Disease relevance of Chondrogenesis

• Midkine is expressed during repair of bone fracture and promotes chondrogenesis [1].
• Hypoxia and HIF-1alpha in chondrogenesis [2].
• In the absence of exogenous BMP-2, Noggin inhibited metatarsal longitudinal growth, chondrocyte proliferation, and chondrocyte hypertrophy, which suggests that endogenous BMPs stimulate longitudinal bone growth and chondrogenesis [3].
• We showed that infection of migratory CNCC with adenovirus Msx2 mutants accelerated the rate and extent of chondrogenesis, as indicated by the expression level of type II collagen and aggrecan, and the amount of alcian blue staining [4].
• Developmental toxicity of valproic acid during embryonic chick vertebral chondrogenesis [5].

High impact information on Chondrogenesis

• During chondrogenesis in the mouse, Sox9 is co-expressed with Col2a1, the gene encoding type-II collagen, the major cartilage matrix protein [6].
• These results demonstrate that COL2A1 expression is directly regulated by SOX9 protein in vivo and implicate abnormal regulation of COL2A1 during, chondrogenesis as a cause of the skeletal abnormalities associated with campomelic dysplasia [6].
• The Sry-related gene Sox9 is expressed during chondrogenesis in mouse embryos [7].
• Our results strongly suggest that chondrogenesis is controlled by interactions between Sox9 and the Wnt/beta-catenin signaling pathway [8].
• Here we show the existence of physical and functional interactions between beta-catenin and Sox9, a transcription factor that is required in successive steps of chondrogenesis [8].

Chemical compound and disease context of Chondrogenesis

• Glucose transport and metabolism in chondrocytes: a key to understanding chondrogenesis, skeletal development and cartilage degradation in osteoarthritis [9].

Biological context of Chondrogenesis

• Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18 [10].
• Abnormal ambient glucose levels inhibit proteoglycan core protein gene expression and reduce proteoglycan accumulation during chondrogenesis: possible mechanism for teratogenic effects of maternal diabetes [11].
• These results establish that SOX9 cooperative dimerization is required for chondrogenesis but not for sex determination and may explain why campomelic dysplasia need not be associated with XY sex reversal [12].
• These findings suggest a role for HMGN1 in chromatin remodeling during embryogenesis and in the activation of Sox9 during chondrogenesis [13].
• Further, we demonstrate that Tbx5 exerts in part its key regulatory role in bone growth and maturation by controlling via Cx40 the expression of Sox9 (a transcription factor essential for chondrogenesis and skeleton growth) [14].

Anatomical context of Chondrogenesis

• Although the signals involved in these later steps have not yet been pinpointed, there is substantial evidence that the analogous stages of limb bud chondrogenesis require bone morphogenetic protein (BMP) signaling [15].
• Signaling to multiple FGFRs positions FGF18 to coordinate chondrogenesis in the growth plate with osteogenesis in cortical and trabecular bone [10].
• Sox9, for instance, is required for chondrogenesis and male sex determination; Sox10 plays key roles in neural crest development and peripheral gliogenesis [16].
• Dual role of the basic helix-loop-helix transcription factor scleraxis in mesoderm formation and chondrogenesis during mouse embryogenesis [17].
• PDGFA stimulated chondrogenesis in somite micromass cultures as well as in embryos when PDGFA was knocked into the Myf5 locus, resulting in increased vertebral and rib development [18].

Associations of Chondrogenesis with chemical compounds

• Insulin cannot be substituted by insulin-like growth factor-I, but dexamethasone concentration can be decreased to 10(-12) M without chondrogenesis being impaired [19].
• The sensitivity to ambient glucose levels of both expression of the cartilage-specific chondroitin sulfate core protein gene and the accumulation of the corresponding extracellular matrix macromolecules during chondrogenesis suggest a molecular mechanism for the well-known adverse effect of maternal diabetes on embryonic skeletogenesis [11].
• Cloning of a retinoic acid-sensitive mRNA expressed in cartilage and during chondrogenesis [20].
• Expression of integrin alpha5beta1 and fibronectin were found to transiently increase during chondrogenesis [21].
• The calcium ionophore, ionomycin, induced chondrogenesis through activation of calcineurin [22].

Gene context of Chondrogenesis

• Expression of Sox5 and Sox6, two other Sox genes involved in chondrogenesis, was no longer detected [23].
• Together, these data suggest that Col10a1 is a direct transcriptional target of Runx2 during chondrogenesis [24].
• Furthermore, using this mouse model, we establish the cellular etiology of these defects and show that Shox2 acts upstream the Runx2 gene, a key regulator of chondrogenesis [25].
• Bmpr1a and Bmpr1b have overlapping functions and are essential for chondrogenesis in vivo [26].
• Also, forkhead, CD10, and MMP13 increased up to day 7 and decreased thereafter, suggesting roles in an intermediate stage of chondrogenesis [27].

Analytical, diagnostic and therapeutic context of Chondrogenesis

• In situ hybridization analysis demonstrated that mouse I-mfa was highly expressed in extraembryonic lineages, in the sclerotome, and subsequently within mesenchymal precursors of the axial and appendicular skeleton, before chondrogenesis occurs [28].
• Estradiol inhibited significantly cell proliferation as well as chondrogenesis in cell cultures from either side of female syrinx [29].
• As shown by Western blotting, the expression of N-cadherin declined as chondrogenesis proceeded and was affected in cultures treated with 1,25-dihydroxyvitamin D3 and TGF-beta 1 [30].
• In contrast to previous studies in chicken using N-cadherin-perturbing antibodies, our organ culture studies with mouse tissue demonstrate that N-cadherin is not essential for limb mesenchymal chondrogenesis [31].
• Microinjection of the Msx2-adenovirus to the proximal position inhibited BMP4-induced chondrogenesis [32].

References