Mouse Acan (Aggrecan core protein) ELISA Kit (DEIA-FN23)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, plasma, cell culture supernatants, tissue homogenate
Species Reactivity
Intended Use
For quantitative detection of Mouse Acan (Aggrecan core protein) in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
0.156-10 ng/mL
0.094 ng/mL
Standard Curve


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Stimulation of Chondrogenic Differentiation of Adult Human Bone Marrow-Derived Stromal Cells by a Moderate-Strength Static Magnetic Field


Authors: Amin, Harsh D.; Brady, Mariea Alice; St-Pierre, Jean-Philippe; Stevens, Molly M.; Overby, Darryl R.; Ethier, C. Ross

Tissue-engineering strategies for the treatment of osteoarthritis would benefit from the ability to induce chondrogenesis in precursor cells. One such cell source is bone marrow-derived stromal cells (BMSCs). Here, we examined the effects of moderate-strength static magnetic fields (SMFs) on chondrogenic differentiation in human BMSCs in vitro. Cells were cultured in pellet form and exposed to several strengths of SMFs for various durations. mRNA transcript levels of the early chondrogenic transcription factor SOX9 and the late marker genes ACAN and COL2A1 were determined by reverse transcription-polymerase chain reaction, and production of the cartilage-specific macromolecules sGAG, collage type 2 (Col2), and proteoglycans was determined both biochemically and histologically. The role of the transforming growth factor (TGF)-beta signaling pathway was also examined. Results showed that a 0.4 T magnetic field applied for 14 days elicited a strong chondrogenic differentiation response in cultured BMSCs, so long as TGF-beta 3 was also present, that is, a synergistic response of a SMF and TGF-beta 3 on BMSC chondrogenic differentiation was observed. Further, SMF alone caused TGF-beta secretion in culture, and the effects of SMF could be abrogated by the TGF-beta receptor blocker SB-431542. These data show that moderate-strength magnetic fields can induce chondrogenesis in BMSCs through a TGF-beta-dependent pathway. This finding has potentially important applications in cartilage tissue-engineering strategies.

Human osteoarthritic synovium impacts chondrogenic differentiation of mesenchymal stem cells via macrophage polarisation state


Authors: Fahy, N.; de Vries-van Melle, M. L.; Lehmann, J.; Wei, W.; Grotenhuis, N.; Farrell, E.; van der Kraan, P. M.; Murphy, J. M.; Bastiaansen-Jenniskens, Y. M.; van Osch, G. J. V. M.

Objective: Mesenchymal stem cells (MSCs) are a promising cell type for the repair of damaged cartilage in osteoarthritis (OA). However, OA synovial fluid and factors secreted by synovium impede chondrogenic differentiation of MSCs, and the mechanism responsible for this effect remains unclear. In this study, we sought to investigate whether M1 and M2 synovial macrophages can contribute to the inhibition of MSC chondrogenesis. Design: The constitution of synovial macrophage subsets was analysed by immunohistochemical staining of human OA synovium sections for CD86 (M1 marker) and CD206 (M2 marker). To assess the effect of synovial macrophages on chondrogenesis, collagen type II (COL2) and aggrecan (ACAN) gene expression were compared between MSCs undergoing chondrogenic differentiation in medium conditioned (CM) by human OA synovial explants, human synovial macrophages and fibroblasts, or peripheral blood derived primary human monocytes differentiated towards an M1 or M2 phenotype. Results: OA synovium contained both M1 and M2 macrophages. Medium conditioned by synovial macrophages (CD45 + plastic adherent cells) down-regulated chondrogenic gene expression by MSCs. Additionally, CM of M1 polarised monocytes significantly decreased COL2 and ACAN gene expression by MSCs; this effect was not observed for treatment with CM of M2 polarised monocytes. Conclusion: MSC chondrogenesis is inhibited by OA synovium CM through factors secreted by synovial macrophages and our findings suggest that M1 polarised subsets are potential mediators of this anti-chondrogenic effect. Modulation of macrophage phenotype may serve as a beneficial strategy to maximise the potential of MSCs for efficient cartilage repair. (C) 2014 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

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