exposure to 50 Hz magnetic fields in repair-proficient and -deficient yeast strains.

Author

Takashima, Y., Ikehata, M., Miyakoshi, J., and Koana, T.

Subjects
*ELF electromagnetic fields, *MAGNETIC fields, *DYNAMICS, *DNA repair, *NUCLEOTIDES, *ULTRAVIOLET radiation
Abstract

Purpose : To assess the possibility that extremely low frequency (ELF) magnetic fields obstruct the damage repair process, the gene conversion frequency and cell cycle kinetics in a DNA repair-proficient and nucleotide excision repair (NER)-deficient strain of diploid yeast Saccharomyces cerevisiae . Materials and methods : DNA repair- or NER-deficient cells were irradiated with sublethal doses of ultraviolet light (UV) radiation followed by exposure to 50 Hz magnetic fields up to 30 mT for 48 h. After exposure, colony-forming ability was scored as revertants in which gene conversion had restored the functional allele of the ARG4 gene conversion hotspot. Cell cycle analysis was performed using flow cytometry. Results : Gene conversion rate was increased by the combined exposure in DNA repair-proficient cells, whereas it remained unchanged between UV alone and the combined exposure in NER-deficient cells. The UV-induced G1 arrest was inhibited by exposure to 30 mT ELF magnetic fields in both repair-proficient and -deficient cells. Conclusions : The results suggest that exposure to high-density (30 mT) ELF magnetic fields decreases the efficiency of NER by suppressing G1 arrest, which in turn led to enhancement of the UV-induced gene conversion. [ABSTRACT FROM AUTHOR]

Published
2003
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