hypertrophic chondrocyte differentiation

To analyse the expression and roles of p38 mitogen-activated protein kinases in this process, we have established a micromass. 5 mediated by integrins, 3 , 4 , and 5 . RhoA, ROCK1, and ROCK2 are expressed throughout chondrogenic differenti-ation. Coupling of hypertrophic chondrocyte differentiation and angiogenesis is a prerequisite for endochondral ossification and involves numerous growth factors that influence chondrocyte differentiation but may require components of the extracellular matrix to be active in cartilage. An . cartilage development endochondral ossification hypertrophic chondrocyte Sox9 C hondrogenesis is an essential process in which sequential aggregation, proliferation, differentiation, and hypertrophy Arrows indicate Zbtb20 + cells (red). Requirements for the degree of . Growth plate chondrocytes go through multiple differentiation steps and eventually become hypertrophic chondrocytes. Coordinated proliferation and differentiation of growth plate chondrocytes is required for normal growth and development of the endochondral skeleton, but little is known about the intracellular signal transduction pathways regulating these processes. We have induced this osteogenic differentiation by cutting through the hypertrophic cartilage of embryonic chick femurs and culturing the explants. However, chondrocyte hypertrophic differentiation is a major obstacle for the application of hBMSCs in articular cartilage defect treatment. Interestingly, these changes occur during or immediately after the period of active chondrocyte proliferation. Longitudinal growth of endochondral bones is accomplished through the co-ordinated proliferation and hypertrophic differentiation of growth plate chondrocytes. In this study, we found that NCAM deficiency accelerates chondrocyte hypertrophy in articular cartilage and growth plate of OA mice. Introduction. RhoA overexpression in chondrogenic ATDC5 cells results in increased proliferation and a marked delay of hypertrophic differentiation, as shown by decreased induc-tion of alkaline phosphatase activity, mineralization, and (30) Yet, such a shift was not observed in the . Increasing evidence suggests that melatonin, an indole hormone, plays a pivotal role in chondrogenesis. A large number of growth factors and hormones have been implicated in the regulation of growth plate biology, however, less is known about the intracellular signaling pathways involved. 1989. Arrows indicate Zbtb20 + cells (red). As BMSC chondrogenic differentiation lies on a continuum, where the terminally differentiated cell type is a hypertrophic chondrocyte 12, the temporal response to induction factors is a critical . Chondrodysplasias are highly heterogeneous genetic cartilage diseases. A continuous cycle of chondrocyte hypertrophic differentiation in the newly Site-1 protease (S1P3; also known as the membrane-bound formed growth plate allows for continuous bone deposition and transcription factor protease, site-1) is a proprotein convertase therefore bone elongation. 274 CHENG ET AL. Hypertrophy is a critical process for chondrocyte differentiation and maturation during endochondral ossification, which is responsible for the formation of long bone and postnatal longitudinal growth. Hormones In addition to locally produced growth factors, systemic hormones - such as growth hormone (GH), insulin-like growth factors (IGFs), thyroid hormone, androgen, estrogen and glucocorticoids - tightly regulate . It has been shown that miR-145 is a key negative regulator of chondrogenic differentiation by directly targeting Sox9 to regulate the mRNA levels of chondrogenic marker genes and it contributes to impaired extracellular matrix in osteoarthritis partly via targeting Smad3 [12, 135 . Both local paracrine regulators and systemic hormones control endochondral bone formation and bone remode-ling throughout life. In this study, we investigated In conclusion, altered cell fate decisions, 33, 41 impaired hypertrophic chondrocyte transdifferentiation, 26 and impaired chondrocyte differentiation are regulated by SHP2 to some extent and contribute to the ossification process through various signaling pathways. In the case of a conditional knock out (CKO) of the R-Smads (1 and 5) in chondrocytes growth plate morphology is dramatically disrupted. hypertrophic and hypertrophic zones; staining was also observed in the pro-liferative zone. [PMC free article] [Google Scholar] Hunziker EB and Schenk RK (1989). Hypertrophic chondrocytes derived from human BMSCs represent a promising option for bone tissue engineering. Objective Calcification of cartilage with basic calcium phosphate (BCP) crystals is a common phenomenon during osteoarthritis (OA). hypertrophic chondrocyte differentiation and endochondral bone formation in spine development and maintenance. of hypertrophic chondrocyte differentiation that acts in a negative feedback loop with the secreted factor Indian hedgehog (Ihh) to regulate endochondral bone formation. The vitamin A derivative retinoic acid positively regulates hypertrophic chondrocyte differentiation and matrix mineralization . FGF9 regulates early hypertrophic chondrocyte differentiation and skeletal vascularization in the developing stylopod. Dev. IGF-1 Gene Transfer to Human Synovial MSCs Promotes Their Chondrogenic Differentiation Potential without Induction of the Hypertrophic Phenotype Bergers et al., "MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes ," Cell, vol. We found that SHP2 depletion, or inhibition of the ERK1/2 pathway, delays the terminal differentiation of chondrocytes from the early-hypertrophic to the late-hypertrophic stage. Moreover, osteoclast-derived exosomal let-7a-5p inhibits Smad2 to decrease the transforming growth factor-β-induced inhibition of chondrocyte hypertrophy. Thus, hypertrophic chondrocyte differentiation is . Collectively, these studies find that Bmp4 acts as a positive regulator of hypertrophic chondrocyte differentiation. INTRODUCTION Idiopathic scoliosis (IS) is the most common pediatric spinal deformity characterized by a lateral curvature of the spine >10°, affecting ~3% of children worldwide (Wise et al., 2008). FGF9 regulates early hypertrophic chondrocyte differentiation and skeletal vascularization in the developing stylopod. To determine which of the 1 integrins contribute to differentiation, we first assessed the . They are characterized by expression of type X collagen encoded by the Col10a1 gene, and synthesis of a calcified cartilage matrix. The presence of graft-derived hypertrophic chondrocytes indicated that P3-BMP9 engineered hyaline cartilage maintains a potential for hypertrophic chondrocyte differentiation. We examined the effect of NAC treatment on intracellular ROS levels during . Remarkably, some characteristics of this joint disease resemble chondrocyte … Hypertrophic differentiation of chondrocytes in osteoarthritis: the developmental aspect of degenerative joint disorders Arthritis Res Ther. trophic chondrocyte differentiation. The molecular mechanisms and signalling cascades controlling these processes are not well understood. Hypertrophic chondrocyte markers such as type X collagen and mmp13, as well as increased intracellular levels of ROS detected by dichlorodihydrofluorescein diacetate (DCF-DA), were induced in ATDC5 cells cultured in differentiation medium for 2 wk (Fig. hypertrophic chondrocyte differentiation, such as a large number of skeletal dysplasias that are characterized by dwarfism, skeletal deformities, and frequently by early-onset osteoarthritis [8]. The Signaling Pathways Involved in Chondrocyte Differentiation and Hypertrophic Differentiation JianmeiLiandShiwuDong Department of Biomedical Materials Science, School of Biomedical Engineering,i rd Military Medical University, Chongqing, China Correspondence should be addressed to Shiwu Dong; dongshiwu@.co m We evaluated the effects of rapamy-cin on chondrocyte differentiation by immunohistochemical detection of col-lagen X in intact metatarsals. [PMC free article] [Google Scholar] Hunziker EB and Schenk RK (1989). Jonathan C. Bernhard . Mef2c expression is upregulated in prehypertrophic chondrocytes. (A) Zbtb20 protein expression in hypertrophic chondrocytes in the normal femur at E14.5. Chondrocyte hypertrophic differentiation is a physiological stage in endochondral ossification which starts from the condensation of mesenchymal stem cells (MSCs) ().Then MSCs which are located within the centre of condensation differentiate to chondrocytes ().After proliferation, chondrocytes present hypertrophic morphology and secrete metal matrix proteinase to facilitate . This last stage is characterized by major phenotypic changes in the cell. 5). multistep differentiation process in which chondrocytes differentiate, proliferate, stop dividing and undergo hypertrophy, which entails a 20-fold increase in size. R-Smad CKO mice exhibited an increased area with Osteoclast-derived exosomes promote the hypertrophic differentiation of chondrocytes. High-cell-density micromass cultures were used to induce ATDC5 and C3H10T1/2 cell differentiation into chondrocytes. Cbfa1-deficient mice lack hypertrophic chondrocytes in some skeletal elements, indicating that Cbfa1 may control hypertrophic chondrocyte differentiation. To clarify the mechanisms of regulation by CTGF/Hcs24 with respect to cartilage metabolism, we investigated the interaction between CTGF/Hcs24 and heparan sulfate proteoglycan perlecan. However, little is known about the effects of melatonin on the terminal differentiation of . They are characterized by expression of type X collagen encoded by the Col10a1 gene, and synthesis of a calcified cartilage matrix. Hypertrophic chondrocytes are specialized cells consid-ered to be the end state of the chondrocyte differentiation pathway, and are essential for bone growth. Furthermore, the MAPK/ERK1/2 pathway phosphorylates and activates RunX2 (Cbfa1), a master 54 transcription factor for chondrocyte hypertrophy and an indispensable collagen X transactivator (10) 55 (11, 12) (13). The parathyroid hormone (PTH)-related peptide (PTHrP) signaling pathway plays a central role in regulation of hypertrophic differentiation, at least in part, through enhancing activity of histone deacetylase 4 (HDAC4), a negative regulator of MEF2 transcription factors that . These Wnt and BMP antagonists were able to inhibit hypertrophic chondrocyte differentiation when added to chondrogenically differentiated mesenchymal stem cells (MSCs). Figure 7S.2: Verification of the hypertrophic chondrocyte differentiation within the tissue For example, fibroblast growth factor (FGF) binds to cell surface . Connective tissue growth factor/hypertrophic chondrocyte‐specific gene product 24 (CTGF/Hcs24) plays important roles in the control of the proliferation and differentiation of chondrocytes in vitro. FRANUM CE, NJ WILSMAN. Condensation of hypertrophic chondrocytes at the chondroosseous junction of growth plate cartilage in Yucatan swine: relationship to long bone . According to the general understanding, the chondrocyte lineage terminates with the elimination of late hypertrophic cells by apoptosis in the growth plate. J. Phys 414, 55-71. Dev. Secondly, we studied chondrocyte maturation and organization in mice with a mosaic postnatal inactivation of Ptpn11 in chondrocytes. In summary, we have demonstrated a novel requirement for p38 signalling in hypertrophic differentiation of chondrocytes and identified myocyte enhancer factor 2C as an important regulator of chondrocyte gene expression. A downstream target of Runx2 is the myocyte enhancer factor 2c (Mef2c), which, like Runx2, is essential for hypertrophic chondrocyte differentiation . hypertrophic chondrocyte differentiation and endochondral bone formation in spine development and maintenance. 1. Visualization of living terminal hypertrophic chondrocytes of growth plate cartilage in situ by differential interference contrast microscopy and time-lapse cinematography. Here, Toguchida and colleagues establish a new induction system to differentiate hypertrophic chondrocytes from iPSCs and analyze these disorders in vitro. Here, we paired an in vitro 3D/pellet culture system that mimics chondrocyte hypertrophy with RNA sequencing (RNA-Seq) and enhanced reduced representation of bisulfite sequencing (ERRBS) to identify transcriptomic and epigenomic changes in murine primary articular chondrocytes undergoing hypertrophy-like differentiation. Mef2c expression is upregulated in prehypertrophic chondrocytes. To address this question we generated transgenic mice expressing Cbfa1 in nonhypertrophic chondrocytes (α1(II) Cbfa1). implicate FoxA transcription factors as key regulators of the hypertrophic chondrocyte differentiation program, showing that they directly drive expression of endogenous collagen X and other hypertrophic chondrocyte . 2010;12(5):216. doi: 10.1186/ar3117. The Signaling Pathways Involved in Chondrocyte Differentiation and Hypertrophic Differentiation JianmeiLiandShiwuDong Department of Biomedical Materials Science, School of Biomedical Engineering,i rd Military Medical University, Chongqing, China Correspondence should be addressed to Shiwu Dong; dongshiwu@.co m Generation of chondrocyte-specific Zbtb20 knockout mice. Chondrogenesis occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. The expressions of chondrocyte differentiation regulation genes, including Sox9, Ihh, CyclinD1, PTH1R, and hypertrophic chondrocyte Hypertrophic chondrocytes are specialized cells considered to be the end state of the chondrocyte differentiation pathway, and are essential for bone growth. The abnormalities of chondrocyte differentiation in osteoarthritis (OA) result in disordered cartilage extracellular matrix homeostasis [1,2].RUNX1 (Runt-related transcription factor 1), a member of Runx family, has been reported to be involved in cartilage formation and fracture healing [].RUNX1 promoted the differentiation of mesenchymal cells into chondrocytes [4,5]. A new induction method enables hypertrophic chondrocyte differentiation from iPSCs • Chondrodysplasia mutants show intracellular MATN3 or COL10 accumulation • Some, but not all, mutants have ER stress with an unfolded protein response • This induction system is applicable to transcriptomic analysis and drug development Ionescu et al. . Accelerated chondrocyte differentiation in the Hdac4-KO skeleton is a milder form of that in the Pthrp-KO skeleton. 1A). On the other hand, miR-181a/b apparently promotes hypertrophic chondrocyte differentiation (Fig. Engineering Hypertrophic Chondrocyte-based Grafts for Enhanced Bone Regeneration . Hypertrophic differentiation is marked by expression of the Discussiontype X collagen (COL10), as well as induction of MMP-13, alkaline phosphatase, and osteocalcin. Rapamycin (50 nM) completely abolished phospho-S6 staining at the end of a 3-day incuba-tion period. We have investigated the early cellular events that take place during the change in lineage commitment from hypertrophic chondrocytes to osteoblast-like cells. The results suggest a more efficient strategy for the cartilage repair of OA treatment using NCAM-overexpressing MSCs. Thus, PTHrP and miR-140 appear to regulate hypertrophic differentiation through independent mechanisms, but nevertheless the PTHrP pathway and miR-140 pathway converge on MEF2C regulation. They found that different chondrodysplasia mutants, despite mutations being in the same gene, showed varying phenotypes and transcriptomic changes. They (30) In their absence, chondrocyte-derived osteoblast differentiation decreased, while chondrocyte-derived adipocyte differentiation increased. Abstract. Hypertrophic chondrocyte differentiation induced by soluble GTP-bound transglutaminase 2 is . Clinical In the current study, we investigate and explore the role of ATF6 in endochondral bone formation, focus on associated molecules of hypertrophic chondrocyte differentiation, as well as the molecular events underlying this process. Runx2 induces Sp7, an essential transcription factor for osteoblast differentiation. Direct stimulation of chondrocyte hypertrophy without prior proliferation has been documented previously using embryonic chicken sternal chondrocytes , but it has been considered that proliferation is a prerequisite step that precedes terminal hypertrophic chondrocyte differentiation in the postnatal epiphyseal growth plate (21, 25, 45). Runx1 chondrocyte-specific knockout (Runx1f/fCol2α1-cre) mice exhibited impaired cartilage formation, decreased bone density, and an osteoporotic phenotype. 1, B and C). To test this, P3-BMP9 engineered hyaline cartilage (36-day cultures) was cultured an additional 20 days in BMP2 (P3-BMP9-BMP2) or, as a control, in BMP9. Hypertrophic chondrocytes are specialized cells considered to be the end state of the chondrocyte differentiation pathway, and are essential for bone growth. Generation of chondrocyte-specific Zbtb20 knockout mice. Early chondrogenic differentiation and hypertrophy of fects of RhoA overexpression on hypertrophic chondrocyte dif- ATDC5 cells are demonstrated by the expression of collagens II ferentiation. Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice. TG2 induces chondrocyte hypertrophic differentiation in a 1 integrin-dependent manner. Thus, PTHrP and miR-140 appear to regulate hypertrophic differentiation through independent mechanisms, but nevertheless the PTHrP pathway and miR-140 pathway converge on MEF2C regulation. Methods Calcification and sulfation of extracellular matrix . Ihh, expressed in prehypertrophic and hypertrophic chondrocytes, is required for the specification of Runx2+ osteoprogenitors in endochondral bone development. Skeletal formation by endochondral ossification involves enlargement of small, immature chondrocytes to form hypertrophic chondrocytes in certain cartilage regions. However, miR-138 appears to prevent formation of large, terminally differentiated hypertrophic chondrocytes and formation of type X collagen (a protein specifically generated by hypertrophic chondrocytes). . Runx2 is a transcription factor that is essential for osteoblast differentiation and chondrocyte maturation. We have investigated the roles of the GTPase RhoA and its effector kinases ROCK1/2 in hypertrophic chondrocyte differentiation. NCAM deficiency leads to hypertrophic chondrocyte differentiation in both murine MSCs and chondrogenic cells, in which extracellular signal-regulated kinase (ERK) signaling plays an important role. Clinical This study also described crosstalk between the Wnt pathway and BMP signaling pathway ( Leijten et al., 2013 ). Introduction. Atf-3 represses cyclinD1 and cyclinA It is directly linked to the severity of the disease and known to be associated to hypertrophic differentiation of chondrocytes. In addition, chondrocyte differentiation is also regulated by some microRNAs via altering the expression of Sox9. both chondrocyte and osteoblast differentiation. Bio 307, 300-313. Col10a1 and Col1a1 mRNA expression, as shown by in situ hybridization, indicates the differentiation of hypertrophic chondrocytes and osteoblasts at E14.5 . Thyroid hormone receptor a1(TRa1), TRa2, and TRb1 proteins were localized to reserve zone progenitor cells and proliferating chondrocytes in INTRODUCTION Idiopathic scoliosis (IS) is the most common pediatric spinal deformity characterized by a lateral curvature of the spine >10°, affecting ~3% of children worldwide (Wise et al., 2008). Keywords: chondrocyte, osteoblast, cartilage, cell signaling, growth/development. 39,40 Perfusion bioreactors have demonstrated the ability to enhance the properties of osteochondral constructs, and in this study, our goal was to determine the effect of perfusion flow on hypertrophic chondrocyte differentiation and . Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats. Submitted in partial fulfillment of the . MEF2 transcription factors drive hypertrophic chondrocyte differentiation. However, whether PRMT5-dependent regulation of Bmp4 expression is a driver of defective terminal hypertrophic chondrocyte differentiation remains to be determined. hypertrophic differentiation of the chondrocytes is hampered given the absence of MEF2C and Dlx5, both hypertrophy-promoting transcription factors. In prehypertrophic chondrocytes the activity of Runx2 is coupled to cell cycle exit by the transcription factor Atf-3 and the inhibition of Sox9 function. by . At the end of in vitro culture, tissue constructs grown without perfusion and at the perfusion rate of 400mm/s were im-planted into an orthotopic, critical-sized femoral defect in that NCAM deficiency enhances chondrocyte hypertrophy in chondrogenic differentiation of MSCs and in experimental OA, and upregulation of NCAM inhibits hypertrophic chon-drocyte differentiation. On the premises of the cell lineage definition proposed by Holtzer, the above data suggest that the hypertrophic chondrocytes represent the terminal stage of differentiation in the chondrogenic cell lineage. The chondrocyte in cartilage matrix has rounded or polygonal structure. Col10a1 and Col1a1 mRNA expression, as shown by in situ hybridization, indicates the differentiation of hypertrophic chondrocytes and osteoblasts at E14.5 . To elucidate a molecular mechanism of Dicam, we checked the major signaling targets in chondrogenesis, which showed an increased expression of Hhip and Zfp521, the target molecule of Ihh and Pthrp . Structure. Chondrocytes undergo terminal differentiation when they become hypertrophic, which happens during endochondral ossification. hypertrophic chondrocyte differentiation into bone in the devel-oping appendicular and axial skeletal elements. 41 Therefore, manipulating SHP2 and SHP2-regulated signaling pathways can . Future research optimizing chondrogenic differentiation and maintenance of mature chondrocytes will provide valuable information for both treatment and prevention of disease. H&E staining of the proximal tibial growth plate (original magnification, ×100 [ A - C , top]; ×40 [ D , top]), the anterior rib cage (original magnification, ×40 [ A and B , bottom]), and the anterior rib cartilage (original . In addition, early and late hypertrophic chondrocyte marker, Col10a1 and MMP13, respectively, also increased in Col2-Dicam-Tg compared to wild-type. Canonical Wnt signaling is also required . 52 chondrocyte differentiation from the pre-hypertrophic stage to the late hypertrophic stage during EO 53 (9). However, recent cell tracking studies have shown that murine hypertrophic chondrocytes can survive beyond ''terminal'' differentiation and give rise to a progeny R-spondin 2 facilitates differentiation of proliferating chondrocytes into hypertrophic chondrocytes by enhancing Wnt/β-catenin signaling in endochondral ossification Full Record Other Related Research The majority of our bones develop through the process of endochondral ossification that involves chondrocyte proliferation and hypertrophic differentiation in the cartilage growth plate. Physiological mechanisms adopted by chondrocytes in regulating longitudinal bone growth in rats. No These results support the notion that chondrogenesis and osteogenesis are one continuous process, in which β-catenin signaling plays an essential role in the cell trans-differentiation of chondrocytes into bone cells during mandibular condylar development and growth. One morphogen regulating hypertrophic chondrocyte differentiation is Wnt3a. Although multiple extracellular signaling molecules and nuclear transcription factors are implicated in hypertrophic chondrocyte differentiation, the precise intracellular . drogenic differentiation at 2 weeks and after construct cul-tivation at 5 weeks, and evaluated for hypertrophic chondrocyte differentiation and bone matrix deposition. (A) Zbtb20 protein expression in hypertrophic chondrocytes in the normal femur at E14.5. Chondrocyte hypertrophy is a mandatory step during endochondral ossification. 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