• Coordinated chondrocyte proliferation and differentiation are required for normal endochondral bone growth. (biomedcentral.com)
  • Growth and development of endochondral bones is controlled through the highly coordinated proliferation and differentiation of growth plate chondrocytes [ 1 - 3 ]. (biomedcentral.com)
  • Local factors, including transcription factors such as SRY-box 9 protein (SOX9), Runt-related transcription factor 2 (RUNX2), and bone morphogenetic proteins (BMPs), along with signaling pathways such as the Wnt pathway, play critical roles in chondrocyte proliferation and differentiation. (pfmjournal.org)
  • FGFR3 inhibits chondrocyte proliferation and differentiation and promotes chondrocyte apoptosis [ 1 ]. (e-apem.org)
  • Gremlin-1 and BMP-4 Overexpressed in Osteoarthritis Drive an Osteochondral-Remodeling Program in Osteoblasts and Hypertrophic Chondrocytes. (nih.gov)
  • In contrast, the Runx2 gene (also known as Cbfa1) is essential for differentiation of osteoblasts, but also promotes hypertrophic chondrocyte differentiation [ 5 , 7 ]. (biomedcentral.com)
  • This, in turn, precipitates chondrocyte apoptosis, thereby, osteoblasts invade the hypertrophic zone and bone formation occurs [ 5 ]. (pfmjournal.org)
  • Statistical variations between your saline and alcoholic beverages organizations for biomechanical and micro-CT evaluation were determined using Student's staining exists inside the cartilage most distal towards the fracture site in keeping with triggered β-catenin/TCF transcription within pre-hypertrophic chondrocytes and immature osteoblasts (arrow). (crispr-reagents.com)
  • Ihh stimulates chondrocyte proliferation and regulates chondrocyte maturation by maintaining the expression of PTHrP. (wikipedia.org)
  • In addition, Atf3 mRNA levels are increased in response to cytochalasin D treatment, an inducer of chondrocyte maturation. (biomedcentral.com)
  • In addition to these key regulators of chondrocyte maturation, numerous other transcription factors have been implicated in this process. (biomedcentral.com)
  • The Runt-domain transcription factors Runx2 and Runx3 are known to drive chondrocyte maturation from prehypertrophic to the terminal stage. (bone-abstracts.org)
  • Indian hedgehog (Ihh) and PTHrP signaling play crucial roles in regulating the onset of chondrocyte hypertrophy by forming a negative feedback loop, in which Ihh signaling regulates chondrocyte hypertrophy by controlling PTHrP expression. (silverchair.com)
  • Therefore, ATF3 induction appears to facilitate cell cycle exit and terminal differentiation of chondrocytes. (biomedcentral.com)
  • Growth, metabolism, and differentiation of chondrocytes, which are the key cellular players in this process, are regulated by systemic hormones, local factors, and cellular signaling pathways. (pfmjournal.org)
  • Chondrocyte hypertrophy is an essential process required for endochondral bone formation. (silverchair.com)
  • HMGB2 was detected at higher levels in human MSC as in comparison with human articular chondrocytes and its expression declined during chondrogenic differentiation of MSC. (cox-inhibitors.com)
  • Curiously, a thick cell layer covered the articular cartilage with arthritis, and cellular debris overlaid this thick cell layer, nonetheless, articular chondrocytes seemed intact. (jakenzyme.com)
  • Normal Sprague-Dawley rat growth plate chondrocytes from the perichondral zone (PC)[the layer of fibrous connective tissue that envelops cartilage] and reserve zone (RZ) were isolated by laser microdissection and then subjected to microarray analysis. (heightquest.com)
  • Proper regulation of chondrocyte hypertrophy is also required in postnatal cartilage homeostasis. (silverchair.com)
  • We found that upregulating Ihh signaling in the developing cartilage by treating PTHrP -/- limb explants with sonic hedgehog (Shh) protein in vitro, or overexpressing Ihh in the cartilage of PTHrP -/- embryos or inactivating patched 1( Ptch1 ), a negative regulator of hedgehog (Hh) signaling, accelerated chondrocyte hypertrophy in the PTHrP -/- embryos. (silverchair.com)
  • Furthermore, we show that upregulated Hh signaling in the postnatal cartilage led to accelerated chondrocyte hypertrophy during secondary ossification, which in turn caused reduction of joint cartilage. (silverchair.com)
  • Our results revealed a novel role of Ihh signaling in promoting chondrocyte hypertrophy independently of PTHrP , which is particularly important in postnatal cartilage development and homeostasis. (silverchair.com)
  • In addition, we found that bone morphogenetic protein (Bmp) and Wnt/β-catenin signaling in the cartilage may both mediate the effect of upregulated Ihh signaling in promoting chondrocyte hypertrophy. (silverchair.com)
  • These condensed mesenchymal cells then differentiate into chondrocytes to form the cartilage anlagen. (silverchair.com)
  • This can be constant with in vivo results from mouse growth plates exhibiting that Hmgb2 is expressed in proliferating and prehypertrophic zones but not in hypertrophic cartilage wherever Col10a1 is strongly expressed. (cox-inhibitors.com)
  • hormone, thyroid and sex hormones) stimulates division of these chondrocytes and increase in the length of the cartilage growth plate and of the long bone. (mhmedical.com)
  • The expression of Sox9 induces the expression of BMP, which causes chondrocytes to proliferate and differentiate. (wikipedia.org)
  • To understand whether there is a PTHrP -independent role of Ihh signaling in regulating chondrocyte hypertrophy, we have both activated and inactivated Ihh signaling in the absence of PTHrP during endochondral skeletal development. (silverchair.com)
  • Conversely, when Hh signaling was blocked by cyclopamine or by removing Smoothened ( Smo ), a positive regulator of Hh signaling,chondrocyte hypertrophy was delayed in the PTHrP -/- embryo. (silverchair.com)
  • Hypertrophic chondrocytes, a progeny of terminally differentiated chondrocytes from the proliferative zone, cease further proliferation, undergo hypertrophy in columns parallel to the axis of longitudinal elongation, and initiate the production of factors that trigger mineralization and vessel invasion. (pfmjournal.org)
  • Growth hormone (GH), sex hormone, thyroid hormone, as well as glucocorticoids affect chondrocyte proliferation and hypertrophy. (pfmjournal.org)
  • And, we furtherly performed single-cell spatial transcriptomic sequencing on postnatal day 1 mouse enthesis, in order to deconvolute bone-tendon junction (BTJ) chondrocytes onto spatial spots. (elifesciences.org)
  • The growth plate can be stratified into three distinct zones based on the size, morphology, orientation, proliferative potential, and function of chondrocytes: resting, proliferative, and hypertrophic zone. (pfmjournal.org)
  • Our data suggest that transcriptional induction of the Atf3 gene in maturing chondrocytes results in down-regulation of cyclin D1 and cyclin A expression as well as activation of RUNX2-dependent transcription. (biomedcentral.com)
  • The regulation of chondrocyte function is mediated by several systemic, local, and cellular signaling pathways. (pfmjournal.org)
  • In this review, we summarized key regulatory factors and signaling pathways involved in chondrocyte functions, to understand how they affect chondrocyte growth and development. (pfmjournal.org)
  • The present study focuses on the relationship between the Evc gene and chondrocytes, and examines Evc gene expression in the rat tibial growth plate at the mRNA and protein levels. (elsevierpure.com)
  • Immunohistochemical analyses localized the Evc protein mainly in prehypertrophic and hypertrophic chondrocytes of the epiphyseal growth plate in the tibia during the embryonic and postnatal periods. (elsevierpure.com)
  • These results indicate that the Evc gene functions mainly in the prehypertrophic and hypertrophic chondrocytes of the epiphyseal growth plate. (elsevierpure.com)
  • This review provides an overview of the structural aspects of the growth plate, factors influencing chondrocyte function, and their impact on longitudinal bone growth. (pfmjournal.org)
  • The resting zone, a source of stemlike progenitor cells that restores the reservoir of proliferative chondrocytes, is located farthest from the primary ossification center and assumes responsibility for preserving the architectural integrity of the growth plate [ 4 ]. (pfmjournal.org)
  • The Sox9 gene is required for the differentiation of mesenchymal precursor cells to chondrocytes and, together with the related L-Sox5 and Sox6 proteins, controls chondrocyte-specific gene expression [ 4 , 5 ]. (biomedcentral.com)
  • L-Sox5 and Sox6 are thought to induce the activation of the Col2a1 and the Col11a2 genes, and to repress the expression of Cbfa1, a marker for late stage Chondrocytes. (wikipedia.org)
  • Effects of transforming growth factor-beta on aggrecanase production and proteoglycan degradation by human chondrocytes in vitro. (nih.gov)
  • We had shown earlier that transcription of the cell cycle genes cyclin D1 and cyclin A in chondrocytes is dependent on CREs. (biomedcentral.com)
  • Here we demonstrate that overexpression of ATF3 in primary mouse chondrocytes results in reduced transcription of both genes, as well as decreased activity of a CRE reporter plasmid. (biomedcentral.com)
  • The expression of Runx2, which plays a significant part in late stage chondrocyte differentiation, was enhanced in Hmgb2 / MSC and HMGB2 negatively regulated the stimulatory result of Wnt/b catenin signaling around the Runx2 proximal promoter. (cox-inhibitors.com)
  • PTHrP acts as a patterning molecule, determining the position in which the chondrocytes initiate differentiation. (wikipedia.org)
  • Based on the described biochemical interactions many of us created regulating product for the core signalling factors IHH, PTCH1, along with PTHrP and provided a pair of cell sorts, proliferating/resting chondrocytes along with (pre-) hypertrophic chondrocytes. (betaamyloid-signal.com)
  • These processes are regulated by a large number of endocrine, paracrine and autocrine hormones and growth factors that, to a large part, act on chondrocyte cell surface receptors. (biomedcentral.com)
  • Chondrocyte growth, metabolism, and differentiation are complex processes. (pfmjournal.org)
  • The differentiation of prehypertrophic into hypertrophic chondrocytes drives an OA-remodeling program and IL-34 expression. (nih.gov)
  • The molecule Indian hedgehog (Ihh) is expressed by prehypertrophic chondrocytes. (wikipedia.org)
  • Additionally, Indian hedgehog (Ihh) and C-type natriuretic peptide (CNP) are involved in the complex signaling network governing chondrocyte function. (pfmjournal.org)
  • In this short mini-review, we discuss the potential use of proteoliposome systems as chondrocyte- and osteoblast-derived MVs biomimetics, as a means of reconstituting a phospholipid microenvironment in a manner that recapitulates the native functional MV microenvironment. (scielo.org)