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Human Chondrocytes, HC, are derived from normal human articular cartilage where they produce and maintain the extracellular matrix of cartilage, including type II collagen. Chondrocytes grown in monolayer culture on a solid surface tend to lose their phenotypic markers and became de-differentiated to a fibroblast-like phenotype. This de-differentiation stage can be reversed by culturing them in a semi-solid gel.
Normal Chondrocytes obtained from Cell Applications, Inc. have been adapted as an in vitro model system in multiple studies looking for cellular mechanisms, such as inflammation-related signaling cascades, abnormal proteinase production, chondrocyte apoptosis and differentiation, as well as novel potential treatments for arthritic disease.
Characterization: Positive for aggrecan after differentiation.
Normal Human Chondrocytes (HC) have been used to:
- Develop a high throughput assay to screen for genes capable of inducing an OA-like phenotype in chondrocytes in order to identify key pathways implicated in the disease (Daouti, 2005)
- Elucidate the signaling cascade leading to induction of proinflammatory cytokines by chondrocytes in RA joints (Aida, 2006; Wang, 2011a,b) and effects of elevated IL-6 signaling on normal chondrocytes (Namba, 2007)
- Investigate mechanisms and identify inhibitors of increased production of proteinases by chondrocytes stimulated by interleukin-1 (Aida, 2005; Wada, 2006), retinoic acid (Hikichi, 2009), proinflammatory cytokines (Tanigawa, 2011a,b), nitric oxide (Wu, 2007; Yang, 2011) and shear stress (Wang, 2011b, 2012);
- Investigate the causes of metalloproteinases induction in patients with Lyme disease-associated arthritis (Lin, 2001; Behera, 2004, 2005)
- Study the factors affecting chondrocyte apoptosis (Cherng, 2008; Malemud, 2012) and differentiation into osteoclasts (Watanabe, 2009a,b; Honda, 2011)
- Show that hyaluronate (HA) can prevent the aggravated cartilage degradation by blocking the matrix metalloproteinases production from cytokine-activated chondrocytes via MKP-1 induction through CD44 signaling (Hashizume, 2009, 2010)
- Demonstrate cytotoxic effects of anti-human Fas/APO-1/CD95 (Fas) monoclonal antibody ARG098 on RA synoviocytes and infiltrating lymphocytes, but not on normal chondrocytes (Tamburstuen, 2010)
Normal Chondrocytes were also utilized in a functional cluster formation agarose assay that allows chondrocytes to maintain their differentiated state (Quintavalla, 2005) and to investigate integrin-mediated mechanotransduction pathways required for proper chondrocyte function (Whitney, 2012). Additionally, they have used extensively in material studies aimed to improve chondrocyte adhesion to medical implants (Gutwein, 2002; Ellison, 2003; Price, 2004; Savaiano, 2004; Burns, 2009) and scaffolds for cartilage regeneration (Jun, 2002; Kay, 2002; Miller, 2002a,b; Price, 2002, 2003; Rao, 2004; Park, 2005; Khang, 2008). Normal chondrocyte RNA was used as a gold standard control in research on cellular reprogramming into chondrocytes (Ishii, 2012).