1995 Fiscal Year Final Research Report Summary
Pathogenesis and molecular mechanisms of arteral restenosis
| Project/Area Number |
06454287
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Gunma University School of Medicine (1995)
The University of Tokyo (1994) |
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Principal Investigator |
NAGAI Ryozo Gunma University School of Medicine 2nd Dept of Int Med, Professor, 医学部, 教授 (60207975)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Tetsuya Gunma University School of Medicine 2nd Dept of Int Med, Assistant, 医学部, 助手 (10272238)
ARAI Masashi Gunma University School of Medicine 2nd Dept of Int Med, Assistant, 医学部, 助手 (60270857)
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| Project Period (FY) |
1994 – 1995
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| Keywords | RESTENOSIS, / SMOOTH MUSCLE, / MYOSIN, / SM1 / 2 GENE, / SMemb GENE, / TRANSCRIPTION FACTOR, / PTCA / 転写因子 |
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| Research Abstract |
We previously demonstrated that rabbit and rat smooth muscles contain at least three types of MHCs ; SM1(204kDa), SM2(200kDa)and SMemb(200kDa). SM1 and SM2 are two smooth muscle specific MHC isoforms arising from a singlegene, and SMemb is a third type of MHC isoform abundantly expressed in embryonic aortas. The expression of three MHC isoforms is developmentallyregulated.
The presence of developmentallyregulated MHC isoforms in vascular smooth muscles provides importantmoleculartools to investigate the molecularmechanism underlying vascular diseases. We first demonstrated that the developmentalregulation of myosin heavy chain expression occurs in proliferating smooth muscle cells after percutaneous angioplasty(PTCA) ; SMemb was reexpressed and SM2 was downregulated. We therefore characterized the promoter region of the SM1/2 and SMemb genes. In this study, we identified an important cis element for the SMemb gene and a transcription factor, BTEB-2, which coordinately regulate the SMemb gene.
We furthermore characterized SM1/2 gene which is most specifically expressed in smooth muscles. SM1/2 gene harbors two CCTCCC elements-80 bp upstream of the transcription initiation site. These elements play a basic role for SM1/2 gene transcription but does not necessarily regulate smooth muscle-specific expression.
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[Publications] Takewaki S,Kuro-o M,Hiroi Y,Watanabe M,Noguchi T,Nakahara K,Aikawa M,Manabe I,Ohkubo A,Yazaki Y,Nagai R.: "Activation of Na^+-H^+antipoter(NHE-1)gene expression during growth, hypertrophy and proliferation of the rabbit cardiovascular system" J.Mol.Cell Cardiol.27. 729-742 (1995)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Kimura K,Nagai R,Sakai T,Aikawa M,Kuro-o M,Kobayashi N,Shirato I,Inagami T,Oshi M,Suzuki N,Oba S,Mise N,Tojo A,Hirata Y,Goto A,Yazaki Y,Omata M.: "Diversity and variability of smooth muscle phenotypes of renal arterioles as revealed by myosin isoform expression." Kidney Int. 48. 372-382 (1995)
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「研究成果報告書概要(欧文)」より
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[Publications] Hiroi J,Kimura K,Sakai T,Aikawa M,Kuro-o M,Kobayashi N,Shirato I,Inagami T,Oshi M,Suzuki N,Oba S,Mise N,Tojo A,Hirata Y,Goto A,Yazaki Y,Omata M,Nagai R.: "Expression of a nonmuscle myosin heavy chain in glomerular cells differentiates various types of glomerular disease in rats." Kidney Int. (in press.).
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「研究成果報告書概要(欧文)」より
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[Publications] Suzuki J,Isobe M,Aikawa M,Kawauchi M,Shiojima I,Kobayashi N,Tojo A,KimuraK,Nishikawa T,Sakai T,Sekiguchi M,Yazaki Y,agai R.: "Nonmuscle and smooth muscle myosin heavy chain expression in rejected cardiac allograft-a study in rat and monkey models." Circulation.(in press.).
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「研究成果報告書概要(欧文)」より
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