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Search on : sox9 and transcription and factor [Words]
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[PMID]: 29507095
[Au] Autor:Sakabe T; Sakai K; Maeda T; Sunaga A; Furuta N; Schweitzer R; Sasaki T; Sakai T
[Ad] Address:University of Liverpool, United Kingdom.
[Ti] Title:Transcription factor scleraxis vitally contributes to progenitor lineage direction in wound healing of adult tendon in mice.
[So] Source:J Biol Chem;, 2018 Mar 05.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Tendon is a dense connective tissue that transmits high mechanical forces from skeletal muscle to bone. The transcription factor scleraxis (Scx) is a highly specific marker of both precursor and mature tendon cells (tenocytes). Mice lacking scx exhibit a specific and virtually complete loss of tendons during development. However, the functional contribution of Scx to wound healing in adult tendon has not yet been fully characterized. Here, using ScxGFP-tracking and loss-of-function systems, we show in an adult mouse model of Achilles tendon injury that paratenon cells, representing a stem cell antigen-1 (Sca-1)-positive and Scx-negative progenitor subpopulation, display Scx induction, migrate to the wound site, and produce extracellular matrix (ECM) to bridge the defect, whereas resident tenocytes exhibit a delayed response. Scx induction in the progenitors is initiated by transforming growth factor ß (TGF-ß)-signaling. Scx-deficient mice had migration of Sca-1-positive progenitor cell to the lesion site, but impaired ECM assembly to bridge the defect. Mechanistically, scx-null progenitors displayed higher chondrogenic potential with up-regulation of SRY-box 9 (Sox9) coactivator PPAR-gamma coactivator 1α (PGC-1α) in vitro, and knock-in analysis revealed that forced-expression of full-length scx significantly inhibited sox9 expression. Accordingly, scx-null wounds formed cartilage-like tissues that developed ectopic ossification. Our findings indicate a critical role of Scx in a progenitor-cell-lineage in wound healing of adult mouse tendon. These progenitor cells could represent targets in strategies to facilitate tendon repair. We propose that this lineage-regulatory mechanism in tissue progenitors could apply to a broader set of tissues or biological systems in the body.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  2 / 2606 MEDLINE  
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[PMID]: 29487295
[Au] Autor:Roberto VP; Gavaia P; Nunes MJ; Rodrigues E; Cancela ML; Tiago DM
[Ad] Address:Centre of Marine Sciences (CCMAR/CIMAR-LA), University of Algarve, 8005-139, Faro, Portugal.
[Ti] Title:Evidences for a New Role of miR-214 in Chondrogenesis.
[So] Source:Sci Rep;8(1):3704, 2018 Feb 27.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:miR-214 is known to play a role in mammalian skeletal development through inhibition of osteogenesis and stimulation of osteoclastogenesis, but data regarding other vertebrates, as well as a possible role in chondrogenesis, remain unknown. Here, we show that miR-214 expression is detected in bone and cartilage of zebrafish skeleton, and is downregulated during murine ATDC5 chondrocyte differentiation. Additionally, we observed a conservation of the transcriptional regulation of miR-214 primary transcript Dnm3os in vertebrates, being regulated by Ets1 in ATDC5 chondrogenic cells. Moreover, overexpression of miR-214 in vitro and in vivo mitigated chondrocyte differentiation probably by targeting activating transcription factor 4 (Atf4). Indeed, miR-214 overexpression in vivo hampered cranial cartilage formation of zebrafish and coincided with downregulation of atf4 and of the key chondrogenic players sox9 and col2a1. We show that miR-214 overexpression exerts a negative role in chondrogenesis by impacting on chondrocyte differentiation possibly through conserved mechanisms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-21735-w

  3 / 2606 MEDLINE  
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[PMID]: 29457374
[Au] Autor:Serrano RL; Chen LY; Lotz MK; Liu-Bryan R; Terkeltaub R
[Ad] Address:Ramon L Serrano, PhD, Liang-Yu Chen, PhD, Ru Liu-Bryan, PhD, Robert Terkeltaub, MD, VA San Diego Healthcare System/UC San DiegoLa Jolla, CA.
[Ti] Title:Proteasomal function is impaired in human osteoarthritic chondrocytes and this can contribute to decreased SOX9 and aggrecan.
[So] Source:Arthritis Rheumatol;, 2018 Feb 18.
[Is] ISSN:2326-5205
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Osteoarthritis (OA) chondrocytes have impaired autophagy, one arm of the proteostasis network that coordinates proteome and organelle quality control and degradation. Deficient proteostasis impacts differentiation and viability, and inflammatory processes in aging and disease. Studying OA chondrocytes, we assessed ubiquitin proteasome system proteasomal function. METHODS: We evaluated human knee cartilages by immunohistochemistry, and assessed proteasomal function, levels of proteasomal core subunits and chaperones, and autophagy in cultured chondrocytes. Assays included Western blotting, quantitative RT-PCR, proteasomal protease activity and cell immunofluorescence. RESULTS: Human knee OA cartilages demonstrated polyubiquitin accumulation, with increased ubiquitin K48-linked polyubiquitinated proteins in situ, suggesting proteasomal impairment. Cultured OA chondrocytes demonstrated accumulation of K48 polyubiquitinated proteins, significantly decreased 20S proteasome core protease activity, and decreased levels of phosphorylated FOXO4 and PSMD11, a FOXO4-inducible promoter of proteasomal activation. Levels of proteasomal core subunits PSMB3, 5, 6, and assembly chaperone PSMG1 were not decreased in OA chondrocytes. In normal chondrocytes, PSMD11 siRNA knockdown stimulated certain autophagy machinery elements, elevated extracellular nitric oxide (NO), and decreased chondrocytic master transcription factor SOX9 protein (and mRNA) and aggrecan (AGC1) mRNA. PSMD11 gain of function by transfection increased proteasomal function, raised levels of SOX9-induced AGC1 mRNA, stimulated elements of the autophagic machinery, and inhibited extracellular levels of IL-1-induced NO and MMP13 in OA chondrocytes. CONCLUSION: Deficient PSMD11, associated with less phosphorylated FOXO4, promotes impaired proteasomal function in OA chondrocytes, dysregulated chondrocytic homeostasis, and decreased levels of SOX9 mRNA, SOX9 protein, and AGC1 mRNA. Chondrocyte proteasomal impairment may be a therapy target for OA. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher
[do] DOI:10.1002/art.40456

  4 / 2606 MEDLINE  
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[PMID]: 29286152
[Au] Autor:Delgado-Enciso I; Paz-Garcia J; Rodriguez-Hernandez A; Madrigal-Perez VM; Cabrera-Licona A; Garcia-Rivera A; Soriano-Hernandez AD; Cortes-Bazan JL; Galvan-Salazar HR; Valtierra-Alvarez J; Guzman-Esquivel J; Rodriguez-Sanchez IP; Martinez-Fierro ML; Paz-Michel B
[Ad] Address:Cancerology State Institute, Colima State Health Services, Colima 28000, Mexico.
[Ti] Title:A promising novel formulation for articular cartilage regeneration: Preclinical evaluation of a treatment that produces SOX9 overexpression in human synovial fluid cells.
[So] Source:Mol Med Rep;17(3):3503-3510, 2018 Mar.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Osteoarthritis (OA) is a chronic disorder of synovial joints, in which there is progressive softening and disintegration of the articular cartilage. OA is the most common form of arthritis, and is the primary cause of disability and impaired quality of life in the elderly. Despite considerable medical necessity, no treatment has yet been proven to act as a disease­modifying agent that may halt or reverse the structural progression of OA. The replacement of the joint with a prosthesis appears to be the best option in the advanced stages of the disease. A formulation (BIOF2) for cartilage regeneration has been recently developed. The present study evaluated the effects of BIOF2 on gene expression in human cell cultures, followed by efficacy trials in three OA animal models. Human synovial fluid cells that were exposed to the formulation exhibited increased transcription factor SOX­9 (SOX9; chondrogenic factor) expression, and decreased mimecan (mineralization inducer) and macrophage­stimulating protein receptor (osteoclastogenic factor) expression. The intra­articular application of BIOF2 in the animal models significantly increased cartilage thickness from 12 to 31% at 28 days, compared with articular cartilage treated with saline solution. The articular area and number of chondrocytes additionally increased significantly, maintaining an unaltered chondrocyte/mm2 proportion. Evaluation of the histological architecture additionally displayed a decrease in the grade of articular damage in the groups treated with BIOF2. In conclusion, BIOF2 has proven to be effective for treating OA in animal models, most likely due to SOX9 overexpression in articular cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Process
[do] DOI:10.3892/mmr.2017.8336

  5 / 2606 MEDLINE  
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[PMID]: 29425963
[Au] Autor:Xu X; Bass B; McKillop WM; Mailloux J; Liu T; Geremia NM; Hryciw T; Brown A
[Ad] Address:Robarts Research Institute, University of Western Ontario, London, Canada.
[Ti] Title:Sox9 knockout mice have improved recovery following stroke.
[So] Source:Exp Neurol;303:59-71, 2018 Feb 06.
[Is] ISSN:1090-2430
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The partial recovery that can occur after a stroke has been attributed to structural and functional plasticity that compensate for damage and lost functions. This plasticity is thought to be limited in part by the presence of growth inhibitors in the central nervous system. Blocking or reducing signals from inhibitors of axonal sprouting such as Nogo and chondroitin sulfate proteoglycans (CSPGs) increases post-stroke axonal sprouting and improves recovery. We previously identified the transcription factor SOX9 as a key up-regulator of CSPG production and demonstrated that conditional Sox9 ablation leads to increased axonal sprouting and improved recovery after spinal cord injury. In the present study we evaluate the effect of conditional Sox9 ablation in a transient middle cerebral artery occlusion (MCAO) model of stroke. We demonstrate that conditional Sox9 ablation leads to reduced CSPG levels, increased tissue sparing and improved post-stroke neurological recovery. Anterograde tract tracing studies demonstrate that in the Sox9 conditional knockout mice corticorubral and corticospinal projections from the contralateral, uninjured cortex increase projections to targets in the midbrain and spinal cord denervated by the injury. These results suggest that targeting SOX9 is a viable strategy to promote reparative axonal sprouting, neuroprotection and recovery after stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:Publisher

  6 / 2606 MEDLINE  
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[PMID]: 29421235
[Au] Autor:Golan-Lagziel T; Lewis YE; Shkedi O; Douvdevany G; Caspi LH; Kehat I
[Ad] Address:The Rappaport Institute and the Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 31096, Israel.
[Ti] Title:Analysis of rat cardiac myocytes and fibroblasts identifies combinatorial enhancer organization and transcription factor families.
[So] Source:J Mol Cell Cardiol;116:91-105, 2018 Feb 05.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cardiac fibroblasts play key roles in both health and disease. Their regulatory elements, transcription factors (TFs), and mechanisms of expression control have not been fully elucidated. We used a differential open chromatin approach, coupled with active enhancer mark, transcriptomic, and computational TFs binding analysis to map cell-type-specific active enhancers in cardiac fibroblasts and cardiomyocytes, and outline the TFs families that control them. This approach was validated by its ability to uncover the known cardiomyocyte TF biology in an unbiased manner, and was then applied to cardiac fibroblasts. We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general "billboard" model for enhancer organization.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:Publisher

  7 / 2606 MEDLINE  
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[PMID]: 29254288
[Au] Autor:Dyszkiewicz-Konwinska M; Bryja A; Jopek K; Budna J; Khozmi R; Jeseta M; Bukowska D; Antosik P; Bruska M; Nowicki M; Zabel M; Kempisty B
[Ad] Address:Department of Biomaterials and Experimental Dentistry, Poznan University of Medical Sciences, Poznan, Poland.
[Ti] Title:Expression of genes responsible for cell morphogenesis involved in differentiation in porcine buccal pouch mucosal cells during long-term primary culture and real-time proliferation in vitro.
[So] Source:J Biol Regul Homeost Agents;31(4):855-864, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:Recently, using experimental animal model, we demonstrated that porcine buccal pouch mucosal cells reflect increased proliferation capability during primary cultivation in vitro. Although the histological structure and morphogenesis in oral cavity is well recognized, the molecular mechanisms which regulate this process still need further investigation. This study was aimed to analyze the molecular marker expression profile involved in morphogenesis and differentiation capacity of porcine buccal pouch mucosal cells during their long-term primary cultivation in vitro. The experiment was performed on buccal pouch mucosal cells isolated from 80 pubertal crossbred Landrace gilts. After collection, the cells were treated enzymatically and transferred into a primary in vitro culture (IVC) system and cultured for 30 days. The cells were collected for RNA isolation after 7, 15 and 30 days of IVC and were checked for their real-time proliferative status using the RTCA system. We found an increased expression of FN1 and SOX9 genes when calculated against ACTB after 7, and 30 days of IVC, (P less than 0.01, P less than 0.001, respectively). The CXCL12 mRNA was down-regulated after 7, 15 and 30 days of IVC, but not statistically significant. Similar expression profile was observed when calculated against HPRT, however, DAB2 was found to be higher expressed at day 15 of IVC, (P less than 0.05). The cell index measured during real-time cell proliferation was substantially increased between 96 h and 147h of IVC and reached the log phase. Since FN1 and SOX9 revealed significant increase of expression after long-term culture in vitro, it is suggested that expression of these differentiation and stemness genes is accompanied by cell proliferation. Moreover, FN1 and SOX9 might be recognized as new markers of buccal pouch mucosal cell proliferation and differentiation in pigs in in vitro primary culture model.
[Mh] MeSH terms primary: Epithelial Cells/metabolism
Gene Expression Regulation, Developmental
Lipocalin-2/genetics
Morphogenesis/genetics
Mouth Mucosa/metabolism
SOX9 Transcription Factor/genetics
[Mh] MeSH terms secundary: Animals
Cell Differentiation
Cell Proliferation
Chemokine CXCL12/genetics
Chemokine CXCL12/metabolism
Epithelial Cells/cytology
Female
Gene Expression Profiling
Hypoxanthine Phosphoribosyltransferase/genetics
Hypoxanthine Phosphoribosyltransferase/metabolism
Lipocalin-2/metabolism
Mouth Mucosa/cytology
Mouth Mucosa/growth & development
Primary Cell Culture
RNA, Messenger/genetics
RNA, Messenger/metabolism
SOX9 Transcription Factor/metabolism
Signal Transduction
Swine
Tumor Suppressor Proteins/genetics
Tumor Suppressor Proteins/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Chemokine CXCL12); 0 (Lipocalin-2); 0 (RNA, Messenger); 0 (SOX9 Transcription Factor); 0 (Tumor Suppressor Proteins); EC 2.4.2.8 (Hypoxanthine Phosphoribosyltransferase)
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:IM
[Da] Date of entry for processing:171220
[St] Status:MEDLINE

  8 / 2606 MEDLINE  
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[PMID]: 29187585
[Au] Autor:Xu J; Lv S; Hou Y; Xu K; Sun D; Zheng Y; Zhang Z; Li X; Li Y; Chi G
[Ad] Address:The Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun 130000, People's Republic of China.
[Ti] Title: promotes type II collagen expression by targetting peroxisome proliferator-activated receptor-γ2 during rat articular chondrocyte differentiation.
[So] Source:Biosci Rep;38(1), 2018 02 28.
[Is] ISSN:1573-4935
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:MicroRNAs (miRNAs) play an essential role in articular cartilage development and growth. However, the exact mechanisms involved in this process remain unknown. In the present study, we investigated the biological functions of during hypertrophic differentiation of rat articular chondrocytes. Based on hybridization and immunohistochemistry, we report that expression is reduced in the hypertrophic zone of articular cartilage, but expression of peroxisome proliferator-activated receptor γ (Pparγ) is increased. Dual-luciferase reporter gene assay and Western blot analysis demonstrated that Pparγ2 is a target of Overexpression of inhibited expression of Pparγ2, as well as type X collagen (Col10a1) and matrix metalloproteinase 13 (Mmp13), while significantly promoting the expression of Sex-determining Region-box 9 (Sox9) and type II collagen (Col2a1) at both the mRNA and protein levels. Rosiglitazone, a Pparγ agonist, suppressed Col2a1 expression, while promoting expression of runt-related transcription factor 2 (Runx2) and Col10a1 in a concentration-dependent manner. siRNA-mediated knockdown of Pparγ2 caused an increase in protein levels of Col2a1. The present study demonstrates that regulates chondrocyte hypertrophy in part by targetting Pparγ2, and that may have important therapeutic implications in cartilage diseases.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1712
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Process

  9 / 2606 MEDLINE  
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[PMID]: 28935584
[Au] Autor:Liu C; Jia X; Zou Z; Wang X; Wang Y; Zhang Z
[Ad] Address:Key Laboratory of Healthy Mariculture for the East China Sea, Ministry of Agriculture, Fisheries College, Jimei University, Xiamen 361021, China.
[Ti] Title:VIH from the mud crab is specifically expressed in the eyestalk and potentially regulated by transactivator of Sox9/Oct4/Oct1.
[So] Source:Gen Comp Endocrinol;255:1-11, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Vitellogenesis-inhibiting hormone (VIH) is known to regulate ovarian maturation by suppressing the synthesis of vitellogenin (Vtg) in crustaceans, which belongs to a member of crustacean hyperglycemic hormone (CHH) family synthesized and secreted from the X-organ/sinus gland complex of eyestalks. In this study, the cDNA, genomic DNA (gDNA) and the 5'-upstream regulatory (promoter region) sequences of VIH gene were obtained by conventional PCR, genome walker and tail-PCR techniques according to our transcriptomic database of Scylla paramamosain. The full-length cDNA of SpVIH is 634bp including 105bp 5'UTR, 151bp 3'UTR and 378bp ORF that encodes a peptide of 125 amino acids. The full length gDNA of SpVIH is 790bp containing two exons and one intron. The 5'-flanking promoter regions of SpVIH we isolated are 3070bp from the translation initiation (ATG) and 2398bp from the predicted transcription initiation (A), which consists of putative core promoter region and multiple potential transcription factor binding sites. SpVIH was only expressed in eyestalk. The expression level of SpVIH in eyestalk of female crab decreased gradually along with the development of ovary. As there is not cell line of crabs available, we chose the mature transfection system HEK293FT cell lines to explore the mechanism of transcription regulation of SpVIH in crabs. Sequential deletion assays using luciferase reporter gene in HEK293FT cells revealed that the possible promoter activity regions (including positive and negative transcription factors binding sites simultaneously) presented between pSpVIH-4 and pSpVIH-6. In order to further identify the crucial transcription factors binding site in this region, the site-directed mutagenesis of Sox9/Oct4/Oct1 binding site of pSpVIH-4 was created. The results demonstrated that the transcriptional activity of pSpVIH-4â–³ decreased significantly (p<0.05). Thus, it is reasonable to deduce that the Sox9/Oct4/Oct1 may be the essential positive transcription factors which regulate the expression of SpVIH.
[Mh] MeSH terms primary: Brachyura/metabolism
Carrier Proteins/metabolism
Eye/metabolism
Invertebrate Hormones/metabolism
Octamer Transcription Factor-1/metabolism
Octamer Transcription Factor-3/metabolism
SOX9 Transcription Factor/metabolism
Trans-Activators/metabolism
[Mh] MeSH terms secundary: 5' Flanking Region/genetics
Amino Acid Sequence
Animals
Base Sequence
Carrier Proteins/chemistry
Carrier Proteins/genetics
DNA, Complementary/genetics
Female
Gene Expression Regulation, Developmental
HEK293 Cells
Humans
Invertebrate Hormones/chemistry
Invertebrate Hormones/genetics
Mutation/genetics
Ovary/embryology
Ovary/metabolism
Phylogeny
Promoter Regions, Genetic/genetics
Sequence Analysis, DNA
Transgenes
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Carrier Proteins); 0 (DNA, Complementary); 0 (Invertebrate Hormones); 0 (Octamer Transcription Factor-1); 0 (Octamer Transcription Factor-3); 0 (SOX9 Transcription Factor); 0 (Trans-Activators); 138360-48-2 (vitellogenesis inhibiting hormone)
[Em] Entry month:1802
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[Js] Journal subset:IM
[Da] Date of entry for processing:170923
[St] Status:MEDLINE

  10 / 2606 MEDLINE  
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[PMID]: 29343853
[Au] Autor:Li IMH; Liu K; Neal A; Clegg PD; De Val S; Bou-Gharios G
[Ad] Address:Institute of Ageing and Chronic Disease, University of Liverpool, William Henry Duncan Building, Liverpool, L7 8TX, UK.
[Ti] Title:Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements.
[So] Source:Sci Rep;8(1):950, 2018 Jan 17.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The transcriptional mechanism through which chondrocytes control the spatial and temporal composition of the cartilage tissue has remained largely elusive. The central aim of this study was to identify whether transcriptional enhancers played a role in the organisation of the chondrocytes in cartilaginous tissue. We focused on the Aggrecan gene (Acan) as it is essential for the normal structure and function of cartilage and it is expressed developmentally in different stages of chondrocyte maturation. Using transgenic reporter studies in mice we identified four elements, two of which showed individual chondrocyte developmental stage specificity. In particular, one enhancer (-80) distinguishes itself from the others by being predominantly active in adult cartilage. Furthermore, the -62 element uniquely drove reporter activity in early chondrocytes. The remaining chondrocyte specific enhancers, +28 and -30, showed no preference to chondrocyte type. The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (-30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity. Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180210
[Lr] Last revision date:180210
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-19186-4


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