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Monomeric, porous type II collagen scaffolds promote chondrogenic differentiation of human bone marrow mesenchymal stem cells in vitro

Abstract:
Osteoarthritis (OA) is a common cause of pain and disability and is often associated with the degeneration of articular cartilage. Lesions to the articular surface, which are thought to progress to OA, have the potential to be repaired using tissue engineering strategies; however, it remains challenging to instruct cell differentiation within a scaffold to produce tissue with appropriate structural, chemical and mechanical properties. We aimed to address this by driving progenitor cells to adopt a chondrogenic phenotype through the tailoring of scaffold composition and physical properties. Monomeric type-I and type-II collagen scaffolds, which avoid potential immunogenicity associated with fibrillar collagens, were fabricated with and without chondroitin sulfate (CS) and their ability to stimulate the chondrogenic differentiation of human bone marrow-derived mesenchymal stem cells was assessed. Immunohistochemical analyses showed that cells produced abundant collagen type-II on type-II scaffolds and collagen type-I on type-I scaffolds. Gene expression analyses indicated that the addition of CS - which was released from scaffolds quickly - significantly upregulated expression of type II collagen, compared to type-I and pure type-II scaffolds. We conclude that collagen type-II and CS can be used to promote a more chondrogenic phenotype in the absence of growth factors, potentially providing an eventual therapy to prevent OA.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/srep43519

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Publisher:
Nature Publishing Group
Journal:
Scientific Reports More from this journal
Volume:
7
Issue:
43519
Pages:
1-10
Publication date:
2017-03-03
Acceptance date:
2017-01-25
DOI:
ISSN:
2045-2322


Language:
English
Keywords:
Pubs id:
pubs:685342
UUID:
uuid:22961cf1-2128-442f-abc1-90616427475b
Local pid:
pubs:685342
Source identifiers:
685342
Deposit date:
2017-04-28

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