Abstract
The aim of this study was to explore the therapeutic effect of iPSC-mesenchymal stem cell (MSC)-derived chondrocytes in a rabbit osteoarthritis (OA) model. The iPSCs were characterized by gene expressions, immunostaining of pluripotent markers, and in vivo teratoma formation. iPSC-differentiated MSCs were characterized by flow cytometry and trilineage differentiation. A rabbit OA model was established by the transection of the anterior cruciate ligament. The therapeutic effect of transplanted iPSC-MSC-chondrocytes on the OA was evaluated by the histology, immunostaining, and qPCR of defective cartilage. The results showed iPSC could express pluripotency markers such as OCT4, SOX2, and NANOG and form an embryoid body and a teratoma. After differentiation of iPSCs for 30 days, MSCs were established. The iPSC-MSC could express typical MSC markers such as CD29, CD44, CD90, CD105, and HLA-ABC. They could differentiate into adipocytes, osteocytes, and chondrocytes. In this model, iPSC-MSC-chondrocytes significantly improved the histology and ICRS (International Cartilage Repair Society) scores. The transplanted cartilage expressed less IL-1β, TNF-α, and MMP13 than control cartilage. In conclusion, the iPSCs we derived might represent an emerging source for differentiated MSC-chondrocyte and might rescue cartilage defects through its anti-inflammatory and anti-catabolic effects.
Highlights
Osteoarthritis (OA) is characterized by a gradual articular cartilage loss due to unknown causes [1]
The pluripotency of induced pluripotent stem cells (iPSCs) was evaluated by demonstrating that iPSCs immunofluorescence staining against NANOG, OCT4, and SOX2 were positive (Figure 1(a))
We proved iPSC-MSCchondrocytes transplanted cartilages were more intact than control cartilage
Summary
Osteoarthritis (OA) is characterized by a gradual articular cartilage loss due to unknown causes [1]. OA has an impact on the health of both men and women worldwide and about 10%–15% of adults over 60 years old have some degree of OA It is becoming an increasingly important disease, ranked as a cause for second disability [4]. The current symptoms’ control treatments of OA include both pharmacological and nonpharmacological approaches [5] as well as knee joint replacement in cases of severe cartilage destruction [6]. These treatment modalities still lack a definite efficacy.
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