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Growth factor and extracellular matrix in glomerulosclerosis

Research Project

Project/Area Number 09671186
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionKAWASAKI UNIVERSITY OF MEDICAL WELFARE (1998)
Kawasaki Medical School (1997)

Principal Investigator

OSAWA Gengo  Kawasaki University of Medical Wefare Faculty of Medical Welfare, Professor, 医療福祉学部, 教授 (00018368)

Co-Investigator(Kenkyū-buntansha) SASAKI Tamaki  Kawasaki Medical School, Department of Medicine, Assisatant Professor, 医学部, 講師 (30187124)
除 義之  川崎医科大学, 医学部, 助手 (90235812)
北野 裕一  川崎医科大学, 医学部, 講師 (60177855)
Project Period (FY) 1997 – 1998
Project Status Completed (Fiscal Year 1998)
Budget Amount *help
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
KeywordsPodocyte / TGF-B / Cyclin-CDK / cyclin kinase inhibitor (CKI) family / p21 / p27 / Osteopontin / Tenascin / BMP7 / 糸球体荒廃像 / Bowman嚢上皮細胞 / 尿細管間質病変
Research Abstract

Podocytes are mostly present in the late G1 phase of the cell cycle even in the proliferative state, and there is no increase in the number of cells. As for the cyclin kinase inhibitor (CKI) family, which suppresses shifting of the cell cycle from the G i to the S phase, p21 and p27 have been identified. Regarding the number of p27-positive cells in podocytes, changes due to administration of FGF2 were not observed, but an increase in p21-positive podocytes was noted. These findings suggest that the reason most podocytes remain in the late GL phase might be upregulation of p21. Furthermore, FGF2 induced podocyte injury related to the transit cell cycle. When two sets of PAN rats were compared, the number of BrdU-positive cells was clearly greater in the rats administered FGF2. This finding demonstrated that a few podocytes entered the DNA synthesis phase. The number of bi - or multi- nucleated podocytes was counted in these rats. Our hypothesis is that podocytes entering the S phase are associated with FGF2-idced cell damage. We have shown that TGF-B isoforms and receptors increase with the podocytes of various glomerular injury models. The smad family was recently isolated and identified in the signalling of TGF-B.Expression of the smad family was observed in the podocytes of various glomerular injury models. TGF-B increases the expression of p21 in certain cells in vitro. Taken together, increases in p21 expression in podocytes may be due to the upregulation of TGF-B.We propose that p21 protects podocytes against damage by preventing damaged cells from entering the cell cycle.

Report

(3 results)
  • 1998 Annual Research Report   Final Research Report Summary
  • 1997 Annual Research Report
  • Research Products

    (21 results)

All Other

All Publications (21 results)

  • [Publications] T. SASAKI, et al: "Cytokines and podocyte injury : the mechanism of fibroblast growth factor 2-induced podocyte injury." Nephrol Dial Transplant. 14. 33-34 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] S. NOMURA, et al: "Microsatellite alterations in serum DNA of end-stage renal disease patients with acquired polycystic kidney." J Am Soc Nephrol. 9. 164A (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] T. SASAKI, et al: "A basic study of antisense therapy for peritoneal mesothelail injury." J Am Soc Nephrol. 9. 288A (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Y. OSHIRO, et al: "In vivo visualization of glomerular circulation in rat mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 340A (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Y. OSHIRO, et al: "Tubular expression of FGFRI and tenascin in reverse mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 498A (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Sasaki, T., et al.: "Cytokines and podocyte injury : the mechanism of fibroblast growth factor 2-induced podocyte injury." Nephrol Dial Transplant. 14. 33-34 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Nomura, S., et al.: "Microsatellite alterations in serum DNA of end-stage renal disease patients with acquired polycystic kidney." J Am Soc Nephrol. 9. 164A (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Sasaki, T., et al.: "A basic study of antisense therapy for peritoneal meshothelail injury." J Am Soc Nephrol. 9. 288A (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Oshiro, Y., et al.: "In vivo visualization of glomerular circulation in rat mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 340A (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Oshiro, Y., et al.: "Tubular expression of FGFR1 and tenascin in reverse mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 498A (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] T.SASAKI,et al: "Cytokines and podocyte injury: the mechanism of fibroblast growth factor 2-induced podocyte injury." Nephrol Dial Transplant. 14. 33-34 (1999)

    • Related Report
      1998 Annual Research Report
  • [Publications] S.NOMURA,et al: "Microsatellite alterations in serum DNA of end-stage renal disease patients with acquired polycystic kidney." J Am Soc Nephrol. 9. 164A (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] T.SASAKI,et al: "A basic study of antisense therapy for peritoneal mesothelail injury." J Am Soc Nephrol. 9. 288A (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Y.OSHIRO,et al: "In vivo visualization of glomerular circulation in rat mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 340A (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] Y.OSHIRO,et al: "Tubular expression of FGFR1 and tenascin in reverse mesangial proliferative glomerulonephritis" J Am Soc Nephrol. 9. 498A (1998)

    • Related Report
      1998 Annual Research Report
  • [Publications] T,SASAKI,et.al.: "Changes in glomerular epithelial cells by FGF2 and FGF2 neutralizing antibody in puromycin aminonucleoside nephropathy" Kidney Int. 51. 301-309 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] T,SASAKI,et.al.: "A Kinetic Study of Glomerular Epithelial Cells Associated with Segmental Glomerular Sclerotic Lesions with Adhesion in Spontaneously Diabetic WBN/Kob rats" Clin Exp Nephrol. 1. 32-40 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] H,KATO,et.al.: "Detection of Osteopontin mRNA in Epithelail Cells of Bowman's Capsule as revealed by in situ Hybridization" Kawasaki Med J. 4. 187-195 (1996)

    • Related Report
      1997 Annual Research Report
  • [Publications] Y,JYO,et.al.: "Expression of Tenascin in Mesangial Injury in Experimenatl Glomerulonephritis" Exp Nephrol. 5. 423-428 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] Y,JYO,et.al.: "Release of FGF2 and Osteopontin augments periglomerular lesions" J Am Soc Nephrol. 8. 498 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] T,SASAKI,et.al.: "The role of FGF2 in peritoneal mesothelial cell injury" J Am Soc Nephrol. 8. 272 (1998)

    • Related Report
      1997 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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