University of Oulu

Jerome Nicolas Janssen, Valerio Izzi, Elvira Henze, Gökhan Cingöz, Florian Lowen, David Küttner, Ruth Neumann, Christof Lenz, Vicki Rosen, Nicolai Miosge, Enhancing the chondrogenic potential of chondrogenic progenitor cells by deleting RAB5C, iScience, Volume 24, Issue 5, 2021, 102464, ISSN 2589-0042,

Enhancing the chondrogenic potential of chondrogenic progenitor cells by deleting RAB5C

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Author: Janssen, Jerome Nicolas1,2; Izzi, Valerio3; Henze, Elvira1;
Organizations: 1Tissue Regeneration Work Group, Department of Prosthodontics, Medical Faculty, Georg-August-University, 37075 Göttingen, Germany
2Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA
3Faculty of Biochemistry and Molecular Medicine, University of Oulu, 90014 Oulu, Finland
4Bioanalytical Mass Spectrometry Group, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany
5Institute of Clinical Chemistry, Medical Faculty, Georg-August-University, 37075 Göttingen, Germany
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 10.1 MB)
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Language: English
Published: Elsevier, 2021
Publish Date: 2021-06-11


Osteoarthritis (OA) is the most prevalent chronic joint disease that affects a large proportion of the elderly population. Chondrogenic progenitor cells (CPCs) reside in late-stage OA cartilage tissue, producing a fibrocartilaginous extracellular matrix; these cells can be manipulated in vitro to deposit proteins of healthy articular cartilage.

CPCs are under the control of SOX9 and RUNX2. In our earlier studies, we showed that a knockdown of RUNX2 enhanced the chondrogenic potential of CPCs. Here we demonstrate that CPCs carrying a knockout of RAB5C, a protein involved in endosomal trafficking, exhibited elevated expression of multiple chondrogenic markers, including the SOX trio, and increased COL2 deposition, whereas no changes in COL1 deposition were observed.

We report RAB5C as an attractive target for future therapeutic approaches designed to increase the COL2 content in the diseased joint.

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Series: iScience
ISSN: 2589-0042
ISSN-E: 2589-0042
ISSN-L: 2589-0042
Volume: 24
Issue: 5
Article number: 102464
DOI: 10.1016/j.isci.2021.102464
Type of Publication: A1 Journal article – refereed
Field of Science: 1182 Biochemistry, cell and molecular biology
Funding: The authors disclosed the receipt of the following financial support for the research, authorship, and/or publication of this article: The Deutsche Forschungsgemeinschaft (Mi-573/10-2) and partial support from the Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences (GSC 226/4).
Copyright information: © 2021. This is an open access article under the CC BY-NC-ND license (