BMP-7 modulates selected matrix-associated changes in human articular chondrocytes during 2D expansion
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Published on: January 31, 2012
Milena Paw1, Dawid Wnuk1, Julita Balcerek2
1Department of Cell Biology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, Kraków, 30-387, Poland.
Background:
Maintenance of cartilage-associated features during in vitro expansion remains an important challenge for the development of chondrocyte-based Advanced Therapy Medicinal Products (ATMPs). Monolayer-cultured human articular chondrocytes (HACs) rapidly downregulate COL2A1 and ACAN while upregulating COL1A1, resulting in fibrocartilage-like matrix formation and reduced therapeutic efficacy. Bone morphogenetic protein-7 (BMP-7) has been reported to support anabolic and anti-fibrotic activity in cartilage, but its relevance to serial 2D expansion protocols relevant to chondrocyte expansion remains insufficiently understood. This study evaluated whether BMP-7 supplementation was associated with maintenance of selected matrix-associated readouts during prolonged 2D expansion of human articular chondrocytes.
Methods:
Primary HACs were isolated from human knee cartilage and expanded up to passage 3 with or without BMP-7, transforming growth factor β1 (TGF-β1) or dexamethasone. Cell morphology, proliferation, selected matrix-associated gene expression markers (COL2A1, COL1A1, ACAN, VCAN) and collagen I/II secretion were assessed.
Results:
During standard 2D expansion, COL2A1/COL1A1 and ACAN/VCAN ratios decreased, collagen I secretion increased, and the collagen II/collagen I protein ratio declined by approximately 10-fold by passage 2. TGF-β1 increased proliferation but markedly suppressed collagen II secretion. In contrast, BMP-7 maintained collagen II expression and secretion at levels comparable to primary culture up to passage 2, without altering proliferation. At passage 3, collagen II levels decreased and collagen I accumulation remained elevated irrespective of BMP-7 supplementation.
Conclusions:
These findings indicate that BMP-7 supports selected cartilage-associated readouts in primary HACs during early 2D expansion. However, BMP-7 did not prevent collagen I up-regulation at later passages, and functional redifferentiation capacity was not assessed. BMP-7 supplementation should therefore be considered a candidate strategy for further studies rather than evidence of complete phenotype preservation or a validated manufacturing approach on chondrogenic phenotype maintenance.
