Relevant bibliographies by topics / Mesothelial

Academic literature on the topic 'Mesothelial'

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Published: 11 March 2023

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Journal articles on the topic "Mesothelial"

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Foley-Comer, Adam J., Sarah E. Herrick, Talib Al-Mishlab, Cecilia M. Prêle, Geoffrey J. Laurent, and Steven E. Mutsaers. "Evidence for incorporation of free-floating mesothelial cells as a mechanism of serosal healing." Journal of Cell Science 115, no. 7 (April 1, 2002): 1383–89. http://dx.doi.org/10.1242/jcs.115.7.1383.

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Regeneration of the mesothelium is unlike that of other epithelial-like surfaces, as healing does not occur solely by centripetal migration of cells from the wound edge. The mechanism of repair of mesothelium is controversial,but it is widely accepted, without compelling evidence, that pluripotent cells beneath the mesothelium migrate to the surface and differentiate into mesothelial cells. In this study we examined an alternative hypothesis, using in vivo cell-tracking studies, that repair involves implantation,proliferation and incorporation of free-floating mesothelial cells into the regenerating mesothelium. Cultured mesothelial cells, fibroblasts and peritoneal lavage cells were DiI- or PKH26-PCL-labelled and injected into rats immediately following mesothelial injury. Implantation of labelled cells was assessed on mesothelial imprints using confocal microscopy, and cell proliferation was determined by proliferating cell nuclear antigen immunolabelling. Incorporation of labelled cells, assessed by the formation of apical junctional complexes, was shown by confocal imaging of zonula occludens-1 protein. Labelled cultured mesothelial and peritoneal lavage cells, but not cultured fibroblasts, implanted onto the wound surface 3, 5 and 8 days after injury. These cells proliferated and incorporated into the regenerated mesothelium, as demonstrated by nuclear proliferating cell nuclear antigen staining and membrane-localised zonula occludens-1 expression,respectively. Furthermore, immunolocalisation of the mesothelial cell marker HBME-1 demonstrated that the incorporated, labelled lavage-derived cells were mesothelial cells and not macrophages as it had previously been suggested. This study has clearly shown that serosal healing involves implantation,proliferation and incorporation of free-floating mesothelial cells into the regenerating mesothelium.
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Madeira, Ana, Carolina Serena, Miriam Ejarque, Elsa Maymó-Masip, Monica Millan, M. Carmen Navarro-Ruiz, Rocío Guzmán-Ruiz, et al. "Crohn’s Disease Increases the Mesothelial Properties of Adipocyte Progenitors in the Creeping Fat." International Journal of Molecular Sciences 22, no. 8 (April 20, 2021): 4292. http://dx.doi.org/10.3390/ijms22084292.

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Our understanding of the interplay between human adipose tissue and the immune system is limited. The mesothelium, an immunologically active structure, emerged as a source of visceral adipose tissue. After investigating the mesothelial properties of human visceral and subcutaneous adipose tissue and their progenitors, we explored whether the dysfunctional obese and Crohn’s disease environments influence the mesothelial/mesenchymal properties of their adipocyte precursors, as well as their ability to mount an immune response. Using a tandem transcriptomic/proteomic approach, we evaluated the mesothelial and mesenchymal expression profiles in adipose tissue, both in subjects covering a wide range of body-mass indexes and in Crohn’s disease patients. We also isolated adipose tissue precursors (adipose-derived stem cells, ASCs) to assess their mesothelial/mesenchymal properties, as well as their antigen-presenting features. Human visceral tissue presented a mesothelial phenotype not detected in the subcutaneous fat. Only ASCs from mesenteric adipose tissue, named creeping fat, had a significantly higher expression of the hallmark mesothelial genes mesothelin (MSLN) and Wilms’ tumor suppressor gene 1 (WT1), supporting a mesothelial nature of these cells. Both lean and Crohn’s disease visceral ASCs expressed equivalent surface percentages of the antigen-presenting molecules human leucocyte antigen—DR isotype (HLA-DR) and CD86. However, lean-derived ASCs were predominantly HLA-DR dim, whereas in Crohn’s disease, the HLA-DR bright subpopulation was increased 3.2-fold. Importantly, the mesothelial-enriched Crohn’s disease precursors activated CD4+ T-lymphocytes. Our study evidences a mesothelial signature in the creeping fat of Crohn’s disease patients and its progenitor cells, the latter being able to present antigens and orchestrate an immune response.
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Yung, Susan, and Chan Tak Mao. "Mesothelial Cells." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 2_suppl (June 2007): 110–15. http://dx.doi.org/10.1177/089686080702702s19.

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♦ Background The introduction of peritoneal dialysis (PD) as a modality of renal replacement therapy has provoked much interest in the biology of the peritoneal mesothelial cell. Mesothelial cells isolated from omental tissue have immunohistochemical markers that are identical to those of mesothelial stem cells, and omental mesothelial cells can be cultivated in vitro to study changes to their biologic functions in the setting of PD. ♦ Method The present article describes the structure and function of mesothelial cells in the normal peritoneum and details the morphologic changes that occur after the introduction of PD. Furthermore, this article reviews the literature of mesothelial cell culture and the limitations of in vitro studies. ♦ Results The mesothelium is now considered to be a dynamic membrane that plays a pivotal role in the homeostasis of the peritoneal cavity, contributing to the control of fluid and solute transport, inflammation, and wound healing. These functional properties of the mesothelium are compromised in the setting of PD. Cultures of peritoneal mesothelial cells from omental tissue provide a relevant in vitro model that allows researchers to assess specific molecular pathways of disease in a distinct population of cells. Structural and functional attributes of mesothelial cells are discussed in relation to long-term culture, proliferation potential, age of tissue donor, use of human or animal in vitro models, and how the foregoing factors may influence in vitro data. ♦ Conclusions The ability to propagate mesothelial cells in culture has resulted, over the past two decades, in an explosion of mesothelial cell research pertaining to PD and peritoneal disorders. Independent researchers have highlighted the potential use of mesothelial cells as targets for gene therapy or transplantation in the search to provide therapeutic strategies for the preservation of the mesothelium during chemical or bacterial injury.
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Kao, Hao-Hsi, Chang-Yi Kuo, Darshan Tagadur Govindaraju, Kuo-Su Chen, and Jyh-Ping Chen. "Polycaprolactone/Chitosan Composite Nanofiber Membrane as a Preferred Scaffold for the Culture of Mesothelial Cells and the Repair of Damaged Mesothelium." International Journal of Molecular Sciences 23, no. 17 (August 23, 2022): 9517. http://dx.doi.org/10.3390/ijms23179517.

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Mesothelial cells are specific epithelial cells lining the serosal cavity and internal organs. Nonetheless, few studies have explored the possibility to culture mesothelial cells in a nanostructure scaffold for tissue engineering applications. Therefore, this study aims to fabricate nanofibers from a polycaprolactone (PCL) and PCL/chitosan (CS) blend by electrospinning, and to elucidate the effect of CS on the cellular response of mesothelial cells. The results demonstrate that a PCL and PCL/CS nanofiber membrane scaffold could be prepared with a comparable fiber diameter (~300 nm) and porosity for cell culture. Blending CS with PCL influenced the mechanical properties of the scaffold due to interference of PCL crystallinity in the nanofibers. However, CS substantially improves scaffold hydrophilicity and results in a ~6-times-higher cell attachment rate in PCL/CS. The mesothelial cells maintain high viability in both nanofiber membranes, but PCL/CS provides better maintenance of cobblestone-like mesothelial morphology. From gene expression analysis and immunofluorescence staining, the incorporation of CS also results in the upregulated expression of mesothelial marker genes and the enhanced production of key mesothelial maker proteins, endorsing PCL/CS to better maintain the mesothelial phenotype. The PCL/CS scaffold was therefore chosen for the in vivo studies, which involved transplanting a cell/scaffold construct containing allograft mesothelial cells for mesothelium reconstruction in rats. In the absence of mesothelial cells, the mesothelium wound covered with PCL/CS showed an inflammatory response. In contrast, a mesothelium layer similar to native mesothelium tissue could be obtained by implanting the cell/scaffold construct, based on hematoxylin and eosin (H&E) and immunohistochemical staining.
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Witz, CA, S. Cho, VE Centonze, IA Montoya-Rodriguez, and RS Schenken. "Time Series Analysis of Transmesothelial Invasion by Endometrial Stromal and Epithelial Cells Using Three-dimensional Confocal Microscopy." Microscopy and Microanalysis 7, S2 (August 2001): 580–81. http://dx.doi.org/10.1017/s143192760002897x.

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Using human peritoneal explants, we have previously demonstrated that endometrial stromal cells (ESCs) and endometrial epithelial cells (EECs) attach to intact mesothelium. Attachment occurs within one hour and mesothelial invasion occurs within 18 hours (Figure 1). We have also demonstrated that, in vivo, the mesothelium overlies a continuous layer of collagen IV (Col IV).More recently we have used CLSM, to study the mechanism and time course of ESC and EEC attachment and invasion through mesothelial monolayers. in these studies, CellTracker® dyes were used to label cells. Mesothelial cells were labeled with chloromethylbenzoylaminotetramethylrhodamine (CellTracker Orange). Mesothelial cells were then plated on human collagen IV coated, laser etched coverslips. Mesothelial cells were cultured to subconfluence. ESCs and EECs, labeled with chloromethylfluorscein diacetate (CellTracker Green) were plated on the mesothelial monolayers. Cultures were examined at 1, 6, 12 and 24 hours with simultaneous differential interference contrast and CLSM.
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Yung, Susan, Fu Keung Li, and Tak Mao Chan. "Peritoneal Mesothelial Cell Culture and Biology." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 26, no. 2 (March 2006): 162–93. http://dx.doi.org/10.1177/089686080602600207.

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The peritoneal mesothelium is composed of an extensive monolayer of mesothelial cells that lines the body's serous cavity and internal organs and was previously thought to act principally as a protective nonadhesive lubricating surface to facilitate intracoelomic movement. With the introduction of peritoneal dialysis over three decades ago, there has been much interest in the cell biology of peritoneal mesothelial cells. Independent studies have highlighted specific properties of the peritoneal mesothelial cell, including antigen presentation, regenerative properties, clearance of fibrin; synthesis of cytokines, growth factors, and matrix proteins; and secretion of lubricants to protect the tissue from abrasion, adhesion, infection, and tumor dissemination. It is now evident that the mesothelium is not merely a passive membrane but, rather, a dynamic membrane that contributes substantially to the structural, functional, and homeostatic properties of the peritoneum. Since peritoneal mesothelial cells in culture possess immunohistochemical markers identical to mesothelial stem cells, the culture of mesothelial cells offers researchers an essential tool to assess their morphologic, structural, and functional properties. This review will discuss current procedures to isolate peritoneal mesothelial cells from human omental specimens, animal sources, and spent dialysate. Furthermore, the functional and morphologic properties of mesothelial cells are discussed, together with the potential use of mesothelial cell culture in research and clinical applications.
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Hilliard, Tyvette S., Brooke Kowalski, Kyle Iwamoto, Elizabeth A. Agadi, Yueying Liu, Jing Yang, Marwa Asem, et al. "Host Mesothelin Expression Increases Ovarian Cancer Metastasis in the Peritoneal Microenvironment." International Journal of Molecular Sciences 22, no. 22 (November 18, 2021): 12443. http://dx.doi.org/10.3390/ijms222212443.

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Mesothelin (MSLN), a glycoprotein normally expressed by mesothelial cells, is overexpressed in ovarian cancer (OvCa) suggesting a role in tumor progression, although the biological function is not fully understood. OvCa has a high mortality rate due to diagnosis at advanced stage disease with intraperitoneal metastasis. Tumor cells detach from the primary tumor as single cells or multicellular aggregates (MCAs) and attach to the mesothelium of organs within the peritoneal cavity producing widely disseminated secondary lesions. To investigate the role of host MSLN in the peritoneal cavity we used a mouse model with a null mutation in the MSLN gene (MSLNKO). The deletion of host MSLN expression modified the peritoneal ultrastructure resulting in abnormal mesothelial cell surface architecture and altered omental collagen fibril organization. Co-culture of murine OvCa cells with primary mesothelial cells regardless of MSLN expression formed compact MCAs. However, co-culture with MSLNKO mesothelial cells resulted in smaller MCAs. An allograft tumor study, using wild-type mice (MSLNWT) or MSLNKO mice injected intraperitoneally with murine OvCa cells demonstrated a significant decrease in peritoneal metastatic tumor burden in MSLNKO mice compared to MSLNWT mice. Together, these data support a role for host MSLN in the progression of OvCa metastasis.
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Kao, Hao-Hsi, Chang-Yi Kuo, Kuo-Su Chen, and Jyh-Ping Chen. "Preparation of Gelatin and Gelatin/Hyaluronic Acid Cryogel Scaffolds for the 3D Culture of Mesothelial Cells and Mesothelium Tissue Regeneration." International Journal of Molecular Sciences 20, no. 18 (September 12, 2019): 4527. http://dx.doi.org/10.3390/ijms20184527.

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Mesothelial cells are specific epithelial cells that are lined in the serosal cavity and internal organs. Nonetheless, few studies have explored the possibility to culture mesothelial cells in a three-dimensional (3D) scaffold for tissue engineering applications. Towards this end, we fabricated macroporous scaffolds from gelatin and gelatin/hyaluronic acid (HA) by cryogelation, and elucidated the influence of HA on cryogel properties and the cellular phenotype of mesothelial cells cultured within the 3D scaffolds. The incorporation of HA was found not to significantly change the pore size, porosity, water uptake kinetics, and swelling ratios of the cryogel scaffolds, but led to a faster scaffold degradation in the collagenase solution. Adding 5% HA in the composite cryogels also decreased the ultimate compressive stress (strain) and toughness of the scaffold, but enhanced the elastic modulus. From the in vitro cell culture, rat mesothelial cells showed quantitative cell viability in gelatin (G) and gelatin/HA (GH) cryogels. Nonetheless, mesothelial cells cultured in GH cryogels showed a change in the cell morphology and cytoskeleton arrangement, reduced cell proliferation rate, and downregulation of the mesothelium specific maker gene expression. The production of key mesothelium proteins E-cadherin and calretinin were also reduced in the GH cryogels. Choosing the best G cryogels for in vivo studies, the cell/cryogel construct was used for the transplantation of allograft mesothelial cells for mesothelium reconstruction in rats. A mesothelium layer similar to the native mesothelium tissue could be obtained 21 days post-implantation, based on hematoxylin and eosin (H&E) and immunohistochemical staining.
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Betjes, Michiel G. H., Harry J. Bos, Raymond T. Krediet, and Lambertus Arisz. "The Mesothelial Cells in CAPD Effluent and Their Relation to Peritonitis Incidence." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 11, no. 1 (January 1991): 22–26. http://dx.doi.org/10.1177/089686089101100106.

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The total cell count and cell differentiation of the overnight peritoneal dialysis effluent (PDE) was analysed in 34 long-term CAPD patients. The mean percentage and yield of mesothelial cells were 3.1% and 0.17 × 106 per PDE. There was a significant lower percentage and yield of mesothelial cells in the PDE of patients with a peritonitis incidence (PI) of more than 2 episodes a year. Independent of dwell time, a positive correlation between the total yield of leucocytes and the yield of mesothelial cells was found. No relation between the amount of phospholipids in the PDE and the yield of mesothelial cells could be shown. Mesothelial cells in the PDE are probably reflecting the turn-over rate of a reactive mesothelium. Whether a low turn-over rate of the mesothelium is causing or is caused by a high PI needs further investigation.
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Yung, Susan, and Tak Mao Chan. "Intrinsic Cells: Mesothelial Cells — Central Players in Regulating Inflammation and Resolution." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 29, no. 2_suppl (February 2009): 21–27. http://dx.doi.org/10.1177/089686080902902s03.

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Background Preservation of the structural and functional integrity of the peritoneum is essential to maintain the dialytic efficacy of the peritoneal membrane. Although much improvement has been made to peritoneal dialysis (PD) fluids, they remain bioincompatible, and together with peritonitis, they continue to induce peritoneal inflammation and fibrosis. Method This article reviews the putative factors that mediate mesothelial cell inflammation during PD, and the mechanisms by which mesothelial cells attempt to regulate and resolve peritoneal inflammation. Results The mesothelium is the first line of defense to foreign particles and chemicals in the peritoneal cavity. Constant exposure of the mesothelium to the bioincompatible constituents of PD solutions results in denudation of the mesothelium and loss of the peritoneal cavity's protective layer. Detached mesothelial cells in PD solutions have the capacity to replenish the mesothelial layer through their ability to migrate and attach to areas of denudation. Mesothelial cells synthesize a plethora of growth factors, matrix proteins, and proteoglycans that aid in the reparative process and regulate the formation of chemotactic gradients that are essential for infiltration of leukocytes to sites of injury. Conclusions Far from being bystanders in peritoneal function, mesothelial cells have been shown to play a dynamic role in peritoneal homeostasis and immunoregulation. Studies have highlighted the potential use of mesothelial cells in gene therapy and cell transplantation, both of which may provide novel therapeutic strategies for the preservation of the peritoneum during PD.
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Dissertations / Theses on the topic "Mesothelial"

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Lin, Judy Li-Wen. "Mechanisms of mesothelial tissue lubrication." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/36249.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2006.
"June 2006."
Includes bibliographical references (p. 63-64).
In the pleural space, sliding between the lung and chest wall induces shear stress that could damage the delicate mesothelial cells covering the tissue surfaces. Normally, the pleural space, which is filled with fluid, is able to sustain continuous shear loading throughout its lifetime. To understand the mechanisms in preventing frictional damage on mesothelial tissue, we conducted experiments using abdominal tissue excised from a rat. We allowed the tissue to slide against a glass surface, and measured the fluid thickness and shear force between them. We also studied independent variables such as location on the tissue, applied normal load, sliding velocity and direction to determine their effects on mesothelial tissue lubrication. Both thickening and thinning of the fluid layer were observed during sliding. The fluid thickness was found to change with sliding velocity and direction, but invariant with location on tissue surface. In tribological experiments, shear force decreased with increasing velocity until it reached a minimum value varying with different tissue samples. Normal load had a strong effect on shear force, but not on friction coefficient.
(cont.) Overall, the friction curves had similar shape as described by the mixed/elasto-hydrodynamic regions of the Stribeck curve. Results were consistent within each tissue sample, but varied among samples. The dependency on velocity and direction suggested elasto-hydrodynamic lubrication. Taken together, we conclude that elasto-hydrodynamic lubrication is likely to be an important lubrication mechanism for mesothelial tissue sliding in the pleural region. Our findings support the existence of a continuous fluid layer separating the pleural surfaces. The fluid pressure gradient generated by surface roughness redistributes fluid from thick to thin regions preventing surface contact.
by Judy Li-Wen Lin.
S.M.
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Davidowitz, Rachel Alexis. "Mechanisms Governing Mesothelial Clearance by Ovarian Cancer Spheroids." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10719.

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Metastatic dissemination of ovarian tumors involves the invasion of multi-cellular tumor cell clusters into the mesothelial cell lining of organs in the peritoneal cavity. We developed an in vitro assay that models this initial step of ovarian cancer metastasis to investigate the mechanisms of invasion. Pre-clustered ovarian cancer multicellular spheroids are incubated with GFP-expressing mesothelial monolayers and the extent of mesothelial invasion is monitored by time-lapse video microscopy.
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Dixit, Radhika Nagaraj. "The contribution of mesothelial cells to lung development." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12825.

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Thesis (Ph.D.)--Boston University
Mesothelium-derived progenitors have been demonstrated to contribute to differentiated mesenchymal components of the heart, liver, and gut during organogenesis. The precise contribution of the mesothelium to lung development, however, has not been fully clarified and the key signals regulating mesothelial cell entry have not been identified. To rigorously address this issue, we employed mice with an inducible Cre expressed from the Wilm's tumor-1 (WT1) locus for high fidelity lineage tracing after confirming that Cre-recombinase was mesothelial-specific and faithfully recapitulated endogenous WT1 gene expression. We visualized WT1+ mesothelial cell entry into the fetal lung by live imaging and identified their progenies in subpopulations of bronchial smooth muscle cells, vascular smooth muscle cells, and desmin+ fibroblasts by lineage tagging. In view of the role of Sonic Hedgehog (Hh) signaling in regulating mesenchymal cell differentiation and epithelial-mesenchymal transition, we hypothesized that this pathway regulates events associated with migration of mesothelial cells into the developing lung. To examine for this, we first used two independent reporter mice to show that Hh signaling is active within the lung mesothelium at time points coinciding with the appearance of mesothelium-derived cells in the lung parenchyma. Using loss-of-function assays in organ cultures, and targeted mesothelial-restricted loss-of hedgehog function mice, we demonstrated that mesothelial cell movement into the lung requires the direct action of Hh signaling. In order to examine whether WT1 interacts with Hh pathway, we conducted ChIP assays on fetal lung mesothelial cells, and found that WT1 directly binds and regulates promoter elements of downstream targets of Hh pathway. Consistent with this observation, Hh pathway gene expression was down-regulated in isolated WT1 deficient fetal lung mesothelial cells. Taken together, these findings lend further support to a paradigm in which mesothelial cells are an important source of progenitors for mesenchymal structures. Our findings also reveal a role for Hh pathway in the early events associated with mesothelial cell entry and indicate that WT1 likely acts upstream of Hh signaling.
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Gulyás, Miklós. "Mesothelial differentiation, mesothelioma and tumor markers in serous cavities /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-566-2/.

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Yung, S. S. Y. "Characterization of proteoglycans synthesized by human peritoneal mesothelial cells." Thesis, Swansea University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636722.

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This thesis consists of three studies on the synthesis of proteoglycans (PGs) and hyaluronan (HA) in relation to peritoneal dialysis. In the first study, newly synthesized proteoglycans from human peritoneal mesothelial cells were labelled in vitro with either 35S-sulphate, 3H-glucosamine or 35S-methionine for 24h, and were characterised using biochemical and immunological techniques. The following were identified: i). a large chondroitin sulphate proteoglycan (CSPG I), Mr > 1000 kDa, protein core > 400 kDA, which was present in both the culture medium (CM) and the cell layer extract (CL). ii). a minor dermatan sulphate proteoglycan (DSPG I), Mr 200 kDa, protein core 45 kDa, also present in the CM and identified as biglycan. iii). a second small dermatan sulphate proteoglycan (DSPG I), Mr 110 kDa, protein core 43 and 47 kDa, and found solely in theCM. This proteoglycan, identified as decorin, was thepredominant species. iv). a large heparan sulphate proteoglycan (HSPG I), Mr 1200 kDa, isolated in both the CM and in the cytoskeletal-matrix which may be related to perlecan. v). a cell surface hybrid proteoglycan (containing both HS and CS chains), Mr 190-210 kDa, and identified as syndecan. vi). a glycosylphosphatidylinositol-anchored heparan sulphate (HSPF II), Mr ≈190 kDa and identified as glypican. In addition to these proteoglycans, a large amount of free CS/HS GAGs were present (70% of the total CL). Pulse chase data revealed that these GAG chains were undergoing degradation. In the second study, proteoglycans were isolated from CAPD fluid and characterised. The results revealed that decorin was the predominant species with minor amounts of biglycan. Finally, the presence of HA in CAPD fluid was monitored. Results showed that the HA levels are elevated during peritonitis, but with successful treatment, the levels returned to normal. In vitro studies suggested that peritoneal mesothelial cells were the likely source of the HA.
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Dauleh, S. "Characterising mesothelial cell cultures derived from the murine omentum." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3004240/.

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Mesothelial cells have been described to possess progenitor characteristics and contribute to regeneration through differentiation. However, it is not clear what the effects of prolonged culture have on the mesothelial cell properties and relative plasticity; as long-term cultures have not yet been established as a result of early senescence. Understanding the effects of time in culture is crucial for the development of novel therapies. In this thesis, we demonstrated that mesothelial cell cultures isolated from murine omentum could be cultured for more than 40 passages and showed relatively stable population doubling times. While initially, the cells did down-regulated the expression of mesothelial markers Wilm’s tumor protein 1 (Wt1) and mesothelin and epithelial genes; their mesenchymal profile was maintained. This along with the increased Snail2 expression suggested the cells were progressing through the mesothelial to mesenchymal (MMT) transdifferentiation programme. TGF-β and more recently EGF are known mediators of MMT. Targeting signalling through these receptors with small molecule inhibitors LY364947 and PD153035, slowed the rate of gap closure, in vitro and increased zonula occludens 1 accumulation at cell-cell contacts. Which seemed to be mediated through the MEK5/ERK5 pathway. Furthermore, siRNA-mediated transient knockdown of Zeb1 and Zeb2 transcription factors also achieved attenuated the rate of migration. Next, we moved onto to accessing the progenitor properties of the mesothelial cells with time in culture. The expression of stem cells markers Bmi1 (Proto-Oncogene, Polycomb Ring Finger), Sox9 ((Sex Determining Region Y)-Box 9) and CD34 were downregulated with repeated passaging. However, the low passage mesothelial cells exhibited clonogenicity and could differentiate into osteoblasts and adipocytes. Finally, in an embryonic kidney rudiment assay, we could show that the mesothelial cells co-existed with the embryonic kidney cells and allowed renal structures to form in their presence. Ultimately, we have demonstrated that the mesothelial cells from the omentum maintain some mesothelial characteristics with prolonged culturing. The cells showed clonogenic and multi-lineage potential and expressed a number of stem cell genes. The MMT programme is complex and could be partly reversed by targeting TGF-βR1 and EGFR tyrosine kinases, which along with transiently silencing the Zeb transcriptional factors seem likely key targets in ameliorating pathological fibrosis.
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Swain, William Alexander. "Cell signalling pathways in mesothelial cells treated with mineral fibres." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/30767.

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Malignant mesothelioma (MM) is a major health problem as it is an invariably fatal disease resulting from occupational exposure to asbestos. The long latency period of this disease means that death rates will continue to rise for 10-20 years before improved exposure regulations take effect. The studies described here were designed to explore mechanisms by which asbestos exposure elicits this malignancy. Cell signalling events germane to malignant transformation were investigated in rat (4/4 RM4) and human (MET5A) mesothelial cells in vitro following exposure to asbestos. The activation state of the MAPK family and Akt were probed, because these pathways are pivotal in determining death or survival of the cell. The results suggest that extracellular signal regulated protein kinase (ERK), p38 and Akt are activated by asbestos exposure. For the former two, at least, this activation depended on oxidative stress. A selective inhibitor of EGFR tyrosine kinase, PKI166, inhibited asbestos-mediated Akt and ERK activation. Asbestos-mediated Akt activation was also inhibited by LY294002, an inhibitor of phosphatidylinositol 3-kinase (P13K). The effect of events triggered by asbestos downstream of these kinases, on the transcription factors activator protein (AP) -1 and nuclear factor-kB (NF-kB) were investigated. Pharmacological inhibition of either the ERK pathway by UO126 or the p38 pathway by SB203580 ameliorated crocidolite-induced AP-1 activation. Inhibition of the Akt pathway by LY294002 or PKI166 reduced crocidolite-induced NF-kB translocation. The same panel of inhibitors were used to investigate the role of these pathways in defined endpoints characteristic of asbestos exposure i.e. cell death and survival/proliferation. In both cell lines the p38 pathway was involved in cell death and the Akt pathway in survival. In 4/4 RM4 cells activation of the ERK pathway also induced cell death. In contrast, in MET5A cells ERK appeared to be involved in survival.
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Mohamed, Moinuddin Mohammed. "Characterisation of peritoneal calcification in encapsulating peritoneal sclerosis." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-peritoneal-calcification-in-encapsulating-peritoneal-sclerosis(003593cd-01f0-4e7b-a22b-d216451f6a93).html.

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Encapsulating peritoneal sclerosis (EPS) is a rare complication of long-term peritoneal dialysis (PD). EPS is associated with extensive thickening and fibrosis of the peritoneum resulting in the formation of a fibrous cocoon encapsulating the bowel leading to intestinal obstruction. The presence of peritoneal thickening, peritoneal calcification and bowel obstruction is considered to be diagnostic of EPS. The current understanding of the pathogenesis of EPS is through the 'two-hit' fibrosis model. This model, however, does not explain the development of peritoneal calcification in patients with EPS. This thesis addresses the hypothesis that altered bone mineral metabolism in ESRF patients together with the mechanical stress of PD influences mesothelial cells to differentiate into osteoblasts promoting calcification in peritoneal tissue. Peritoneal calcification leads to increased tissue stiffness causing progressive fibrosis and the development of EPS. We compared the temporal evolution of the levels of bone mineral markers during PD between patients who developed EPS and control patients on PD. We found that raised serum levels of calcium, phosphate and alkaline phosphatase during PD increased the risk of development of EPS. We compared peritoneum from patients with EPS with that of PD patients without EPS using histological techniques. We found that calcification, organised fibrillary collagen and elastic fibres were significantly more abundant in the EPS peritoneum. Peritoneal calcification was also generalised and distributed not only on the peritoneal surface but also in the sub-mesothelial zone of fibrosis. EPS peritoneum also exhibited osteocalcin, an osteogenic protein, suggesting a cellular mechanism of calcification. Atomic force microscopy of EPS peritoneum showed increased stiffness when compared to control PD peritoneum with the areas of calcification possibly contributing to the increase in tissue stiffness. Human omental cells (HOMCs) were isolated by protease digestion and characterised using a panel of mesothelial markers. HOMCs were cultured in phosphate rich media and phosphate and calcium rich media. HOMCs when cultured with high extracellular levels of calcium showed accelerated mineralisation with upregulation of osteogenic transcription factor runx-2 suggesting osteoblastic transformation. In summary, this thesis indicates that poorly controlled secondary hyperparathyroidism is a risk factor for the development of EPS. On a background of PD related simple sclerosis, uncontrolled secondary hyperparathyroidism can lead to the transformation of mesothelial cells to osteoblasts. This leads to increased matrix deposition and matrix mineralisation causing increased matrix stiffness. Increase in matrix stiffness leads to progressive fibrosis culminating in EPS. Peritoneal calcification can act as the second hit leading to progressive fibrosis and development of EPS.
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Medcalf, James Frederick. "The role of mesothelial cell biology in peritoneal fibrosis on CAPD." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29376.

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Worldwide 100,000 people are dependent on peritoneal dialysis (PD) for treatment of end-stage renal failure. Long term technique survival is limited by peritoneal membrane fibrosis and loss of membrane function. The human peritoneal mesothelial cell (HPMC) is the one of the most abundant cells in the peritoneal cavity, and is in direct contact with the peritoneal dialysate. The aim of these experiments was to investigate the role of the HPMC in the regulation of peritoneal fibrosis in the context of peritoneal dialysis. Hyperosmolar glucose lactate-buffered dialysate is the most widely used dialysis solution. A culture system was developed to grow HPMC from uraemic patients undergoing PD catheter insertion. The effect exposure to a 50:50 mixture of dialysate and M199 for 12 hours was examined. Glucose was varied between 5-40mmol/L. Increases in glucose concentration caused a decrease in cell viability, a decrease in proliferation, and increase in fibronectin mRNA and protein amount. The mechanism responsible for glucose induced increase in fibronectin was examined. Increasing glucose caused an increase in HPMC TGF- protein amount. Exogenous TGF- caused a dose dependent increase in HPMC fibronectin production, and increase mRNA for fibronectin and TGF- itself. An anti TGF- Antibody prevented glucose induced HPMC fibronectin production. Two alternative dialysis solutions were investigated; a different osmotic agent (amino acid dialysate), and a different dialysate buffer (bicarbonate). Amino acid dialysate showed less cytotoxicity, but inhibited proliferation, and caused TGF- mediated fibronectin production. Although amino acid dialysate contains 3.3 mmo1/L L-arginine, NO was not shown to mediate this response. Dialysate with bicarbonate:lactate buffer allowed greater HPMC proliferation, and no inhibition of proliferation with hyperosmolar glucose previously seen with lactate buffered dialysate. These studies suggest the HPMC has a role in the production and regulation of ECM, and that TGF- is an important intermediary.
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Sun, Xiaojuan. "Studies on mesothelial differentiation : prognostic and therapeutic approaches to malignant mesothelioma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-513-5/.

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Books on the topic "Mesothelial"

1

Robinson, Robert Joseph. Metastatic or mesothelial cells: Two more antibodies. [s.l: The Author], 1991.

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McKee, Janet. The use of lectins to distinguish between reactive mesothelial cells, malignant mesothelioma and adenocarcinoma in serous fluids. [s.l: The Author], 1991.

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Jones, J. S. P., ed. Pathology of the Mesothelium. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1404-8.

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Jones, J. S. P., 1929-, ed. Pathology of the mesothelium. London: Springer-Verlag, 1987.

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Czyżewska, Krystyna. Funkcje mezotelium otrzewnej: Studium problemu w medycynie eksperymentalnej. Warszawa: Wydawn. Nauk. PWN, 1992.

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Zarogiannis, Sotirios G., ed. Mesothelial Physiology and Pathophysiology. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-541-6.

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1944-, Jaurand Marie-Claude, and Bignon Jean, eds. The Mesothelial cell and mesothelioma. New York: M. Dekker, 1994.

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8

Pass, Harvey I., John A. Dingell, and Susan Vento. 100 Questions & Answers About Mesothelioma (100 Questions & Answers about . . .). Jones and Bartlett Publishers, Inc., 2004.

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Lake, Sarah, Sarah Ann Lake, Harvey I. Pass, and Mary Hesdorffer. 100 Questions and Answers about Mesothelioma. Jones & Bartlett Learning, LLC, 2022.

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Tumors Of The Serosal Membranes (Atlas of Tumor Pathology 3rd Series). AMERICAN REGISTRY OF PATHOLOGY, 1995.

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Book chapters on the topic "Mesothelial"

1

Fisher, Cyril. "Mesothelial Lesions." In Atlas of Soft Tissue Tumor Pathology, 75–78. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7025-0_7.

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Hoffhines, Adam. "Mesothelial Cell Hyperplasia." In Encyclopedia of Pathology, 279–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-66796-6_371.

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Brcic, Iva. "Mesothelial Cyst, Mediastinal." In Encyclopedia of Pathology, 281–83. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-66796-6_41.

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Ali, Syed Z., and Edmund S. Cibas. "Reactive Mesothelial Hyperplasia." In Serous Cavity Fluid and Cerebrospinal Fluid Cytopathology, 19–34. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1776-7_3.

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Bomeisl III, Philip E., and Claire W. Michael. "Mesothelial Cells, Reactive." In Encyclopedia of Pathology, 265–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33286-4_920.

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Weissferdt, Annikka. "Mesothelial Tumors of the Pleura." In Diagnostic Thoracic Pathology, 697–725. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36438-0_22.

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Nistal, Manuel, Pilar González-Peramato, and Álvaro Serrano. "Reactive Mesothelial Hyperplasia Versus Mesothelioma." In Clues in the Diagnosis of Non-tumoral Testicular Pathology, 311–17. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49364-0_35.

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Mullen, Mary, Hollie Noia, and Katherine Fuh. "Culturing Primary Human Mesothelial Cells." In Methods in Molecular Biology, 147–54. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1956-8_9.

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Weissferdt, Annikka. "Non-mesothelial Tumors of the Pleura." In Diagnostic Thoracic Pathology, 727–66. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36438-0_23.

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Davidson, Ben, and Bojana Djordjevic. "Mesothelial Tumors, Pathology of the Peritoneum." In Encyclopedia of Pathology, 1–6. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-319-28845-1_5674-1.

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Conference papers on the topic "Mesothelial"

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Tucker, T. A., Y. Tsukasaki, T. Sakai, S. Mitsuhashi, A. Jeffers, S. Idell, and M. Ikebe. "Myocardin Is Involved in Mesothelial-Mesenchymal Transition of Human Pleural Mesothelial Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5348.

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Choo, Y., T. Sakai, R. Ikebe, A. Jeffers, S. Idell, T. A. Tucker, and M. Ikebe. "Calponin 1 Promotes Myofibroblast Differentiation of Human Pleural Mesothelial Cells During Mesothelial Mesenchymal Transition." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4420.

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Malkawi, A., A. I. Saeed, and A. Wright. "Transforming or Coexisting: Pleural Mesothelial Hyperplasia and Mesothelioma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7002.

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Dixit, Radhika N., Xingbin Ai, and Alan Fine. "The Contribution Of Mesothelial-Derived Cells To Lung Development." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2237.

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Tucker, T. A., A. Jeffers, S. Owens, W. Qin, and S. Idell. "NOX1 Targeting Attenuates Mesothelial Mesenchymal Transition and Pleural Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6390.

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Zolak, Jason S., Rajesh Jagirdar, Qiang Ding, Rui-Ming Liu, Octavio Oliva, Victor J. Thannickal, and Veena B. Antony. "Pleural Mesothelial Cells In The Pathogenesis Of Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5559.

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Nakamura, Koji, Kenjiro Sawada, Yasuto Kinose, Akihiko Yoshimura, Erika Nakatsuka, Seiji Mabuchi, and Tadashi Kimura. "Abstract 5060: Exosome transfer from ovarian cancer cells to mesothelial cells promotes cell invasion by upregulating MMP-9 secretion and increasing clearance of mesothelial cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5060.

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Tucker, T. A., O. Ogunsakin, A. Jeffers, S. Owens, W. Qin, S. Komatsu, M. Ikebe, and S. Idell. "NOX1 Attenuates Mesothelial-Mesenchymal Transition Through Modulation of ROS Mediated Signaling." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5347.

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Solenov, Evgeniy, Alexander Ershov, Galina Baturina, Lubov Katkova, Chrissi Hatzoglou, Konstantinos Gourgoulianis, and Sotirios Zarogiannis. "Water and urea transport in benign and malignant pleural mesothelial cells." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2864.

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Tucker, Torry A., LaTerrica Williams, Kathy Koenig, Hema Kothari, Andrey Komissarov, Galina Florova, Andrew P. Mazar, L. V. M. Rao, and Steven Idell. "Lrp1 Regulates Urokinase Receptor-Dependent Pathophysiologic Responses Of Human Pleural Mesothelial Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3485.

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Reports on the topic "Mesothelial"

1

Tilly, Jonathan L. Role of Oocyte Loss in Ovarian Surface Mesothelial Cell Transformation. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada434130.

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Tilly, Jonathan L., and Grant R. MacGregor. Role of Oocyte Loss in Ovarian Surface Mesothelial Cell Transformation. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada413259.

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Tilly, Jonathan L. Role of Oocyte Loss in Ovarian Surface Mesothelial Cell Transformation. Fort Belvoir, VA: Defense Technical Information Center, November 2003. http://dx.doi.org/10.21236/ada424569.

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