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Elucidation of the mechanism of TGF-βsignaling in the repair process of full-thickness defects of rat articular cartilage.

Research Project

Project/Area Number 10671368
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Orthopaedic surgery
Research InstitutionDepartment of Orthopedic Surgery Kumamoto University

Principal Investigator

MIZUTA Hiroshi  Department of Orthopedic Surgery of Kumamoto University School of Medicine, Assistant professor, 医学部, 助教授 (60174025)

Co-Investigator(Kenkyū-buntansha) NAKAMURA Eiichi  Department of Orthopedic Surgery of Kumamoto University School of Medicine, Assistant, 医学部・附属病院, 助手 (70274719)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsFull-thickness defect / rat model / type II collagen / PCNA / N-CAM / TGF-βsignaling / immunohistochemistry / in situ hybridization / 軟骨全層欠損 / TGF-β1 / TGF-β受容体 / 軟骨欠損 / TGFβ
Research Abstract

To create full-thickness defects in rat femoral patellar groove uniformly, we invented a twin blade device. The repair process using this device was studied histologically, and the character of cells in the reparative tissue was elucidated by observing the localization of cell proliferation, N-CAM, and type II collagen mRNA.Further, the expression of TGF-β1, TGF-βRI, and TGF-βRII during the repair processes was investigated. At four days, proliferating undifferentiated spindle-shaped cells filled the entire defect, and N-CAM expression was restricted to spindlier undifferentiated cells beneath the surface area. Subsequently, these cells changed into polygonal-shaped cells, and type II collagen mRNA was detected in these cells deep in the defects at ten days. At two weeks, the first evidence of cartilage matrix indicated by safranin-O was observed, and chondrocytes surrounded by this cartilage matrix showed a high proliferative capacity. New subchondral bone at the bottom of the defects had formed through intramembranous ossification from four days. It progressed and reached to the same level of residual osteochondral junction by four weeks. By that time, new cartilage tissue similar to residual articular cartilage regenerated, and safranin-O and type II collagen wholly stained the newly synthesized cartilage matrix. TGF-β1, TGF-βRI, and TGF-β RII were coexpressed in the spindle-shaped undifferentiated cells that infiltrated into the defects, in the polygonal-shaped cells, and in proliferating chondrocytes located in the deep and middle layers. These results suggested that TGF-β signaling was involved through the chondrogenesis pathway of repair process, which included undifferentiated cell proliferation, cellular condensation, chondrocyte proliferation, and matrix synthesis.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report

URL: 

Published: 1998-04-01   Modified: 2016-04-21  

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