2003 Fiscal Year Final Research Report Summary
A novel mutant gene inhibiting the progression of autoimmune glomerulonephritis
| Project/Area Number |
14370077
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Ehime University |
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Principal Investigator |
NOSE Masato Ehime Univ., Med., Pathol., Prof., 医学部, 教授 (70030913)
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| Co-Investigator(Kenkyū-buntansha) |
MAEYAMA Kazutaka Ehime Univ., Med., Pharmacol., Prof., 医学部, 教授 (00157158)
ONO Masao Ehime Univ., Med., Pathol., Ass.Prof., 医学系研究科, 教授 (20302218)
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| Project Period (FY) |
2002 – 2003
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| Keywords | crescentic glomerulonephritis / coat color / linkage analysis / susceptibility loci / mutant gene / platelet function / pathogenomics / EOD mice |
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| Research Abstract |
Crescentic glomerulonephritis (CreGN) is a representative outcome of autoimmune glomerulopathy, morphologically characteristics of extracapillary proliferative lesions in renal Bowman's space. Its rapid progression for irreversible renal failureis is of clinical importance. We previously had reported the establishment of murine disease-model (named EOD strain), of which the mice die of CreGN by 3 month-old. Recently, among these EOD mice, we found a spontaneous mutant strain of mice that exhibited much longer life-span and improved CreGN. Comparative pathological study using wild-type disease and mutant healthy mice demonstrated that a defect in platelet function was responsible for the improvement of CreGN. Furthermore, genetic analysis successfully identified the gene of mutation, which turned out to code a novel protein. Protein analysis showed that this mutation caused a loss of expression of this protein. The present study put forth an idea for therapeutic strategy against CreGN, that targets that molecular or a platelet function.
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[Publications] Takahashi, S., Araki, K., Araki, M., Ito, M.R., Nakatani, K., Fujii, H., Izui, S., Vassalli, P., Nose, M.: "Suppression of experimental lupus nephritis by aberrant expression of the solublu E-selectin gene."Pathol Int. 52(3). 175-180 (2002)
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「研究成果報告書概要(欧文)」より
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[Publications] Kamogawa, J., Terada, M., Mizuki, S., Nishihara, M., Yamamoto, H., Mori, S., Abe, Y., Morimoto, K., Nakatsuru, S., Nakamura, Y., Nose, M.: "Arthritis in MRL/lpr mice is under the control of multiple gene loci with an allelic combination derived from the original inbred strains."Arthritis Rheum. 46(4). 1067-1074 (2002)
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[Publications] Qu, W.M., Miyazaki, T., Terada, M., Okada, K., Mori, S., Kanno, H., Nose, M.: "A novel autoimmune pancreatitis model in MRL mice treated with polyinosinic : polycytidylic acid."Clin Exp Immunol. 129(1). 27-34 (2002)
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[Publications] Masui, N., Takagi, Y., Nishikawa, T., Yanabe, M., Nose, M., Sato, K.: "New PCR-RFLP analysis for the mouse Tnfsf6gld gene caused by a point mutation in the Tnfsf6 (tumor necrosis factor (Ligand) superfamily, member 6) locus."Exp Anim. 51(5). 501-503 (2002)
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「研究成果報告書概要(欧文)」より
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[Publications] Murata, K., Nose, M., Ndhlovu, L.C., Sato, T., Sugamura, K., Ishii, N.: "Constitutive OX40/OX40 ligand interaction induces autoimmune-like diseases."J Immunol. 169(8). 4628-4636 (2002)
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