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2015 Fiscal Year Final Research Report

Inhibition of CD44 cleavage suppresses the chondrocyte de-differentiation

Research Project

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Project/Area Number 25462366
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Orthopaedic surgery
Research InstitutionNagoya University

Principal Investigator

Takahashi Nobunori  名古屋大学, 医学部附属病院, 病院講師 (20570196)

Co-Investigator(Kenkyū-buntansha) KOJIMA Toshihisa  名古屋大学, 医学部附属病院, 講師 (70378032)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords変形性関節症 / ヒアルロン酸 / CD44 / 断片化 / メカニカルストレス
Outline of Final Research Achievements

We mainly demonstrated that the excess mechanical stress loading can induce the CD44 fragmentation via the activation of TRPV4, a primary mechano-receptor, and the increased ADAM10 expression. CD44 fragmentation results in decreased ‘functional’ hyaluronan receptors and increased CD44 intracellular domain, leading to the diminished extracellular matrix in a chondrocyte. We also demonstrated that we successfully suppress the CD44 fragmentation using a TRPV4 antagonist or ADAM10 inhibitors under the mechanical stress loading condition. We will be able to start the in vivo study using animal osteoarthritis models as a next step.

Free Research Field

整形外科

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Published: 2017-05-10  

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