Abstract
Articular cartilage has limited capacity for natural regeneration and repair. In the present study, we evaluated kartogenin (KGN), a bioactive small heterocyclic molecule, for its effect on in vitro proliferation and chondrogenic differentiation of human bone marrow-derived mesenchymal stromal cells (hBMSCs) in monolayer culture and in co-culture models in vitro. OA osteochondral cylinders and hBMSCs were collected during total knee replacement. The effect of KGN on hBMSCs during 21 days of culture was monitored by real-time proliferation assay, immunofluorescence staining, histological assay, scanning electron microscopy (SEM) (imaging and multiplex enzyme-linked immunosorbent assay) ELISA assay. The rate of proliferation of hBMSCs was significantly increased by treatment with 10 µM KGN during nine days of culture. Histological and SEM analyses showed the ability of hBMSCs in the presence of KGN to colonize the surface of OA cartilage and to produce glycosaminoglycans and proteoglycans after 21 days of co-culture. KGN treated hBMSCs secreted higher concentrations of TIMPs and the secretion of pro-inflammatory molecules (MMP 13, TNF-α) were significantly suppressed in comparison with control without hBMSCs. Our preliminary results support the concept that 10 µM KGN enhances proliferation and chondrogenic differentiation of hBMSCs and suggest that KGN is a potential promoter for cell-based therapeutic application for cartilage regeneration.
Highlights
Osteoarthritis (OA) is a progressively destructive joint disorder that causes articular cartilage erosion and fibrillation, as well as subchondral bone changes, including sclerosis, bone cysts, osteophytes, and synovitis
The donor human bone marrow-derived mesenchymal stromal cells (hBMSCs) used in this study showed that >95% of the cell population expressed CD73 (99.81%), CD90 (99.38%), and CD105 (98.77%), and23
mesenchymal stromal cells (MSCs) has been proposed as a therapeutic strategy for promoting the use of chondrogenically-differentiated MSCs has been proposed as a therapeutic strategy for cartilage regeneration
Summary
Osteoarthritis (OA) is a progressively destructive joint disorder that causes articular cartilage erosion and fibrillation, as well as subchondral bone changes, including sclerosis, bone cysts, osteophytes, and synovitis. This socially-prevalent disease is characterized by complex interactions of cartilage, bone, the synovium, and systemic factors [1]. Articular cartilage represents an avascularised and non-innervated tissue with low cell mobility and a decreased number of progenitor cells, and has a limited capacity to self-repair. Considerable efforts have been made to develop suitable cartilage repair procedures resulting in defect filling and restoration of the articular surface with the best possible tissue repair. There is Molecules 2018, 23, 181; doi:10.3390/molecules23010181 www.mdpi.com/journal/molecules
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