Disease relevance of Chondrocytes

• Conversely, overexpression of HDAC4 in proliferating chondrocytes in vivo inhibits chondrocyte hypertrophy and differentiation, mimicking a Runx2 loss-of-function phenotype [1].
• Hypoxia in cartilage: HIF-1alpha is essential for chondrocyte growth arrest and survival [2].
• In this study, gene delivery to human osteoarthritis chondrocytes in monolayer culture was demonstrated using two adenoviral vectors (Ad.CMVlacZ and Ad.RSVntlacZ) carrying the Escherichia coli beta-galactosidase marker gene, and a third vector (Ad.RSV hIL-1ra) containing the cDNA for human interleukin-1 receptor antagonist [3].
• At an moi of 10(3) plaque-forming units/chondrocyte, > 90% of the infected cells stained positive for E. coli beta-galactosidase activity, indicating a high efficiency of transduction [3].
• Immortalized human chondrocytes were established by transfection of primary cultures of juvenile costal chondrocytes with vectors encoding simian virus 40 large T antigen and selection in suspension culture over agarose [4].

Psychiatry related information on Chondrocytes

• VCAM-1 and ICAM-1 contribute to adhesion of T lymphocytes to chondrocytes, and may thus participate in host defense mechanisms during inflammatory joint conditions such as rheumatoid arthritis and after cartilage transplantation [5].
• Inhibition of either RA or BMP signaling, with selective inhibitors, interfered with the inductive effects of these agents but also inhibited the complementary pathway, demonstrating a codependence of RA and BMP signaling during chondrocyte maturation [6].

High impact information on Chondrocytes

• CILP colocalized with TGF-beta1 in clustering chondrocytes and their territorial matrices in intervertebral discs [7].
• The Cbfb(GFP/GFP) mice exhibited a delay in endochondral and intramembranous ossification as well as in chondrocyte differentiation, similar to but less severe than delays observed in Runx2(-/-) mice [8].
• PTHrP delays the hypertrophic differentiation of proliferating chondrocytes, whereas IHH promotes chondrocyte proliferation [9].
• Further, we find that Ror2 is selectively expressed in the chondrocytes of all developing cartilage anlagen, where it essential during initial growth and patterning, as well as subsequently in the proliferating chondrocytes of mature growth plates, where it is required for normal expansion [10].
• Thus, Ror2 encodes a receptor-like tyrosine kinase that is selectively expressed in, and particularly important for, the chondrocyte lineage [10].

Chemical compound and disease context of Chondrocytes

• Thyroid hormone, insulin, and glucocorticoids are sufficient to support chondrocyte differentiation to hypertrophy: a serum-free analysis [11].
• Induction of proliferation or hypertrophy of chondrocytes in serum-free culture: the role of insulin-like growth factor-I, insulin, or thyroxine [12].
• Incorporation of sulfate into sulfated proteoglycans by isolated chicken chondrocytes was inhibited up to 74% by transformation with the Rous sarcoma virus, and a similar inhibitory effect was observed on acetate incorporation into chondroitin sulfate [13].
• Osteopontin (OPN) is an extracellular matrix protein containing Arg-Gly-Asp (RGD) sequence, which interacts with alpha(v)beta3 integrins, promotes cell attachment, and cell migration and is expressed in both synovial cells and chondrocytes in rheumatoid arthritis; however, its functional relationship to arthritis has not been known [14].
• Ankylosis protein (Ank), which transports intracellular inorganic pyrophosphate (PP(i)) to the extracellular milieu, is expressed by hypertrophic and, especially highly, by terminally differentiated mineralizing growth plate chondrocytes [15].

Biological context of Chondrocytes

• Reduced Indian hedgehog (Ihh) expression was observed in prehypertrophic chondrocytes, and apoptosis was inhibited in hypertrophic chondrocytes [16].
• Chick sternal chondrocytes cultured at high cell density lack fibronectin as a surface protein, while vitamin A-treated chondrocytes contain it as the major cell surface protein [17].
• Indian hedgehog signaling regulates proliferation and differentiation of chondrocytes and is essential for bone formation [18].
• FGF signaling inhibits chondrocyte proliferation and regulates bone development through the STAT-1 pathway [19].
• In particular, we provide evidence that VEGF expression is up-regulated in a HIF-1alpha-independent manner in chondrocytes surrounding areas of cell death, and this in turn induces ectopic angiogenesis [2].

Anatomical context of Chondrocytes

• Fibronectin alters the phenotypic properties of cultured chick embryo chondroblasts [20].
• Clonal and 2D protein gel analyses demonstrate that 5-azacytidine converts 10T1/2 cells into three stably determined, but undifferentiated, stem cell lineages which can differentiate into myofibers, chondrocytes, and adipocytes [21].
• The OPGL receptor, RANK, is expressed on chondrocytes, osteoclast precursors and mature osteoclasts [22].
• Since lactose also blocks elastic fiber formation by cultured chondroblasts, the galactoside-binding property of the elastin receptor is implicated in this process [23].
• These results identify Cbfa1 as a hypertrophic chondrocyte differentiation factor and provide a genetic argument for a common regulation of osteoblast and chondrocyte differentiation mediated by Cbfa1 [24].

Associations of Chondrocytes with chemical compounds

• Enhanced cellular fibronectin accumulation in chondrocytes treated with vitamin A [17].
• This protein component is also released from the surface of cultured chondroblasts by incubation with lactose, and its association with immobilized elastin is inhibited by lactose [23].
• Cyclic GMP-dependent protein kinase II is a molecular switch from proliferation to hypertrophic differentiation of chondrocytes [25].
• Furthermore, electron-dense deposits were seen near the surface of chondrocytes and corresponded with deposits of IgG and C3 [26].
• These studies, together with others, also suggest that PGE2 may be differentially regulated in normal and OA-affected chondrocytes [27].

Gene context of Chondrocytes

• Because Osx null preosteoblasts express typical chondrocyte marker genes, we propose that Runx2/Cbfa1-expressing preosteoblasts are still bipotential cells [28].
• Here, Sox9 is identified as a regulator of the chondrocyte lineage [29].
• In Hspg2-/- cartilage, proliferation of chondrocytes was reduced and the prehypertrophic zone was diminished [30].
• Analysis of PTHrP (-/-) mutant mice indicated that the PTHrP protein signals to its receptor in the prehypertrophic chondrocytes, thereby blocking hypertrophic differentiation [31].
• Misexpression of Ihh prevents proliferating chondrocytes from initiating the hypertrophic differentiation process [31].

Analytical, diagnostic and therapeutic context of Chondrocytes

• Scanning electron microscopy and light microscopy were used to relate the concentrations of NADH and NAD+ to stages of chondrocyte maturation [32].
• Constitutive low abundance PC-1 mRNA expression was detected in U20S cells and chondrocytes by a nested RNA-PCR assay and by Northern blotting [33].
• In situ hybridization of cartilage organ cultures revealed MCP-1 transcripts in chondrocytes in the superficial tangential zone within 2 h of stimulation with IL-1 [34].
• Transplantation of transduced chondrocytes protects articular cartilage from interleukin 1-induced extracellular matrix degradation [3].
• We infused IGF-I or growth hormone (GH), two key regulators of skeletal growth, into hypophysectomized rats and compared their effects on growth plate chondrocyte differentiation using qualitative and quantitative autoradiography, stereology, and incident light fluorescence microscopy [35].

References