Дисертації: "Cartilage cells"

1

Cook, James L. "Three-dimensional chondrocyte culture : in vitro and in vivo applications /." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9924877.

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2

Srinivasan, Jayendran. "Investigation of internal fluid pressure in cells." Morgantown, W. Va. : [West Virginia University Libraries], 2005. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4177.

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Thesis (M.S.)--West Virginia University, 2005.
Title from document title page. Document formatted into pages; contains x, 114 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 69-77).

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3

Mouw, Janna Kay. "Mechanoregulation of chondrocytes and chondroprogenitors the role of TGF-BETA and SMAD signaling /." Diss., Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-11232005-103041/.

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Thesis (Ph. D.)--Bioengineering, Georgia Institute of Technology, 2006.
Harish Radhakrishna, Committee Member ; Christopher Jacobs, Committee Member ; Andres Garcia, Committee Member ; Marc E. Levenston, Committee Chair ; Barbara Boyan, Committee Member.

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4

Yang, Ziquan. "Repair of cartilage injury using gene modified stem cells and acellular cartilage matrix." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501585.

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5

Bishop, Joanna Charlotte. "Biology of the articular cartilage progenitor cells." Thesis, Cardiff University, 2004. http://orca.cf.ac.uk/55374/.

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6

Brodkin, Kathryn Rhea. "Chondrocyte behavior in monolayer culture : the effects of protein substrates and culture media." Thesis, Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/20216.

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7

Tsang, Kwok-yeung. "Molecular pathogenesis of abnormal chondrocyte differentiation in a transgenic mouse model /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B35132796.

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8

Togo, Takeshi. "Identification of cartilage progenitor cells in the adult ear perichondrium : utilization for cartilage reconstruction." Kyoto University, 2008. http://hdl.handle.net/2433/135826.

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9

Kraft, Jeffrey J. "Developing a cartilage tissue equivalent using chondrocytes and mesenchymal stem cells." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 90 p, 2007. http://proquest.umi.com/pqdweb?did=1397900431&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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10

Clements, Kristen Mary. "Mechanical disruption of articular cartilage cells and matrix." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340082.

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11

Marcus, Paula Louise. "Plasticity and interactions of articular cartilage progenitor cells." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/54742/.

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Articular cartilage is an avascular and aneural tissue and this is, in part, attributable to its low intrinsic capacity for repair after injury. Research is now focusing on alternate cell sources for tissue engineering of damaged cartilage, and recently a population of progenitor cells has been identified within the surface zone of bovine articular cartilage. These cells are capable of differentiating along a variety of mesenchymal lineages and are thought to be required for the appositional growth of the cartilage. The aims of this thesis were to further characterise these cells and determine factors affecting their differentiation. Prolonged growth of the clonal cells in culture was found to alter the ability of the cells to differentiate into a hyaline-like tissue, although these changes didn't always result in a decrease in the chondrogenic capacity. The rate of cell growth was also found to slightly affect the ability of the cells to differentiate, with more rapidly growing cells producing a matrix high in glycosaminoglycans. After short term culture, the cells also altered their expression of three different glycosaminoglycans sulphate epitopes 3B3(-), 4C3 and 7D4. When injected intramuscularly, the chondroprogenitor cells failed to form cartilage pellets despite expressing cartilage related genes. The progenitor cells also appeared unable to functionally engraft into the surrounding tissue, although one clonal cell line expressed the endothelial marker PECAM-1. Within this study we also assessed the ability of the chondroprogenitor cells to express connexins, and form functional gap junctions. The cells were found to fluctuate their connexin expression, although they maintained Cx43 expression throughout culture. Using a novel ultrasound standing wave trap, it was found that the cells failed to upregulate connexin after cell contact resulting in non-functional junctions, whilst the cells were able to form functional gap junctions with terminally differentiated chondrocytes. Treating the clonal cells with growth factors to enhance chondrogenesis also failed to cause the cells to functionally communicate. Finally we looked at the cellular organisation of the tissue to determine if paired cells within the surface zone of the cartilage may contain a progenitor population. These paired cells labelled positively for Notch-1, which is known to affect the clonality of the progenitor cells and could possibly signify the presence of the progenitor cell population. Cellular interactions are vital for controlling and coordinating cell differentiation, and manipulating cellular interactions could be an excellent way to enhance the chondrogenic differentiation of the cells and possibly improve tissue integration.

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12

Zhang, Shang. "Mesenchymal stem cells, cartilage regeneration and immune privilege." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633157.

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Many studies have shown that mesenchymal stem cells (MSCs) can be used as immunosuppressants to treat graft-versus-host disease (GVHO) and autoimmune diseases. The injection of MSCs prolonged allogeneic solid organ transplantation in animal models. The current project aimed to investigate whether tissue-engineered cartilage derived from MSCs could be transplanted allogeneically. We mainly looked at murine MSCs (mMSCs) in this project. mMSCs are more difficult to isolate than human MSCs. We tried several methods to isolate mMSCs and found that a FACS isolated subpopulation of mMSCs, i.e. PaS cells (POGFRa+, Sca-1 +), had clear chondrogenic differentiation potential. The mechanisms involved in the immunosuppressive effect of MSCs are still under debate. Our in vitro data showed that the immunosuppressive effect of MSCs is through a negativefeedback loop. Pro-inflammatory cytokines from proliferating Iymphocytes activate MSCs to produce immunosuppressive molecules that suppress the proliferation of Iymphocytes. This immunosuppressive effect is shared with other stromal cells. A species difference exists in terms of the immunosuppressive effect of MSCs.

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13

Ayyalasomayajula, Madhavi V. S. "Influence of rearrangement of actin cytoskeleton on the overall material properties of ATDC5 cells during chondrogenesis." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3580.

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Thesis (M.S.)--West Virginia University, 2004.
Title from document title page. Document formatted into pages; contains xi, 97 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 68-70).

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14

Yoshimatsu, Masayoshi. "In vivo regeneration of rat laryngeal cartilage with mesenchymal stem cells derived from human induced pluripotent stem cells via neural crest cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/265189.

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京都大学
新制・課程博士
博士(医学)
甲第23417号
医博第4762号
新制||医||1052(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授松田秀一特定拠点, 教授妻木範行, 教授安達泰治
学位規則第4条第1項該当
Doctor of Medical Science
Kyoto University
DFAM

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15

Fellows, Christopher R. "Analyses of articular cartilage-derived stem cells : identification of cellular markers for stem cells within the healthy and osteoarthritic knee articular cartilage." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/70446/.

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Previous studies have identified stem cell populations in articular cartilage using colony forming assays and mesenchymal stem cell (MSC) marker expression. The specificity of classical MSC markers for isolation of stem cells within articular cartilage is insufficient, with large and highly variable quantities being reported in the literature. This study has demonstrated, for the first time, a panel of stem cell markers specific for articular cartilage-derived stem cells (ACSC). ACSCs were isolated, quantified and cultured from healthy and OA joints. Stem cells were clonally-derived cell lines that proliferated beyond 50 population doublings whilst maintaining a phenotype, and demonstrated tri-lineage potential. We discovered that OA cartilage had a two-fold increase in stem cell number, consisting of two divergent stem cell sub-populations. These divergent populations varied in proliferative capacity with only 50% of stem cells from the OA joint capable of extended proliferation in vitro. Using transcriptomic next generation sequencing of culture-expanded chondrocytes and ACSCs we successfully identified differentially expressed genes and a panel of novel markers of cartilage-specific stem cells. Novel markers were validated using qPCR and protein labelling and, were specifically expressed in ACSCs, with no expression in the culture-expanded full-depth chondrocytes. Using immunofluorescence for novel stem cell markers we found articular cartilage-derived stem cells are localised within the transitional zone in normal cartilage and the superficial zone in OA cartilage. OA cartilage was found to contain a 2-fold increase in stem cells using immunofluorescence. Subsequently, we used the panel of novel markers and fluorescent active cell sorting to isolate a sub-population from full-depth cartilage with stem cell characteristics. These cells were plastic adherent, clonogenic, with proliferative capacity greater than 50PD and displayed tri-lineage potential, therefore meeting all criteria for classification as a MSC population. The use of specific markers to isolate ACSCs will allow for further characterisation of stem cells, including a more in-depth understanding of the mechanisms of proliferation, differentiation and degeneration within articular cartilage.

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16

Stoker, Aaron. "Evaluation of the metabolic responses of normal and osteoarthritic cartilage in vitro and in vivo /." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3144460.

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17

Yu, Yin. "Identification and characterization of cartilage progenitor cells by single cell sorting and cloning." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/3414.

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Cartilage lesion is a fairly common problem in orthopaedic practise. It is often a consequence of traumas, inflammatory conditions, and biomechanics alterations. However, as an avascular and aneural tissue, articular cartilage has minimal healing ability. Over the past decades, surgeons and scientists have proposed a nubmer of treatment strategies to promote restoration of articular cartilage, like arthroscopic lavage, microfracture surgery, osteochoncral autografts and allografts, autologous chondrocyte implantation, and other cell-based repairs. Nevertheless, these solutions often result in fibrocartilage, which has inferior mechanical and biochemical properties, with increased susceptibility to injury, which usually ultimately leads to osteoarthritis (OA). Stem cell therapy techniques are widely applied in treating disease or injury. Many medical researchers have proposed stem cell transplantation treatment for enhancing cartilage repair by using mesenchymal stem cells (MSCs) along with biocompatible scaffolds. In addition to that, chondrogenic progenitor cells (CPCs) have also been discovered in OA patients and healthy articular cartilage. However, neither the method for isolating CPCs is not well established, nor the origin and function is not fully understood. Stem cells may be measured in CFUs (Colony-forming units). Ideally, adult stem cells should be clonogenic. In other words, a single adult stem cell should be able to generate a line of genetically identical cells. Fully characteraization of stem/progenitor cell potential requires purified population. Single-cell cloned population maybe serve as a convincing source for study of stem/progenitor cells. Therefore, a single cell clonogenecity screening system was developed to identify and isolate putative stem/progenitor cells from cartilage based on fluorescence-activated cell sorting (FACS). Also, genetical and functional characterization of isolated cells was taken.

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18

Tan, Zhijia, and 谭志佳. "Molecular analyses of chondrocyte differentiation and adaptation to ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209435.

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Endochondral bone development depends on the progression of chondrocyte proliferation, hypertrophy and terminal differentiation, which requires precise transcriptional regulation and signaling coordination. Disturbance of this process would disrupt chondrocyte differentiation and lead to chondrodysplasias. In cells, a highly conserved mechanism, ER stress signaling, has been developed to sense the protein load and maintain the cellular homeostasis. In humans, mutations in COL10A1 induce ER stress and result in metaphyseal chondrodysplasia type Schmid (MCDS). Previous analysis of a MCDS mouse model (13deltg mouse) had revealed a novel mechanism of chondrocyte adaptation to ER stress. The hypertrophic chondrocytes survive ER stress by reverting to a pre-hypertrophic like state (Tsang et al., 2007). To dissect the underlying mechanisms that coordinate chondrocyte survival, reverted differentiation and adaptation to ER stress, different chondrocyte populations in the wild type and 13del growth plates were fractionated for global gene expression analyses. The genome-wide expression profiles of proliferating chondrocytes, prehypertrophic chondrocytes, hypertrophic chondrocytes and terminally differentiated chondrocytes in the wild type growth plate provide molecular bases to understand the processes underlying both physiological and pathological bone growth. Systematic analyses of these transcriptomic data revealed the gene expression patterns and correlation in the dynamics of endochondral ossification. Genes associated with sterol metabolism and cholesterol biosynthesis are enriched in the prehypertrophic chondrocytes. Selected genes (Wwp2, Zbtb20, Ppa1 and Ptgis) that may potentially contribute to endochondral ossification were identified differentially expressed in the growth plate. Bioinformatics approaches were applied to predict regulatory networks in chondrocytes at different differentiation stages, implying the essential and dominant roles of Sox9 in coordination of stage specific gene expression. We further confirmed that Sox9 directly regulates the transcription of Cyr61, Lmo4, Ppa1, Ptch1 and Trps1, suggesting that Sox9 integrates different steps of chondrocyte differentiation via regulation of its target genes and partially crosstalk with IHH signaling pathway. The information on gene expression and regulation from physiological growth plate provides important basis to understand the molecular defects of chondrodysplasia. The hypertrophic zone in 13del growth plate was fractionated into upper, middle and lower parts for microarray profiling, corresponding for the onset of ER stress, onset of reverted differentiation and adaptation phase. Comparative transcriptomics of wild type and 13del growth plates revealed genes related to glucose, amino acid and lipid metabolisms are up regulated in response to ER stress. Fgf21 was identified as a novel ER stress inducible factor regulated by ATF4. Removal of Fgf21 results in increasing cell apoptosis in 13del hypertrophic zone without affecting the reverted differentiation process. Up regulation of genes expression related to hypoxic stress (Slc2a1, Hyou1, Stc2 and Galectin3) in 13del hypertrophic chondrocytes suggested that survival and adaptation of chondrocytes to ER stress involve cross-regulation by other stress pathways. Our findings have provided a new insight into the mechanisms that facilitate chondrocyte survival under ER stress in vivo, and propose the integrative effects of hypoxic stress pathway during the stress adaptation process, which broaden the molecular horizons underlying chondrodysplasias caused by protein folding mutations.
published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy

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19

Yu, Yin. "Articular cartilage tissue engineering using chondrogenic progenitor cell homing and 3D bioprinting." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/6895.

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Articular cartilage damage associated with joint trauma seldom heals and often leads to osteoarthritis (OA). Current treatment often fails to regenerated functional cartilage close to native tissue. We previously identified a migratory chondrogenic progenitor cell (CPC) population that responded chemotactically to cell death and rapidly repopulated the injured cartilage matrix, which suggested their potential for cartilage repair. To test that potential we filled experimental full thickness chondral defects with an acellular hydrogel containing SDF-1α. We expect that SDF-1α can increase the recruitment of CPCs, and then promote the formation of a functional cartilage matrix with chondrogenic factors. Full-thickness bovine chondral defects were filled with hydrogel comprised of fibrin and hyaluronic acid and containing SDF-1α. Cell migration was monitored, followed by chondrogenic induction. Regenerated tissue was evaluated by histology, immunohistochemistry, and scanning electron microscopy. Push-out tests were performed to assess the strength of integration between regenerated tissue and host cartilage. Significant numbers of progenitor cells were recruited by SDF-1α within 12 days. By 5 weeks chondrogenesis, repair tissue cell morphology, proteoglycan density and surface ultrastructure were similar to native cartilage. SDF-1α treated defects had significantly greater interfacial strength than untreated controls. However, regenerated neocartilage had relatively inferior mechanical properties compared with native cartilage. In addition to that, we developed a 3D bioprinting platform, which can directly print chondrocytes as well as CPCs to fabricated articular cartilage tissue in vitro. We successfully implanted the printed tissue into an osteochondral defect, and observed tissue repair after implantation. The regerated tissue has biochemical and mechanical properties within the physiological range of native articular cartilage. This study showed that, when CPC chemotaxis and chondrogenesis are stimulated sequentially, in situ full thickness cartilage regeneration and bonding of repair tissue to surrounding cartilage could occur without the need for cell transplantation from exogenous sources. This study also demonstrated the potential of using 3D bioprinting to engineer articular cartilage implants for repairing cartilage defect.

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20

Lu, Luhui, and 陆璐慧. "Molecular control of osteo-chondroprogenitors formation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B44673966.

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21

Esa, Adam. "Characterising the role of articular cartilage progenitor cells in osteoarthritis." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/90195/.

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Osteoarthritis (OA) is a chronic and highly prevalent degenerative disease of the synovial joint leading to cartilage destruction and bone remodelling. The current management of end-stage OA is joint replacement, however, this procedure is not suitable for a subset of patients hence there is a growing need for alternative treatments and technologies to address this limitation. One such approach to this problem is the application of cell-based therapies that regenerate areas of damaged cartilage. Recently discovered articular cartilage progenitor cells (CPC) have been hallmarked as a potential cell source for repair and/or regeneration of damaged articular cartilage. Initial focus was on the characterisation of human CPC isolated from healthy donors and compared with OA derived CPC and patient matched OA Bone Marrow Mesenchymal Stem Cells (BM-MSCs). Comparison of all cell types showed similar morphology and proliferative capacity. In addition, all cell types isolated showed positive expression of the putative mesenchymal stem cell makers; CD-90, CD-105 and CD-166 while lacking expression of CD-34. All cell types investigated showed successful osteogenic, chondrogenic and adipogenic differentiation, hence providing evidence of the mesenchymal stem cell properties of isolated CPC. A gene profiler array was used to identify the expression of Wnt pathway genes from RNA isolated from CPC cell lines originating from healthy and OA cartilage. Interestingly, the expression of Dkk-1 was observed to have the highest up-regulation in OA-derived CPC. The role of Dkk-1 was further studied in a number of CPC and chondrocyte cell lines from healthy and OA cartilage. It was found that normal CPC cell lines showed homogenously low expression and secretion of Dkk-1, however, OA-derived CPC cell lines exhibited a heterogeneous expression and secretion of Dkk-1. In a pellet culture model of chondrogenic differentiation, CPC cell lines secreting high levels of Dkk-1 failed to undergo chondrogenic differentiation, measured by diminished expression of chondrogenic differentiation markers, Type II collagen, ACAN and Sox-9 at both molecular and protein levels. Immunolocalisation of Dkk-1 in OA osteochondral plugs showed peri-cellular expression in chondrocytes located in all zones and around migratory endothelial cells invading articular cartilage where there was a quantifiable increase of blood vessel invasion. This later observation was further studied through a series of experiments to investigate the role of Dkk-1 in relation to endothelial cell migration and angiogenesis using an in vitro model of angiogenesis and migration/invasion assays. A novel finding emerged from these studies, which provides evidence for a pro-angiogenic and pro-migratory role of Dkk-1 and to a lesser extent Dkk-2 in human endothelial cell lines. A novel in vitro Transwell co-culture model was developed to study the interaction between chondrocytes and endothelial cells mimicking the osteochondral interface. A novel finding from these studies included the observation that normal or OA-derived chondrocytes appeared to induce an endothelial to mesenchymal transformation (EndMT) of the co-culture endothelial cells. This was assessed by a loss of the endothelial cobble stone morphology and a down-regulation of key factors implicated in endothelial cell phenotype, including VE-cadherin, Tie-2, e-NOS, PDGF-AA and PECAM-1. As endothelial cells lost their phenotype they adopted a spindle morphology and expressed mesenchymal cell markers including: Lumican, Snail, α-SMA, Vimentin and MMPs. Interestingly, this was also associated with an increase in Dkk-1 expression. To confirm a role for Dkk-1 in this process endothelial cells were cultured in the presence of Dkk-1 and were found to undergo EndMT when compared to the control. In summary, this thesis has uncovered several interesting differences in CPC phenotype. In addition, my results suggest that Dkk-1 has potential as a biomarker of OA pathology. This thesis highlights further the complex role of the Wnt Pathway and in particular Dkk-1 may play a role in the pathogenesis of osteoarthritis.

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22

Nelson, Larissa. "Evaluation of the potential for repair of degenerate hyaline cartilage in the osteoarthritic knee by cartilage stem cells." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/42362/.

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Osteoarthritis (OA) is a highly prevalent, debilitating disease affecting many joints including the knee. Despite the involvement of several tissues, it is believed that the articular cartilage is the primary site of pathogenesis in humans. Within this study, a new scoring system of OA was devised, incorporating the articular cartilage and underlying bone, aimed at providing a more comprehensive means of grading the severity of tissue damage. We examined changes progressively from mild to severe and were able to deduce from the scoring system that bone changes may precede those of the overlying cartilage. Immunohistochemistry was used to assess stem cell marker expression, proliferation and progressive changes within the extracellular matrix of sectioned osteochondral plugs, however no distinct pattern of change could be extrapolated, highlighting the variable nature of this taxing disease. Previous studies have demonstrated the presence of a sub-population of chondroprogenitor cells present in normal hyaline cartilage. We demonstrated in this study that a similar group of cells reside in osteoarthritic articular cartilage. We were able to isolate and expand clonally derived primary cell lines to beyond 50 population doublings whilst maintaining a chondrogenic phenotype, and demonstrated the tri-lineage potential of these cells. That said, a significant amount of variation was observed and it was, therefore, postulated that there may be a smaller cohort of viable cells within this sub-population isolated from osteoarthritic cartilage. A preliminary study was also carried out comparing chondroprogenitors from normal articular cartilage to those isolated from OA tissue. Heterogeneity was again encountered, suggesting that there was a group of OA chondroprogenitors with similar characteristics to the normal cells, which differed from the other less metabolically active cells. This finding was agreeable with the aforementioned postulation. Data from our preliminary integration study was promising as we demonstrated the potential for using these chondroprogenitor cells in combination with other cells whilst achieving successful integration. However, further work is necessary to distinguish between the cell lines with the potential for integration from those that lacked this ability, thereby eliminating the heterogeneity. The presence of viable chondroprogenitor cells in OA tissue challenges the dogma that the tissue is irrecoverable, and opens the scope for regenerative medicine using resident progenitor cells. This is an exciting prospect that could significantly contribute to articular cartilage repair.

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23

Tsang, Kwok-yeung, and 曾國揚. "Molecular pathogenesis of abnormal chondrocyte differentiation in a transgenic mouse model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B4501551X.

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24

Ahmed, Yasser Abdel Galil. "Analysis of physiological death in equine chondrocytes /." Connect to thesis, 2007. http://eprints.unimelb.edu.au/archive/00003656.

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25

Yang, Liu, and 楊柳. "Genetic analyses of terminal differentiation of hypertrophic chondrocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hdl.handle.net/10722/210320.

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26

Yang, Liu. "Genetic analyses of terminal differentiation of hypertrophic chondrocytes." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43223758.

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27

衛永剛 and Wing-kong Wai. "Abnormal chondrocyte differentiation: a transgenic model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237800.

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28

Wai, Wing-kong. "Abnormal chondrocyte differentiation : a transgenic model /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19656439.

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29

Music, Ena. "Optimisation of methods for driving Chondrogenesis of human and ovine bone marrow–derived stromal cells." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/207820/1/Ena_Music_Thesis.pdf.

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This thesis investigated the effects of different molecules and oxygen levels on the quality of engineered cartilage tissues produced using both human and sheep bone marrow–derived stromal cells. As damaged cartilage cannot repair naturally, it is hoped that cell-based repair strategies can delay the need for joint replacement surgery due to osteoarthritis, which affects 1 in 10 Australians.

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30

Denison, Tracy Adam. "The effect of fluid shear stress on growth plate." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/29603.

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Thesis (Ph.D)--Biomedical Engineering, Georgia Institute of Technology, 2009.
Committee Chair: Boyan, Barbara; Committee Co-Chair: Schwartz, Zvi; Committee Member: Bonewald, Lynda; Committee Member: Jo, Hanjoong; Committee Member: Sambanis, Athanassios. Part of the SMARTech Electronic Thesis and Dissertation Collection.

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31

Heymer, Andrea. "Chondrogenic differentiation of human mesenchymal stem cells and articular cartilage reconstruction." kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2944/.

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32

Lee, Christopher S. D. "Directing the paracrine actions of adipose stem cells for cartilage regeneration." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/44713.

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Current cartilage repair methods are ineffective in restoring the mechanical and biological functions of native hyaline cartilage. Therefore, using the paracrine actions of stem cell therapies to stimulate endogenous cartilage regeneration has gained momentum. Adipose stem cells (ASCs) are an attractive option for this endeavor because of their accessibility, chondrogenic potential, and secretion of factors that promote connective tissue repair. In order to use the factors secreted by ASCs to stimulate cartilage regeneration, the signaling pathways that affect postnatal cartilage development and morphology need to be understood. Next, approaches need to be developed to tailor the secretory profile of ASCs to promote cartilage regeneration. Finally, delivery methods that localize ASCs within a defect site while facilitating paracrine factor secretion need to be optimized. The overall objective of this thesis was to develop an ASC therapy that could be effectively delivered in cartilage defects and stimulate regeneration via its paracrine actions. The general hypothesis was that the secretory profile of ASCs can be tailored to enhance cartilage regeneration and be effectively delivered to regenerate cartilage in vivo. The overall approach used the growth plate as an initial model to study changes in postnatal cartilage morphology and the molecular mechanisms that regulate it, different media treatments and microencapsulation to tailor growth factor production, and alginate microbeads to deliver ASCs in vivo to repair cartilage focal defects.

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33

Boyer, Sam. "Characterisation of articular cartilage progenitor cells : potential use in tissue engineering." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/56057/.

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Articular cartilage is a resilient and load bearing material that provides diarthrodial joints with excellent friction, lubrication and wear characteristics required for continuous motion. However, articular cartilage has a poor regenerative capacity and its degeneration is a common cause of morbidity in terms of loss of joint function and osteoarthritis, frequently resulting in the need for total knee replacement. Articular cartilage has a distinct zonal architecture with biochemical and cellular variations existing from the surface zone to the deeper calcified layers. Thus, the development of the tissue must be stringently controlled, both spatially and temporally in order for the complex structure to be established. Importantly, the surface zone is believed to be responsible for the appositional growth of articular cartilage during development and this growth is believed to be driven by a population of slow cycling progenitor cells within the surface zone itself. The focus of this thesis is the isolation and characterisation of articular cartilage progenitor cells together with an exploration of the cells capabilities in potential cartilage repair therapies. The cells were identified on the basis of differential adhesion assays and colony forming ability. Subsequent experiments were carried out to show the differential expression of various cell surface markers eg Notch 1 receptors and the role of the onco-foetal form of fibronectin, known as fibronectin-EDA on the modulation of cell behaviour. In terms of the potential of the cells for use in tissue engineering, a promising feature of the cells is the discovery that enriched populations of the cells can undergo extensive expansion in simple monolayer cultures and yet retain their ability to undergo chondrogenic differentiation. This property may enable the use of the cells in commercial cartilage repair and/or tissue engineering strategies.

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34

Ferng, Alice Shirong. "ENGINEERING ARTICULAR CARTILAGE FROM HUMAN AND CANINE NON-EMBRYONIC STEM CELLS." Thesis, The University of Arizona, 2009. http://hdl.handle.net/10150/192338.

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35

Al-Obaidi, Aida Hameed Hassan. "Preclinical studies for cartilage tissue engineering using induced pluripotent stem cells." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.738237.

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36

Streppa, Heather Kirsten. "A novel co-culture model for the study of osteoarthritis in dogs /." free to MU campus, to others for purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p1422968.

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37

Lin, Zhen. "Chondrocyte : a target for the treatment of osteoarthritis." University of Western Australia. Orthopaedics Unit, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0203.

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[Truncated abstract] Osteoarthritis (OA) is the most common form of arthritis, characterized by progressively degeneration of articular cartilage. Chondrocyte is the only cell type in articular cartilage tissue and responsible for cartilage matrix turnover. This thesis focuses on the biological and genetic behaviors of human chondrocyte and potential therapeutic strategies that target on chondrocyte. Chondrocytes have been used for the tissue-engineered cartilage construction, especially in articular cartilage repair. The technique of chondrocyte-base tissue engineering utilizes in vitro propagated chondrocytes combined with several manufactured biomaterials to regenerate cartilage tissue. Although these technologies have been successfully applied in clinic, the biological characteristics of chondrocyte during in vitro propagation and after implantation remain unclear. This thesis reviewed the present studies of chondrocyte biology and its potential uses in tissue engineering. Particularly, chondrocytes have been shown to de-differentiate into fibroblastic-cells when they are exposed to inflammatory conditions or cultured on monolayer in vitro. This thesis investigated the gene expression profile of chondrocytes when they are cultured and serially passaged on monolayer in vitro. Human chondrocytes obtained from OA patients were cultured up to passage 6. Twenty-eight chondrocyte associated genes were measured by Real-time PCR. The results showed that a number of genes were changed in expression levels at various stages of passage as indications of chondrocyte de-differentiation. Chondrocytes derived from OA patients or normal donors exhibited a very similar gene expression pattern. Interestingly, transcription factor Sox-9, which plays a key role in chondrogenesis remained unchanged with increasing passage number, indicating that the de-differentiation process of chondrocyte is reversible. This thesis also focused on the development of novel pharmacological approaches for OA that target on articular chondrocyte. The clinical feature, etiology, pathogenesis, diagnostic approaches, conventional and potential future treatments for OA were briefly reviewed in this thesis. ... The effects of natural compounds on chondrocyte gene expression, proteoglycan degradation and nitric oxide production were measured. The results showed that parthenolide, a NF-kB inhibitor, regulated chondrocyte function by suppressing the up-regulation of gene expression of inflammatory factors and matrix proteinases induced by lipopolysaccharide, and down-regulating COX-2 expression. Parthenolide was able to reduce proteoglycan degradation in human chondrocytes, but had no effect on nitric oxide production. These results suggest that parthenolide mediates inflammatory-activated NF-kB pathway, and subsequently reduces inflammatory response, prevents cartilage destruction and relieves pain, and hence may be useful for OA treatment.

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38

Fabre, Hugo. "Cartilage Tissue Engineering Using Mesenchymal Stem Cells : development of a screening method by flow cytometry to characterize diverse sources of human mesenchymal stem cells and to evaluate the quality of their chondrogenic conversion." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10186.

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Articular cartilage is made up of dense, connective tissue localized at the junction of several locations in the skeleton. It covers the surface of the joints to ensure that bones can move. It is an avascular tissue that is not innervated and is composed primarily of a single cell type, the chondrocyte, which synthesizes an abundant extracellular matrix (ECM). Osteoarthritis (OA), a degenerative disease of articular cartilage, is characterized by the degradation of the ECM, associated with increased secretion of matrix metalloproteinases (MMPs) and aggrecanases. In addition, the OA process induces chondrocyte dedifferentiation characterized at least in part by increased synthesis of type I collagen, an atypical isoform in articular cartilage. Moreover, due to the poor intrinsic healing capacity of articular cartilage, there is currently no treatment to restore the chondrocyte phenotype and, in the most advanced stages of OA, the joint must be replaced with a prosthesis, requiring surgery. Therefore, various drug and surgical treatments have been developed in an attempt to prevent the destruction of cartilage which, in light of their relative success, then lead to new, improved therapeutic strategies. One of the most promising approaches is the cartilage tissue engineering based on the procedure described by Brittberg using autologous chondrocyte implantation (ACI). Applied in the earliest stages of OA or chondral lesions, ACI is based on the use of chondrocytes from a healthy, non-bearing region of the diseased joint. The cells are then amplified in monolayer culture and then re-implanted in the lesion. However, amplification of autologous chondrocytes in two-dimensional culture mimics, at least in part, some of the characteristics of the OA process and is accompanied by cell dedifferentiation leading to the formation of nonfunctional fibrocartilage. The numerous pharmaceutical approaches and surgical techniques developed to repair cartilage lesions have revealed their limitations. Ideally, traumatic cartilage lesions should be treated earlier to prevent OA and postpone prosthetic surgery. In the interest of preventing OA, cartilage cell therapy has proven to be a pivotal approach for repairing damaged tissue. Cell therapy consists not only in filling the cartilage lesion with healthy chondrocytes, but also in reconstituting the structure, the physico-chemical properties and the functionality of the hyaline matrix. The transplantation of autologous chondrocytes is the foundation of cell therapy and cartilage tissue engineering and there have been several generations of ACI, each improving on the previous one. However, even the most recent ACI techniques are showing limitations and consequently, research efforts are now focused on improving this technique in order to obtain, after amplification, a differentiated and stable chondrocyte phenotype. This is to be achieved by using new types of biomaterials that can fill more important lesions, molecules and growth factors to better control the chondrogenic differentiation and more suitable cell sources that avoid morbidity at the donor site as it is the case with articular chondrocytes. Today, MSCs hold much promise for biomedical research because they are able to recapitulate many tissues, including cartilage. However, for future advances in the field of regeneration and tissue engineering it is important to know the exact nature of these cells. With this goal, in this work, we first fully characterized 4 categories of serum free amplified mesenchymal stem cells extracted from adipose tissue (AT), bone marrow (BM), dental pulp (DP) and Wharton’s jelly (WJ) of the umbilical cord. The cells were characterized in terms of efficiency of isolation, amplification kinetics and according to an extensive immunophenotyping using flow cytometry... [etc]

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Nettles, Dana Lynn. "Evaluation of chitosan as a cell scaffolding material for cartilage tissue engineering." Master's thesis, Mississippi State : Mississippi State University, 2001. http://library.msstate.edu/etd/show.asp?etd=etd-10262001-114635.

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40

Nasu, Akira. "Genetically Matched Human iPS Cells Reveal that Propensity for Cartilage and Bone Differentiation Differs with Clones, not Cell Type of Origin." Kyoto University, 2014. http://hdl.handle.net/2433/189661.

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41

Viswanathan, Sundar. "Finite element analysis of interaction between actin cytoskeleton and intracellular fluid in prechondrocytes and chondrocytes subjected to compressive loading." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3664.

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Thesis (M.S.)--West Virginia University, 2004.
Title from document title page. Document formatted into pages; contains ix, 138 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 93-94).

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Leung, Y. L., and 梁宇亮. "Transcriptional regulators of col10al in chondrocyte differentiation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31244440.

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43

Chen, Xike. "Integration Capacity of Human Induced Pluripotent Stem Cell-Derived Cartilage." Kyoto University, 2019. http://hdl.handle.net/2433/242390.

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Yagi, Rieko. "Bcl-2 Regulates Chondrocyte Phenotype Through MEK-ERK1/2 Pathway; Relevance to Osteoarthritis and Cartilage Biology." [Kent, Ohio] : Kent State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1118329494.

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Thesis (Ph.D.)--Kent State University, 2005.
Title from PDF t.p. (viewed Sept. 5, 2006). Advisor: Walter E. Horton. Keywords: chondrocytes; osteoarthritis; Sox9; Bcl-2; MEK-ERK 1/2. Includes bibliographical references (p. 91-106).

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45

Vail, Daniel Joseph. "Mapping the Way Toward an Engineered Articular Cartilage:A Complete Transcriptional Characterization of Native and MSC-Derived Cartilage." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case162644731682198.

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46

Ahmed, Saima. "Repairing injured articular cartilage : investigation of potential mechanisms using mesenchymal stem cells." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/17872/.

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47

Leung, Ching-man, and 梁靜雯. "Effects of Ext1 and Ext2 mutations in a chondrocyte cell line on heparan sulfate synthesis and in vitro chondrogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31227569.

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48

Loke, Chee Wui. "Finite element modeling of cells in response to loading effect of cytoskeleton /." Morgantown, W. Va. : [West Virginia University Libraries], 2005. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=4036.

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Thesis (M.S.)--West Virginia University, 2005.
Title from document title page. Document formatted into pages; contains xi, 86 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 59-62).

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49

Mazor, Marija. "Changes in chondrogenic progenitor populations associated with osteoarthritis grades." Thesis, Orléans, 2016. http://www.theses.fr/2016ORLE2084.

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L'arthrose (OA) est une maladie dégénérative avec un impact remarquable sur la qualité de vie. Pourtant, aucune intervention pharmacologique entièrement appropriée, aucune thérapie biologique ou procédure n'entraînent la dégradation progressive de l'articulation OA. Ici, nous explorons les cellules souches mésenchymateuses (MSC) - précurseurs multi-potentiels de cellules qui peuvent être isolées à partir de différents niveaux de dégradation du cartilage. Nous émettons l'hypothèse que les cellules progénitrices mésenchymateuses (CPM) pourraient servir comme une thérapie potentielle. Le cartilage ostéoarthritique humain a été obtenu de 25 patients subissant un remplacement total du genou et classé en différents niveaux de dégradation. Les niveaux d'expression de l'ARNm de CD105, CD166, Notch 1, Sox9, Acan, Col II A1 et Col I A1 ont été mesurés au jour 0, au jour 14 (2 semaines in vitro) et au jour 35 (après chondrogénèse). Les cellules de toutes les classes d'OA ont augmenté de façon significative les marqueurs MPC de l'ARNm avec expression in vitro. Les cellules proliférées ont exprimées des marqueurs spécifiques aux MPC: CD105, CD166, CD73, CD90, Notch – 1 and Nucleostemin. La chondrogénèse induit une diminution de l'ARNm de CD105, de Notch 1 et de Sox9 seulement dans l'OA légère et modérée. Cependant, seules les pastilles modérées dérivées d 'OA ont révélé des signes de cartilage hyaline élevé - collagène II et faible expression de fibrocartilage - collagène I à la fois au niveau de l’ARNm et de la protéine. Une nouvelle conclusion émerge de nos données et confirme les différences dans les marqueurs MPC entre les différents niveaux de dégradation. Seules les cellules dérivées d 'OA modérées ont été capables de former une matrice hyaline composée de protéoglycanes et de collagène II avec le niveau faible en collagène I fibrocartilagineux. Nos résultats montrent que les CPM provenant d’un cartilage d’un niveau de dégradation modéré ont un fort potentiel d'auto-réparation
Osteoarthritis (OA) is a degenerative disease with a remarkable impact on quality of life. Yet no fully appropriate pharmacological intervention, biologic therapy or procedure stops the progressive degradation of the OA joint. Herein, we explore mesenchymal stem cells (MSCs)—multipotent precursors of cells that can be isolated from different grades of OA cartilage. We hypothesize that mesenchymal progenitors cells (MPC), could emerge as a potential therapy. Human osteoarthritic cartilage were obtained and scored (according to the OARSI) from 25 patients undergoing total knee replacement. mRNA expression levels of CD105, CD166, Notch 1, Sox9, Acan, Col II A1 and Col I A1 were measured at day 0, day 14 (2 weeks in vitro) and day 35 (after chondrogenesis). Cells from all OA grades significantly increased MPC markers mRNA with in vitro expression. Proliferated cells expressed MPC specific antigens: CD105, CD166, CD73, CD90, Notch – 1 and Nucleostemin. The chondrogenesis induced decrease in CD105, Notch 1 and Sox9 mRNA only in mild and moderate OA. Yet, only moderate OA – derived pellets revealed high hyaline cartilage marker – collagen II and low fibrocartilage marker – Collagen I expression at both mRNA and protein level. A novel finding emerges from our data and confirms differences in MPC markers between OA grades. Only moderate – OA derived cells were able to form hyaline – like matrix composed of proteoglycans and collagen II with law level of fibrocartilaginous collagen I. Further studies that investigate the mechanistic effects of chondrogenic progenitor populations associated with aging and the progression of OA are crucial to our understanding of the clinical relevance of these cells for use in cartilage repair therapies

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Huang, Zhao [Verfasser]. "In vitro differentiation of chondrogenic cells in three-dimensional scaffold-assisted culture for cartilage repair and characterization of cartilage sources / Zhao Huang." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1127045490/34.

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