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1
Drag, Melvyn I. « Epithelium : The lightweight, customizable epithelial tissue simulator ». The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1430011382.
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Rowley, Jessica. « The interaction of Aspergillus fumigatus with the respiratory epithelium ». Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/the-interaction-of-aspergillus-fumigatus-with-the-respiratory-epithelium(0fc10449-977d-4f14-a169-172e8204fee4).html.
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Aspergillus fumigatus is a filamentous fungus and the main pathogen responsible for the often fatal respiratory condition, aspergillosis. Airway epithelial cells (AECs) are likely to be the first line of host defence that come into contact with the inhaled conidia of A. fumigatus. Recent evidence strongly suggests that the response of the airway epithelium to inhaled pathogens is pivotal in orchestrating immune responses by inducing phagocytic-like reactions and the secretion of inflammatory cytokines and antimicrobial peptides. However, the majority of previous work investigating A. fumigatus-host interactions has been performed using macrophages and neutrophils, thereby neglecting the epithelium. AECs have been shown to secrete inflammatory cytokines in response to A. fumigatus although these studies predominantly used transformed AEC lines that lack tight junctions and do not fully differentiate. Furthermore, most studies used culture filtrate or extract of A. fumigatus rather than live, whole organism and as a result, the direct interaction of the germinating fungus and the airway epithelium has been overlooked. During the early germination and growth period, the cell wall composition of A. fumigatus is dynamic, with various antigens exposed at different morphological stages. The aim of this thesis was to determine whether AECsare able to alter the germination and growth rate of A. fumigatus, and, conversely, if A. fumigatus affects AECs in terms of the secretion of inflammatory mediators. These studies used live, germinating A. fumigatus, and human primary differentiated AECs to obtain a more realistic in vitro model than those used in previous studies. Data showed that AECs are able to significantly inhibit the germination and growth of A. fumigatus, although this effect was less pronounced in differentiated primary AEC than in transformed AEC lines. A. fumigatus also significantly inducedthe expression and secretion of the inflammatory cytokines, IL-6 and IL-8, probably via the interaction of fungal cell wall β-glucans, and as of yet unidentified AEC receptor. The A1160pyrG+ strain of A. fumigatus secreted factors capable of inducing cytokine secretion whereas Af293 strain did not, highlighting diverse mechanisms of action for different strains. Upregulation of both cytokines was dependent on the stage of A. fumigatus growth with induction synchronous with germination. Despite being associated with fungal sensitisation in asthmatics, AEC-derived cytokines associated with this disease, namely TSLP, IL33 and IL25,did not appear to be upregulated by transformed AECs in response to A. fumigatus. Similarly, A. fumigatus did not seem to induce synthesis and secretion of the acute phase response protein, fibrinogen above baseline levels. The data presented in this thesis confirms the importance of the airway epithelium in directing anti-A. fumigatus immunity and the involvement of complex ligand-receptor interactions.
3
Zhu, Yihong. « Tight junction in ovarian surface epithelium and epithelial ovarian tumors / ». Göteborg : Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska University Hospital, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/3167.
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Tipoe, George Lim. « A histological and ultrastructural morphometric assessment of malignant potential in human colorectal epithelium ». Thesis, [Hong Kong : University of Hong Kong], 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13641347.
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Stevens, Paul. « Intrinsic differences of the airway epithelium in childhood allergic asthma ». University of Western Australia. School of Paediatrics and Child Health, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0022.
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[Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms and the role of respiratory viruses in asthma exacerbations, there is little known regarding the role of the epithelium in commonly observed structural changes in the airway wall. The epithelium of the airways provides an essential protective barrier between the environment and underlying structures and is responsible for the secretion of diverse compounds. Since it is likely that dysregulated epithelial characteristics and function in childhood asthma are critical determinants of disease progression in adults, it is pertinent to investigate the cellular mechanisms involved in paediatric asthma. However, full comprehension of paediatric respiratory diseases and the childhood antecedents of adult respiratory disease are currently hampered by the difficulty in obtaining relevant target organ tissue and most of the data to date have been generated from studies involving adults or commercially derived cell lines. This laboratory has successfully developed methodologies of obtaining and studying samples of paediatric primary airway epithelial cells (pAECs) and has identified significant biochemical and functional differences between healthy non-atopic (pAECHNA) and atopic asthmatic (pAECAA) airway cells, which have assisted in the identification of potential mechanisms responsible for abnormal epithelial function. Stevens 2009 ... Exposure of pAECs with RV resulted in elevated PAI-1 mRNA expression and reduced MMP-9 release in both pAECAA and pAECHNA samples. Collectively, the data presented indicate that RV exposure induces a pronounced antiproliferative and retardative repair effect in pAECAA and that the presence of virus may have a role in the PAI-1 and MMP expression witnessed in these cells. In conclusion, this investigation has further characterised the essential role the airway epithelium plays in childhood asthma by demonstrating for the first time that pAECs from asthmatic children lack the ability to successfully repair mechanically induced wounds. This investigation also showed that PAI-1 is elevated in pAECAA and has a functional role in the pAEC proliferative and regenerative processes. It was demonstrated that MMP-2 and MMP-9 activities and the MMP-9/TIMP-1 as well as MMP2/TIMP2 ratios were significantly reduced in pAECAA thereby providing additional evidence that there is a dysregulation in the mechanisms that monitor the turnover of the ECM in childhood asthma. Furthermore, this study has shown for the first time that pAECs from untreated mild atopic-asthmatic children are more sensitive to the pathogenic effects of RV than healthy control cells and that RV exposure delays cellular proliferation and repair. Ultimately, these findings support the hypothesis postulated and provide evidence that indeed the dysregulated epithelial functional characteristics seen in childhood mild asthma may be a critical determinant of disease progression in adults.
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Hong, Hee Ling. « Regulation of neutral proteinase and plasminogen activator secretion by epithelial cells in vitro ». Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24687.
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The aim of this thesis was to study the regulation of proteinase secretion by epithelial cells (E-cells) derived from the epithelial cell rests of Malassez. Since these epithelial cell rests are present only in small numbers in-vivo, E-cells derived from porcine cell rests were cultured according to Brunette et al. (1976) and conditions chosen so that detectable amounts of the proteinases, neutral proteinase and plasminogen activator, could be obtained. The regulation of the secretion of these enzymes was investigated by varying the cell population density, adding E.Coli lipopolysaccharide to the cultures and altering the shape of the E-cells by both chemical and physical means.
Cell population density modulated both neutral proteinase and plasminogen activator secretion. Neutral proteinase secretion was highest at low cell population densities and the activity decreased with increasing cell population density. Plasminogen activator secretion followed a similar pattern. Escherichia coli lipopolysaccharide (E.coli LPS) stimulated both neutral proteinase and plasminogen activator secretion. LPS extracted by the phenol method and LPS extracted by the trichloroacetic acid method caused similar increases in neutral proteinase activity but the increase in plasminogen activator activity was greater when the trichloroacetic acid extracted LPS was used. These findings support the proposal that bacterial LPS in contact with periapical tissues could stimulate the epithelial cell rests into increased production of proteinases, thereby contributing to the degradation of connective tissue associated with dental cyst formation. E-cell shape was altered by physical and chemical means. Addition of cholera toxin and dibutyryl cAMP caused E-cells to flatten. Phorbol myristate acetate, however, caused the cells to retract slightly. Mechanical stretching was applied to the cells to cause cell flattening, and cell rounding was effected by mechanical relaxation. Another method made use of E-cells grown on a substrate with V-shaped grooves which caused the cells to adopt a rounder shape more frequently than cells grown on a flat substrate. In addition, dishes coated with increasing concentrations of poly(HEMA) solution, which altered dish adhesivity to the cell, caused the cells to become less well-spread. In all experiments, a more flattened cell shape correlated with a reduced level of neutral proteinase and plasminogen activator secretion while a more rounded shape correlated with increased amounts of neutral proteinase and plasminogen activator secretion.Dentistry, Faculty of
Graduate
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FORTNER, CHRISTOPHER NEIL. « EPITHELIUM-DEPENDENT RELAXATION OF AIRWAY SMOOTH MUSCLE IS LINKED TO EPITHELIAL CHLORIDE CURRENTS ». University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin983467525.
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Meredith, David. « Oligopeptide transport in lung epithelium ». Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357416.
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Thomas, Biju. « Ciliated epithelium in respiratory diseases ». Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9568.
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Background: The ciliated respiratory epithelium that covers the surface of human airway forms an immunologically active natural barrier to invasion and injury by inhaled noxious agents. Ciliary dysfunction and or epithelial damage compromise this innate defence mechanism. Aim: To study the ciliary function and epithelial ultrastructure of adult patients with asthma and paediatric lung transplant recipients. To study the response of bronchial epithelial cells of patients with atopic severe asthma, to allergen and bacteria. Methods: Digital high speed video microscopy was used to study the ciliary function on bronchoscopic bronchial epithelial brushings. Transmission electron microscopy was used to study the detailed epithelial ultrastructure. Cytokines and chemokines released by primary bronchial epithelial cells were measured using SECTOR Imager 6000 (MSD, USA). Results: Ciliary dysfunction and ultrastructural abnormalities are closely related to asthma severity. Ciliary dysfunction is a feature of moderate to severe asthma and profound ultrastructural abnormalities are restricted to severe disease. Primary bronchial epithelial cells of patients with atopic severe asthma and healthy controls are capable of releasing chemokines and cytokines in response to Dermatophagoides Pteronyssinus allergen 1 and Streptococcus pneumoniae in a dose and time dependent manner. Ciliary dysfunction is a feature of native airway epithelium in paediatric Cystic Fibrosis lung transplant recipients. The allograft epithelium shows profound ultrastructural abnormalities in both Cystic Fibrosis and non-suppurative lung disease lung transplant recipients. Summary: The phenotype of secondary ciliary dyskinesia and the differential cytokine/chemokine response of the epithelium of patients with severe asthma seen in this study extend our current paradigm of severe asthma and present a new therapeutic target. The damaged allograft epithelium seen in paediatric lung transplant recipients may increase risk of microbial colonisation of the allograft airway, which may play a role in the development of Bronchiolitis Obliterans Syndrome (BOS).
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Talebizadeh, Nooshin. « Caspase-3 in lens epithelium ». Doctoral thesis, Uppsala universitet, Oftalmiatrik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-267543.
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Purpose: To model the time evolution of active caspase-3 protein expression in a healthy lens, and in a lens exposed to UVR-300 nm (UVR-B). To develop an automated method to classify the fluorescent signal of biomarkers in the lens epithelial cells. Methods: Six-week old Sprague-Dawley rats were used. Firstly, expression of active caspase-3 was studied in the lens epithelium of healthy rats. Secondly, rats were unilaterally exposed in vivo to 1 kJ/m2 UVR-B for 15 minutes. At 0.5, 8, 16, and 24 hours after the UVR-B exposure, the exposed and the contralateral non-exposed lenses were removed. Immunohistochemistry was done on three mid-sagittal sections from each lens. The florescent labelling for active caspase-3 in each lens section was counted three times. The time evolution of active caspase-3 expression in response to UVR-B exposure was modelled as a function of cell position in the lens epithelium. An automated objective method was developed to quantify the lens epithelial cells and to classify the fluorescent signal of active caspase-3. Active caspase-3 was selected as a model signal. Results: Active caspase-3 was abundant in the anterior pole of the normal lenses. Spatial distribution of active caspase-3 labelling in the lens epithelium was fitted to a logistic model. The probability of active caspase-3 expression was higher in the UVR-B exposed lenses (95% CI = 0.12 ± 0.01). There was no difference in the expression of active caspase-3 between the 0.5 and the 24 hours groups or between the 8 and the 16 hours groups. A difference was noted, when comparing the 0.5 and 24 hours groups with the 8 and 16 hours groups (Test statistic 7.01, F1;36;0.95= 4.11). Exposure to UVR-B has an impact on the average probability of labelling for active caspase-3 as a function of cell position. The probability of labelling as a function of cell number also varied as a function of time after UVR-B exposure. The automated method counted the lens epithelial cells and estimated the proportion of active caspase-3 labelling in the lens epithelium. Conclusions: Active caspase-3 is present in the healthy lens epithelial cells. Active caspase-3 exhibits higher expression at the anterior pole of the lens and the expression decreases towards the periphery. After UVR-B exposure, the expression of active caspase-3 in the lens epithelium increases with a peak of expression occurring around 16 hours after exposure. The average probability of labelling in the lens epithelium is dependent on both the UVR-B exposure and the time period elapsed after the exposure. The automated method enables objective and fast quantification of lens epithelial cells and the expression of fluorescent signal in the lens cells.
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Domínguez, Hüttinger Elisa. « Mathematical modelling of epithelium homeostasis ». Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/47969.
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The body and organs of all animals are covered by epithelial tissues, such as the epidermis and the airway epithelium. Epithelial tissues play a key role in protecting the body from environmental aggressors. Failure to maintain a competent epithelium can lead to the onset of many diseases, including Atopic dermatitis (AD) and infection by Streptococcus pneumoniae. Treatment of AD is currently restricted to the relief of symptoms, mainly because the underlying mechanisms remain elusive. Antibiotic resistance threatens the effectiveness of the prevalent treatments for infection. Devising new and effective therapeutic strategies that halt the progression of these diseases requires an understanding of the different disease mechanisms that can cause loss of epithelial homeostasis in different patients. Intricate regulatory networks of several biochemical and cellular interactions maintain epithelium homeostasis in healthy individuals, but can also propagate different disturbances, resulting in a wide spectrum of possible disease phenotypes. In this thesis, we propose mathematical models of these regulatory networks to analyse the mechanisms that lead to the onset and progression of AD and pneumococcal infection from a systems-level perspective. Our mathematical model of AD reproduced, for the first time, the different stages of the disease that have been observed in the clinic. Moreover, we proposed different pathogenic mechanisms, triggered by different genetic and environmental risk factors that are known to predispose to AD. By assessing the effects of common treatments for AD, we suggested effective treatment strategies that can prevent the aggravation of the disease, in a patient-specific way. Our data-driven mathematical model of pneumococcal infection identified four qualitatively different mechanisms by which co-infection can drive the pathogenic process. They can be counteracted by distinctive treatment strategies that only partially involve antibiotics. Our work provides a theoretical framework for the integration and analysis of clinical and experimental data describing epithelial homeostasis.
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Kalair, Waseem. « Isolation and transplantation of murine intestinal stem cells ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/MQ59179.pdf.
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Brocchieri, Cristian. « A study on the regulation of Epithelial to Mesenchymal Transition in the Ovarian Surface Epithelium ». Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611315.
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Carter, Lauren. « Defining the Epithelial-to-Mesenchymal Transition and Regulation of Stemness in the Ovarian Surface Epithelium ». Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38491.
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The ovarian surface epithelium (OSE) is a monolayer of cells surrounding the ovary that is ruptured during ovulation. After ovulation the wound is repaired, however this process, and the mechanisms to maintain OSE homeostasis after the wound is repaired are poorly understood. We have shown the mouse OSE (mOSE) contains a stem cell population that is expanded by Transforming Growth Factor Beta 1 (TGFB1), a factor present in follicular fluid. These data suggest that components in the follicular fluid such as TGFB1 may promote wound repair and OSE homeostasis through maintenance of the OSE stem cell population. Additionally, TGFB1 may promote wound repair through induction of an epithelial-to-mesenchymal transition (EMT) and activation of pro-survival pathways, as seen in other tissues.
To elucidate the mechanism for TGFB1-mediated ovulatory wound repair, mOSE cells were treated with TGFB1, which induced an EMT seen with increased Snai1 expression and cell migration. Snai1 overexpression also increased cell migration and sphere formation (a stem cell characteristic). RNA sequencing results suggest this is at least in part through elevated collagen deposition in SNAI1 overexpressing cells. A TGFB signalling targets array identified Cox2 induction following TGFB1 treatment. Constitutive Cox2 expression did not promote an EMT, but enhanced sphere formation and cell survival. Finally, TGFB1 treatment decreased Brca1 expression, which when deleted from mOSE cells also increased sphere formation. RNA sequencing results suggest that Brca1 deletion promotes stemness through activation of the stem cell genes Ly6a and Lgr5. RNA sequencing was also used to compare mOSE cells cultured as monolayers and as spheroids, with and without TGFB1. These results validate our findings that TGFB1 promotes an EMT partially through Snail induction and the upregulation of Cox2. mOSE cells cultured as spheroids acquire a mesenchymal transcriptional profile that is further enhanced with TGFB1 treatment.
These data suggest that TGFB1 may promote ovulatory wound repair and maintain OSE homeostasis through the induction of an EMT, maintenance of the stem cell population and activation of a pro-survival pathway. Interestingly, mOSE spheroids also decrease Brca1 expression and upregulate cancer associated genes such as Pax8 and Greb1. The induction of survival pathways, while simultaneously increasing stemness and repressing Brca1 could render cells more susceptible to transformation. This work provides novel insights as to why ovulation is the primary non-hereditary risk factor for ovarian cancer.
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Lau, Janet. « Hedgehog signaling in the pancreas epithelium ». Diss., Search in ProQuest Dissertations & ; Theses. UC Only, 2010. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3398879.
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Schmachtenberg, Oliver. « Nitric oxide in the olfactory epithelium ». [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962820598.
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Nilsson, Jan Anders. « Aldehyde toxicity in human oral epithelium / ». Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-141-5/.
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Calderon-Zapatal, Moises Antonio. « The nasal epithelium, atopy and inflammation ». Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286273.
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O'Connor, M. G. « Apoptosis in intestinal epithelium during regeneration ». Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411844.
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McLennan, Ross Kenneth James. « Vesicle trafficking in a Drosophila epithelium ». Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398536.
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Wei, Jun. « Development of the first vertebrate epithelium ». Thesis, University of Bath, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538125.
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A conserved feature of early vertebrate embryos is the formation of simple epithelial layer of cells which surrounds the embryo and protects it from the external environment. This epithelium is called the trophectoderm in mammals, the superficial layer in Xenopus and the enveloping layer in zebrafish. This project investigates what promotes differentiation of this cell type. In Xenopus embryos aPKC and Notch signalling were found to be unable to promote differentiation of the superficial layer. In contrast, BMP signalling can promote expression of a number of transcriptional regulators, including members of the Grhl and Msx families and differentiation of the superficial layer. This pathway is initiated in the underlying deep cells, but not all target genes are activated so differentiation does not occur in these cells. The role of BMP signalling in mouse development was investigated by using mouse embryonic stem cells (mESCs) as the model. BMP4 is sufficient to induce mESCs to form a polarised epithelial cell type and that these epithelial cells appear trophoblast in fate. BMP signalling activates Grhl and Msx genes in mESCs, as it does in Xenopus embryos. This suggests that similar target genes are activated by BMP signalling in the first epithelium of Xenopus and mouse. Based on this data it is tempting to propose that BMP signalling acts in a conserved manor to promote differentiation of the first epithelium in diverse vertebrates.
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Owen-Jones, Catrin Eleri. « Stem cells in human oral epithelium ». Thesis, Cardiff University, 2004. http://orca.cf.ac.uk/55544/.
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The stratifying epithelia of skin and mucosa continuously renew their structure by cell division, but only a small fraction of proliferative cells, the stem cells, are capable of continuous self-renewal. The staining distribution of various stem cell and differentiation markers were investigated in normal human mucosal epithelium. To determine the extent of regional variation in patterns of stem cell behaviour in human epithelia, human mucosal keratinocytes were amplified in vitro. Using retroviral vectors, a sub-population of these cells were transduced with genes for histochemically detectable markers to permit lineage analyses. Organotypic culture methods were used to generate epithelia with normal patterns of cell kinetics and differentiation and these were examined after maintenance in vitro or after transplantation back to in vivo sites in immune deficient mice. The clonal lineages resulting from stem cell patterns were compared and the number of functional stem cells were assessed from the size of stable clonal units regenerated. The cell cycles of keratinocytes grown on plastic compared to organotypic culture were also investigated by flow cytometry to see if the organotypic cultures provided a suitable stem cell model. Results included the following. Antibody staining in palate revealed that K15 and K19 identified zones of positively stained basal cells at the epithelial rete tips. These K15 and K19 positive regions were negative for differentiation markers K6 and K16, indicating that cells in these regions were undifferentiated and could include stem cells Organotypic cultures gave similar staining profiles to palate, and using retrovirally stained subpopulations of cells and transplantation to SCID mice, clonal units were identified which did not correspond to the primitive rete that had reformed. Flow cytometry work showed that the cell cycles of cells grown in vitro on plastic were faster than the cell cycles of organotypic cultures.
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Anantharam, Arun. « Structure and regulation of the epithelial sodium channel / ». Access full-text from WCMC :, 2007. http://proquest.umi.com/pqdweb?did=1445057221&sid=9&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Liu, Ke. « Role of second messengers in controlling growth patterns of corneal epithelial cells / ». View thesis, 2002. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030718.102224/index.html.
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Thesis (Ph. D.)--University of Western Sydney, 2002."This thesis is submitted in fulfilment of the requirements of the degree of Doctor of Philosophy to the University of Western Sydney School of Biological Sciences."t.p. Includes bibliographical references (leaves 138-150).
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Johnston, Richard A. « Characterization of the airway epithelial bioelectric mechanisms associated with the effects of epithelium-derived relaxing factor in guinea-pig isolated trachea ». Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1776.
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Thesis (Ph. D.)--West Virginia University, 2000.Title from document title page. Document formatted into pages; contains ix, 135 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 127-135).
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Papacleovoulou, Georgia. « Steroid signalling in the human ovarian surface epithelium wound healing ». Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4237.
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The human ovarian surface epithelium (hOSE) is a cell monolayer that covers the surface of the ovary. Natural events like incessant ovulation, associated reproductive hormone action prior to and post-ovulation, along with the ovulationassociated inflammation, that result in injury and repair of hOSE, are considered to have a role in the development of epithelial ovarian cancer (EOC). Progesterone is apoptotic and anti-inflammatory, whereas androgens appear cytoproliferative for hOSE. Local generation of these steroid hormones is subject to 3β-hydroxysteroid dehydrogenase (3β-HSD) activity. Moreover, action of these hormones is achieved through coupling to their cognate receptors, progesterone (PR) and androgen receptors (AR). The overall aim of this thesis is to elucidate in vitro the regulation of progesterone and androgen biosynthesis and downstream signalling during the injury and repair of primary hOSE cells that were collected from pre-menopausal women who underwent surgery for benign gynaecological disorders. Injury was mimicked by treatment of cells with several pro-inflammatory cytokines, whereas repair was mimicked with T-lymphocyte, ‘anti-inflammatory’ cytokines. Immunohistochemical studies showed immunodetectable 3β-HSD in the human ovarian cell surface of whole ovary and three-week cultured hOSE cells, establishing 3β-HSD expression in vivo and in vitro. Cross-reaction of the 3β-HSD antibody with both enzyme isoforms did not allow investigation of isoform expression pattern. However, mRNA transcriptional studies with isoform specific primers and probe sets for semi-quantitative (sq) and quantitative (q) PCR revealed expression of both isoforms in hOSE cells; 3β-HSD1 mRNA was expressed at higher levels relative to 3β-HSD2 mRNA in accordance with the preference of this isoform in peripheral non-steroidogenic tissues. Of the cytokines tested, only IL-1α and IL-4 affected 3β-HSD expression. IL- 1α suppressed 3β-HSD1 mRNA, whereas it up-regulated 3β-HSD2 mRNA as assessed with qPCR, without though affecting total 3β-HSD protein and activity levels as assessed with western immunoblotting and radiometric activity assays, respectively. IL-1α did not affect AR or PR mRNA levels, suggesting a balance in androgen and progesterone biosynthesis during post-ovulatory wounding. IL-4 massively induced 3β-HSD1 and 3β-HSD2 mRNA and total 3β-HSD protein and activity. It also attenuated AR mRNA and protein, without affecting PR mRNA. Collectively, these data demonstrate that IL-4 sustains progesterone rather than androgen signalling and this may be part of the anti-inflammatory steroid action that protects hOSE from genetic damage. IL-1α effects appear to be mediated by NF-κB signalling pathway. PI-3K and p38 MAPK appeared involved in IL-1α-induced 3β- HSD2. IL-4-induced 3β-HSDs required STAT-6 and PI-3K pathways and also p38 MAPK at the case of 3β-HSD2. IL-4-attenuated AR was reversed by a p38 MAPK inhibitor. These data suggest that steroid signalling by IL-1α and IL-4 involve multiple signalling pathways. In primary EOC, 3β-HSD1 and 3β-HSD2 transcripts were attenuated relative to hOSE cells, suggestive of an acquired feature of neoplastic transformation. However, both transcripts could be restored after IL-4 treatment, attesting a therapeutic advantage of this cytokine. In conclusion, we have shown that 3β-HSD is under inflammatory control during ovarian post-ovulatory wound healing of hOSE. IL-1α- and IL-4-mediated 3β-HSD1 and 3β-HSD2 are regulated by multiple signalling pathways. Also, IL-4 was identified as an anti-inflammatory agent in hOSE with putative therapeutic benefit in malignancy.
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Chowdhury, Ferdousi. « Epithelial tight junction function in a co-culture model of the human bronchial epithelium and endothelium ». Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404190.
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Scull, Margaret Adele Pickles Raymond J. « Myxovirus interaction with the human airway epithelium ». Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2848.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
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Al-Hosaini, Heba. « Age-related changes in retinal pigment epithelium ». Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444089/.
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The retinal pigment epithelium (RPE) is a monolayer of hexagonal organized cells located between the choriocapillaris and the neurosensory retina. As the RPE is implicated in a range of eye diseases, an understanding of its structure and ability for self renewal is critical for therapeutic strategies. Analysis of human RPE cells at the extreme periphery of the retina reveals a population larger in size than those in the centre, they are highly irregular and form an annulus of 4-5 mm. Although binucleation in humans is rare, 10% of these cells are binucleated. In the central region these large binucleated cells are only found adjacent to drusen, which are age-related lipid-rich deposits. Compared with humans, rat RPE is relatively homogeneous, however, the majority of its cells are binucleated, particularly in the central region. Human and rat RPE also shows different patterns of aging. In humans, the centre of the retina shows a significant reduction in RPE cell density with age, which was not observed in aged rats. The capacity of mature RPE cells to enter the cell cycle was investigated using a proliferative marker in rats. Here a subpopulation of mature peripheral RPE cells had the capacity to enter the cell cycle, and one-third of these cells completed cellular division. As RPE proliferation occur in response to retinal detachment, this was performed on rats and the patterns of gene expression in RPE examined. An increase was observed in nestin, PCNA and Ki67 expression, which was also confirmed at a protein level by immunohistochemistry. These results suggest that RPE cells have the capacity to proliferate and may possibly differentiate if subjected to appropriate stimuli in a normal retina.
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Donahue, Vicki S. « Phospholipase c activity in retinal pigment epithelium ». Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1041916.
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The role of the retinal pigment epithelial cells on the viability and renewal of photoreceptors has been well demonstrated in the Royal College of Surgeons (RCS) strain of rat. These rats are characterized by an inherited time-dependent degeneration of their photoreceptors. This degeneration is apparently due to the inability of the retinal pigment epithelial cells to adequately ingest fragments of photoreceptor membrane that are shed during the course of photoreceptor membrane renewal. The buildup of photoreceptor material in the interphotoreceptor space ultimately leads to the degeneration of photoreceptors in these animals. With regard to the pigment epithelial cells, neither the mechanism mediating the ingestion process in normal rats nor the nature of the defect of this process in RCS rats is understood.It is the goal of this proposed research to assay for the presence of phospholipase C in retinal pigment epithelial (RPE) cells and to determine possible modulators of the enzyme in an attempt to associate this with the process of phagocytosis.Department of Biology
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MacPherson, Matthew. « Calcium signalling in a fluid transporting epithelium ». Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341710.
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Warner, Jacqueline. « Ionic transport across mammalian retinal pigment epithelium ». Thesis, University of Westminster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292857.
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Walker, Dawn Carol. « Modelling the electrical properties of cervical epithelium ». Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392721.
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Scully, Jaqueline Susan. « Insertion of oncogenes into mouse mammary epithelium ». Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315287.
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Milward, Michael Robert. « Oral epithelium in the pathogenesis of periodontitis ». Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1007/.
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Pocket/sulcular epithelium is the first line of defence to plaque bacteria and its potential role in periodontitis is investigated. This thesis describes the development of a model system, utilising an immortal epithelial cell line (H400) in order to investigate responses to periodontal pathogen stimulation (P. gingivalis and F. nucleatum) in terms of NF-\(\kappa\)B activation, differential gene expression and cytokine production. The pathogenesis of periodontitis suggests that susceptible patients exhibit a hyper-inflammatory response to plaque bacteria, so an attempt to modulate the pro-inflammatory epithelial response using a natural di-thiol antioxidant \(\alpha\)-lipoate was also investigated. Data demonstrated that periodontal pathogens P. gingivalis and F. nucleatum elicited a pro-inflammatory response in the H400 model system. This was confirmed by demonstrating NF-\(\kappa\)B activation, gene expression changes and downstream cytokine production. Ontological grouping of gene expression changes revealed a range of gene functions which support the hypothesis that the epithelium may play a role in the initiation and propagation of the periodontal lesion. In addition, alipoate was able to modulate this inflammatory response but not completely block this essential defence mechanism. Data obtained indicates the potential of utilising \(\alpha\)-lipoate as an adjunct in the management of periodontitis.
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Chen, F. K. « Retinal pigment epithelium transplantation in retinal diseases ». Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318070/.
Texte intégralRésumé :
Age-related macular degeneration (AMD) and inherited macular diseases (IMD) are retinal disorders that can cause blindness through atrophy of the retinal pigment epithelium (RPE) or choroidal neovascularisation (CNV). RPE transplantation in severe forms of neovascular AMD has been performed with promising short-term outcomes. However, this approach has not been evaluated in atrophic types of AMD or IMD. Furthermore, the long-term outcomes of photoreceptors cell function rescue by RPE reconstruction in neovascular AMD is unknown. Current surgical techniques are complex with associated high complication rates. Therefore, other treatment approaches to reconstruct the RPE are required. This thesis aims to examine whether long-term photoreceptor cell function rescue can be achieved through RPE reconstruction by investigating the outcomes of autologous RPE transplantation or full macular translocation in AMD and IMD. A further aim is to determine the feasibility of a new approach to reconstruct the RPE using human embryonic stem cell (hESC). A prospective study of autologous RPE-choroid grafts in 9 patients with atrophic macular disease secondary to AMD or IMD demonstrated that submacular RPE graft can support retinal function and fixation. However, there was a high surgical and post-operative complication rates and the overall visual acuity and reading ability declined. Long-term follow-up demonstrated that the graft can maintain retinal function for over 2 years in some patients. A retrospective review of long-term outcomes following autologous RPE-choroid grafts and full macular translocation in 12 and 40 patients with neovascular AMD, respectively, showed that rescue of retinal function beyond 2 years is possible. A visual acuity of 6/12 was achieved and maintained for over 2 years in 8% and 15% of patients who had patch graft and translocation, respectively. However, overall visual acuity outcomes were limited by delayed post-operative complications such as recurrent CNV and cystoid macular oedema. A prospective porcine experiment showed that subretinal implant of hESC derived-RPE was feasible and human donor cell can survive in vivo for up to 6 weeks. However, there was significant loss of the hESC-RPE which may have occurred intra-operatively or during the first 2 weeks post-operatively. Macrophages were noted at the site of the graft suggesting some inflammatory and immunological responses to the human cells, polyester substrate or surgical trauma. The work in this thesis has provided the proof of principle that reconstruction of the RPE can maintain retinal function in atrophic and neovascular macular diseases over the long-term. A novel approach using hESC-RPE on an artificial substrate may be a more feasible and safer alternative to current clinical techniques of RPE reconstruction.
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Thomas, Rebecca Ann. « Effect of stretch on the bronchial epithelium ». Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29487.
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This thesis describes the use of a model of cell deformation to measure the effect of stretch on mediator release or expression by airway epithelial cells, and to assess the method of mechanotransduction in these cells. Cells were cyclically stretched using the Flexercell system delivering biaxial stretch. IL-8 release by BEAS 2B cells was increased by cytokine stimulation and stretch, in a dose, time and rate dependent manner, whereas RANTES levels in the cell supernatant and cell surface ICAM-1 expression decreased after stretch. 30% elongation at 20 cycles/minute for 24 hours increased IL-8 levels by over 100% (p<0.01). Changes in IL-8 and RANTES RNA correlated with the effect on protein levels. Stretch did not adversely effect cell viability. The novel use of primary bronchial epithelial cells in stretch experiments is reported, with, in contrast to the BEAS 2B cell line, no effect of stretch on IL-8 release by these cells.;To interpret how the cells were sensing the stretch stimulus, signalling via integrins was blocked using an inhibitor of Rho (R&barbelow;as Homologous) associated kinases, which inhibited the effect of stretch on IL-8 release by the BEAS 2B cells, but not the effect on RANTES release or ICAM-1 expression. Blocking individual integrins did not affect the stretch response. Paxillin was visualised by indirect immunofluorescence to study the effect of stretch on the distribution of focal contacts and the organisation of the actin cytoskeleton. This demonstrated that stretch caused dramatic disassembly of focal adhesions and resulted in the redistribution of paxillin to the peri-nuclear region.
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Moradi, Emilia. « Folate-mediated macromolecule delivery across the epithelium ». Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/27899/.
Texte intégralRésumé :
Folate uses the natural endocytosis pathway via the folate receptor (FR) to enter the cells. Folate conjugation to small or macromolecular therapeutics has hence been exploited for intracellular delivery to, particularly, cancerous cells. This work reports on the expression and functionality of FR in polarised cell monolayer models of respiratory and gastrointestinal mucosa with the view to assess its potential for delivery of folate-modified macromolecular therapeutics either intracellularly or across the epithelium. Four cell lines representing bronchial and intestinal epithelium; cancer-derived intestinal Caco-2 and bronchial cell line Calu-3, and noncancerous intestinal and bronchial cell lines IEC-6 and HBEC were cultured on permeable membranes to produce polarised monolayers. Expression of FR was confirmed by RT-PCR and Western blot analysis for all the tested cell types and shown to be dependent on culturing time. The functionality of the receptor for endocytosis was demonstrated by a model macromolecular folate conjugate (fluorescent ovalbumin-folate (OVA-FA)), whereby significantly higher cellular uptake of the folate-conjugate, relative to non-folate control, was clearly demonstrated. Importantly the data showed that the expressed folate receptor was capable of mediating transport of the macromolecular folate conjugate across (transcytosis) the cells in the polarised monolayers. Preliminary studies led to investigation of the folate mediated uptake and transport of folate modified nanoparticles (NPs). It was shown that folate modified NPs traversed the Calu-3 layers and studies characterizing this transport indicated folate involvement in this process. Adsorption of OVA-FA on the surface of NPs was seen to promote their cellular uptake and transport across the cell layers. To examine the mechanism of cellular uptake and transport of folate modified nanoparticles, various endocytic inhibitors were employed. The study demonstrated an involvement of the caveolar pathway in internalization of folate modified nanoparticles; as judged from a significant reduction of internalization in filipin (inhibitor of caveolar pathway) treated cells. Moreover, the work also showed evidence of transport of folate-modified nanoparticles via the caveolar pathway, since translocation of nanoparticles across the cell monolayer was absent when this path was inhibited. Disruption of actin filament and microtubules caused no difference in cellular uptake of NPs but increased the transcytosis of folate modified NPs. Confocal microscopy, Transmission Electron Microscopy (TEM), Total Internal Reflection Microscopy (TIRM) and Total Internal Reflection Florescence microscopy (TIRFM) were used to confirm and visualize quantitative data. This study also investigated the effects of surface ligand distribution pattern (ligand clustering and density) on the internalization of nanoparticles by Calu-3 cells cultured as polarised layers. The density of the displayed ligand was manipulated by controlling the conjugation level of folate-ovalbumin, while ligand clustering was achieved by co-adsorption of varying mixtures of folate-ovalbumin conjugate (at different ligand density levels) and unconjugated ovalbumin. Increasing ligand density on the nanoparticle surface resulted in increased internalization of modified nanoparticles by the cells, up to a saturation level. Surface ligand density also affected the cellular uptake pathway; from predominantly clathrin to predominantly caveolae-mediated as the ligand density was increased. It was further demonstrated that surface clustering of the folate ligand enhanced cellular internalization of nanoparticles, relative to its dispersed surface distribution.
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Bhattacharya, Pradipta. « The corneal epithelium in health and disease ». Thesis, Queensland University of Technology, 2022.
Trouver le texte intégralRésumé :
The cornea is the anterior transparent layer of the eye, and understanding corneal epithelial morphology is valuable in monitoring ocular surface diseases. A meta-analysis showed that central corneal basal cell density and nerve parameters were reduced in diseases affecting the ocular surface including limbal stem cell deficiency. Using newly developed image analysis techniques it was observed that epithelial cell density was highest at the corneal nerve whorl region. A decrease in epithelial cell density was observed in eyes with conjunctival ultraviolet autofluorescence, i.e. with sunlight-induced UV damage.
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Lan, Li, et 藍莉. « A study of apoptosis in a human epithelial tumour cell line ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238762.
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Hunjan, Anoop Singh, et Anoop Singh Hunjan. « Chronic Arsenite Exposure in Lung Epithelium Modulates Endocytosis ». Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/626765.
Texte intégralRésumé :
Arsenic exposure in humans has been implicated in the development of a myriad of non-cancerous and cancerous diseases. A reductionist approach to understanding this unusual phenomenon would suggest that arsenic-induced perturbation of a small number of fundamental biological processes could manifest as this diverse array of disease endpoints. Endocytosis is a fundamental cellular process involved in the internalization and transport of various extracellular molecules and membranous components. BEAS-2B, a human bronchial epithelial cell line, was used to characterize the effects of chronic arsenite exposure on endocytosis. Fluorophore-labeled bovine albumin, human transferrin, and human low-density lipoprotein (LDL) were the substrates utilized to measure endocytosis in BEAS-2B cells. The uptake of albumin in unexposed BEAS-2B cells is both dose-dependent and temperature sensitive. Chronic arsenite exposure in BEAS-2B cells increased the uptake of albumin by 3.4-fold after 8 hours of uptake relative to unexposed BEAS-2B cells. Pharmacological studies utilizing endocytosis inhibitors suggested that the uptake of albumin in both unexposed and arsenite-exposed BEAS-2B cells occurs through a combination of receptor-mediated endocytosis and macropinocytosis. Chronic arsenite exposure in BEAS-2B cells also increased the endocytic uptake of transferrin by 2.9-fold at 30 minutes and LDL by 1.3-fold at 2 hours relative to unexposed BEAS-2B cells. Together, the data suggests that chronic arsenite exposure can increase the rate of endocytosis. This novel finding could add mechanistic insight to the conundrum of arsenic-associated human diseases.
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Ivert, Lena. « Interactions between neural retina, retinal epithelium and choroid / ». Stockholm : Section of ophthalmology and vision, Department of clinical neuroscience, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-797-9/.
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Stumpff, Friederike [Verfasser]. « Ionic conductances of the ruminal epithelium / Friederike Stumpff ». Berlin : Freie Universität Berlin, 2011. http://d-nb.info/1025355377/34.
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Fox, Emma. « Systemic delivery of DNA to the airway epithelium ». Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409742.
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Mort, Richard Lester. « Stem cell function in the mouse corneal epithelium ». Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/8187.
Texte intégralRésumé :
Limbal stem cells maintain the corneal epithelium through a process of clonal growth and ordered migration. In X-inactivation mosaic female mice, that express LacZ from one of their X-chromosomes, random clumps of LacZ-positive cells are seen in the cornea at 3-6 weeks of life. This pattern resolves between 6-10 weeks forming radial stripes thought to represent chords of clonally related, inwardly migrating cells. By measuring the number and width of stripes and correcting for the effects of different proportions of LacZ-positive cells, an estimate of the number of coherent stem cell clones maintaining the tissue can be derived. Analysis at 5 ages demonstrated that the estimated number of coherent stem cell clones is reduced from ~100 at 15 weeks to ~50 at 39 weeks and is then stable at least until 52 weeks. An automated method was developed using image analysis software to analyse these striping patterns. This method produced results that did not differ significantly from the above. The dosage of the transcription factor Pax6 is crucial for normal eye development. In Pax6 heterozygous animals the estimated number of coherent stem cell clones is reduced to ~50 at 15 weeks with no further reduction up to 30 weeks. Mice hemizygous for the PAX77 transgene over-express human PAX6. In PAX77 hemizygous X-inactivation mosaics, estimated clone number was similarly reduced to ~50 with no further decline. Mice heterozygous for both Gli3 and Pax6 have a distinct striping phenotype, highlighted by an increase in coherent clones. When the corneal epithelium is injured the surrounding epithelial cells migrate along the corneal stroma to cover the wound. X-gal staining of healed, centrally wounded X-inactivation eyes reveals that striping patterns are reconstituted during wound healing in ex-vivo culture. In GFP mosaics the healing process can be imaged using time-lapse confocal microscopy. This technique demonstrated that clones remain contiguous throughout their migration. Healing of peripheral wounds was observed to form de-novo whorling patterns, revealing that basal cells in the epithelium can migrate both away from and towards the limbal region.
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Foley, Charlotte Louise. « Characterisation of human prostate epithelium colony forming cells ». Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444718/.
Texte intégralRésumé :
Objectives: Rare prostate epithelial stem cells have been implicated in the aetiology of prostate disease, yet are overlooked in studies on the whole tissue. When prostate epithelial cells are cultured at low density, two distinct colony types arise, postulated to represent the progeny of stem cells (type II colonies) and committed 'transit amplifying' cells (type I). This project aimed to further characterize these rare colonies and confirm their position in the prostate epithelial cell hierarchy, in benign, and for the first time, malignant tissue. Methods: Colonies derived from transurethral resection tissue were compared for proliferation, differentiation, colony self-renewal and gene expression. Paired benign and malignant radical prostatectomy samples were cultured. To confirm the benign / malignant nature of individual colonies, loss of heterozygosity and expression of known prostate cancer markers were assessed. Results: There was a trend to greater type II colony proliferation, but no difference in ability to differentiate into multi-layered acinus-like structures expressing early and late epithelial markers. When passaged, type II colonies never re-created themselves, but resembled type I colonies. Using cDNA microarrays, comparison of gene expression in the two colony types showed a limited magnitude of differences, most notably in differentiation markers. Malignant tissue yielded both colony types, which were indistinguishable from their benign counterparts. Neither loss of heterozygosity analysis nor prostate cancer marker expression distinguished benign from malignant colonies. Conclusions: These colonies behave like differently-aged populations of transit amplifying cells - the committed offspring of the stem cell. If a stem cell does generate type II colonies, it appears to lose self-renewal ability and differentiate in culture. Colonies derived from cancer tissue show neither a malignant genotype nor phenotype suggesting that malignant cells are not cultured in these conditions. This highlights the need to confirm malignancy in primary prostate cancer cultures, hitherto assumed by many authors.
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Ahmad, Sajjad. « The culture of human limbal epithelium for transplantation ». Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440580.
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Devine, Lesley. « Cellular interactions between lymphocytes and retinal pigment epithelium ». Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338652.
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Sheridan, Carl Michael. « The retinal pigment epithelium and its extracellular matrix ». Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366682.
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Green, Graeme Lister. « The bacterial flora associated with the human epithelium ». Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441254.
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