Journal articles on the topic 'Mesothelial'
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1
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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Lucas, P. A. "Stem Cells for Mesothelial Repair: An Understudied Modality." International Journal of Artificial Organs 30, no. 6 (June 2007): 550–56. http://dx.doi.org/10.1177/039139880703000613.
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Adhesions are bands of fibrous tissue that form between opposing organs and the peritoneum, restricting vital intrapleural and abdominal movement. They remain a major problem in abdominal surgery, occurring in more than three fourths of patients following laparotomy. Adhesions result when injury to the mesothelium is not repaired by mesothelial cells and can be viewed as scar tissue formation. The mechanism of mesothelial healing suggested the involvement of stem cells in the process. It has long been known that peritoneal wounds heal in the same amount of time regardless of size. Therefore, the mesothelium could not regenerate solely by proliferation and centripetal migration of cells at the wound edge as occurs in the healing of skin epithelium. Several studies suggest the presence of i) mesothelial stem cells that can differentiate into mesothelial cells and a few other phenotypes and/or ii) that mesothelial cells are themselves stem cells. Other studies have suggested that adult stem cells in the muscle underlying the peritoneum can differentiate into mesothelial cells and contribute to healing. Prevention of abdominal adhesions have been accomplished by delivery of autologous mesothelial cells and multipotent adult stem cells isolated from skeletal muscle. Adult stem cells from sources other than the serosal tissue offer an alternative treatment modality to prevent the formation of abdominal adhesions.
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Isotalo, Phillip A., John P. Veinot, and Maha Jabi. "Hyperplastic Mesothelial Cells in Mediastinal Lymph Node Sinuses With Extranodal Lymphatic Involvement." Archives of Pathology & Laboratory Medicine 124, no. 4 (April 1, 2000): 609–13. http://dx.doi.org/10.5858/2000-124-0609-hmciml.
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Abstract We describe a patient with hyperplastic mesothelial cells localized to mediastinal lymph node sinuses. These mesothelial cells were originally misdiagnosed as metastatic carcinoma, and the patient received radiotherapy. Histologic review, immunohistochemistry, and ultrastructural studies confirmed mesothelial cell origin. These nodal mesothelial cells were associated with pericardial and pleural effusions. Extranodal lymphatics also contained hyperplastic mesothelial cells, confirming their mode of lymphatic transport to node sinuses. This finding supports the theory that hyperplastic mesothelial cells derive from reactive serosal mesothelium and are dislodged into draining lymphatics. This is the first report, to our knowledge, that demonstrates the pathogenetic significance of this lymphatic transport mechanism. Awareness of intralymphatic and nodal benign hyperplastic mesothelial cells and their mimicry of invasive malignant neoplasms is important for accurate diagnoses and appropriate therapy.
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Breborowicz, Andrzej, Elias Balaskas, George D. Oreopoulos, Leo Martis, Kenneth Serkes, and Dimitrios G. Oreopoulos. "In Vitro Study of the Effect of Osmotic Solutes on the Interactions between Cells from the Peritoneum and Peritoneal Cavity." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 14, no. 2 (April 1994): 149–54. http://dx.doi.org/10.1177/089686089401400210.
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Objective To study how the presence of osmotic solutes in medium affects growth of the peritoneal mesothelial cells and fibroblasts and how osmotic solutes influence the production of factors regulating growth of these cells. Design The proliferation of mesothelial cells and fibroblasts was evaluated by measuring the incorporation of 3H-thymidine into the cells. Cells were exposed to osmotic solutes; the concentration of the latter in the medium was continuously lowered over the time of the experiment to simulate changes of their concentration in the dialysate. The synthesis of factors influencing the proliferation of the mesothelial cells or fibroblasts, by mesothelial cells or fibroblasts themselves, or by peritoneal leukocytes, was tested by the characteristics of the “conditioned” medium. The conditioned medium was produced by exposing standard medium to mesothelial or fibroblasts monolayer or to peritoneal leukocytes over 24 hours; following filtration it was applied to growing test cells for the study of growth factors. Results The effect of osmotic solutes on the growth of mesothelial cells is less inhibitory when their concentration is gradually lowered over the time of the study, compared to previous findings with a constant concentration. Peritoneal leukocytes produce growth factors for mesothelial cells and fibroblasts. Glucose and amino acids inhibit production of peritonealleukocyte-derived growth factors for mesothelial cells, while glycerol increases synthesis of such growth factors for fibroblasts. Mesothelial cells produce factors stimulating the proliferation of mesothelial cells and fibroblasts. In the presence of glycerol or amino acids synthesis of mesothelium derived growth factors for fibroblasts is augmented. Finally, fibroblasts produce factors that inhibit the proliferation of the mesothelial cells, and this effect is potentiated in the presence of amino acids. Conclusions Cytotoxicity of the osmotic solutes measured by the inhibition of growth of the mesothelial cells or their increased damage is significantly reduced during in vitro kinetic study when the concentration of these solutes is gradually lowered. Presence of osmotic solutes in the medium affects synthesis of growth factors derived from mesothelium, fibroblasts, or peritoneal leukocytes, which affect the proliferation of mesothelial cells or fibroblasts.
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Tsai, Jonathan M., Rahul Sinha, Jun Seita, Nathaniel Fernhoff, Simon Christ, Tim Koopmans, Geoffrey W. Krampitz, et al. "Surgical adhesions in mice are derived from mesothelial cells and can be targeted by antibodies against mesothelial markers." Science Translational Medicine 10, no. 469 (November 28, 2018): eaan6735. http://dx.doi.org/10.1126/scitranslmed.aan6735.
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Peritoneal adhesions are fibrous tissues that tether organs to one another or to the peritoneal wall and are a major cause of postsurgical and infectious morbidity. The primary molecular chain of events leading to the initiation of adhesions has been elusive, chiefly due to the lack of an identifiable cell of origin. Using clonal analysis and lineage tracing, we have identified injured surface mesothelium expressing podoplanin (PDPN) and mesothelin (MSLN) as a primary instigator of peritoneal adhesions after surgery in mice. We demonstrate that an anti-MSLN antibody diminished adhesion formation in a mouse model where adhesions were induced by surgical ligation to form ischemic buttons and subsequent surgical abrasion of the peritoneum. RNA sequencing and bioinformatics analyses of mouse mesothelial cells from injured mesothelium revealed aspects of the pathological mechanism of adhesion development and yielded several potential regulators of this process. Specifically, we show that PDPN+MSLN+ mesothelium responded to hypoxia by early up-regulation of hypoxia-inducible factor 1 alpha (HIF1α) that preceded adhesion development. Inhibition of HIF1α with small molecules ameliorated the injury program in damaged mesothelium and was sufficient to diminish adhesion severity in a mouse model. Analyses of human adhesion tissue suggested that similar surface markers and signaling pathways may contribute to surgical adhesions in human patients.
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Garosi, Guido, Enzo Gaggiotti, Giulio Monaci, Simone Brardi, and Nicola Di Paolo. "Biocompatibility of a Peritoneal Dialysis Solution with Amino Acids: Histological Evaluation in the Rabbit." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 18, no. 6 (November 1998): 610–19. http://dx.doi.org/10.1177/089686089801800609.
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Objective To determine the biocompatibility of a peritoneal dialysis (PD) solution containing amino acids compared to PD solutions containing glucose. Design The biocompatibility of three dialysis solutions containing 1.1% amino acids, 1.36% glucose, and 3.86% glucose, respectively, was evaluated in vivo in rabbits. Methods After 60 days of PD, peritoneal histological changes in rabbits were investigated by light and transmission electron microscopy. The parameters investigated were: (1) mesothelial damage; (2) submesothelial edema; (3) submesothelial cell infiltration; (4) submesothelial fibrosis; and (5) vascular alterations. Semiquantitative evaluations were performed for all the above alterations; quantitative morphometric evaluation was performed for mesothelial damage (cubic transformation of the mesothelium, areas devoid of mesothelium, submesothelial edema) and thickness of peritoneal arteriole walls. Results (1) Mesothelial damage was practically nonexistent in rabbits dialyzed with the solution containing amino acids, and intermediate and severe with low glucose and high-glucose solutions, respectively. Both controls and rabbits dialyzed with amino acid solution showed flat continuous mesothelium; rabbits dialyzed with low-glucose solution showed cubic continuous mesothelium; and rabbits dialyzed with high-glucose solution showed cubic discontinuous mesothelium. Cytopathic mesothelial effects were slight with the solution containing amino acids and severe with both the low and high-glucose solutions. Duplication and thickening of mesothelial basement membrane were never observed. (2) Submesothelial edema showed a worsening trend from controls to rabbits dialyzed with solution containing amino acids, low glucose, and high glucose. (3) No difference in submesothelial infiltration was found between groups. (4) Submesothelial fibrosis was never observed. (5) Vascular alterations were never observed. Conclusion These results are evidence that PD solution with amino acids is more biocompatible than high and also low-glucose solutions.
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Breborowicz, Andrzej, Justyna Wisniewska, Alicja Polubinska, Katarzyna Wieczorowska Tobis, Leo Martis, and Dimitrios G. Oreopoulos. "Role of Peritoneal Mesothelial Cells and Fibroblasts in the Synthesis of Hyaluronan during Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 18, no. 4 (July 1998): 382–86. http://dx.doi.org/10.1177/089686089801800406.
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Objective To assess the in vitro synthesis rate of hyaluronan (HA) by human peritoneal mesothelial cells and peritoneal fibroblasts in the presence of effluent dialysate from continuous ambulatory peritoneal dialysis (CAPD) patients. Methods We used primary cultures of human peritoneal mesothelial cells and peritoneal fibroblasts from nonuremic patients to study the effect of interleukin-1 β (11–1 β) and pooled effluent dialysate, from noninfected and infected CAPD patients, on the synthesis of HA by the studied cells. We also tested the effect of the exogenous HA on the synthesis rate of that glycosaminoglycan. We studied the correlation between HA concentration in effluent dialysate and the stimulatory effect of that solution on in vitro synthesis of HA by mesothelium. Results Peritoneal fibroblasts produce more HA than mesothelial cells. Noninfected effluent dialysates or dialysates from CAPD patients with peritonitis stimulate synthesis of HA by mesothelial cells and fibroblasts. Interleukin-1 β has a stimulating effect, which was synergistic with effluent dialysates, on the synthesis of HA by mesothelium and peritoneal fibroblasts. A weak correlation was demonstrated between the level of HA in effluent dialysate and the stimulatory effect of that dialysate on in vitro synthesis of HA by mesothelial cells. Conclusions Peritoneal fibroblasts are a more potent source of HA than are mesothelial cells, but probably the latter are the main source of HA in drained dialysate. Although effluent dialysates contain factors that stimulate the production of HA by mesothelium, there is weak correlation between that stimulatory effect and the actual HA concentration in the dialysate, which, in some patients, might suggest low “responsiveness” of the membrane.
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Mutsaers, S. E., C. Prêle, S. M. Lansley, and S. E. Herrick. "The Origin of Regenerating Mesothelium: A Historical Perspective." International Journal of Artificial Organs 30, no. 6 (June 2007): 484–94. http://dx.doi.org/10.1177/039139880703000606.
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Bichat first described the mesothelium in 1827 but despite its early discovery, it has only been in recent years that its importance both in health and disease has been realised. One area still poorly understood is that of the mechanisms regulating mesothelial repair. Mesothelial cells are derived from the mesoderm but express many epithelial characteristics. However, mesothelium does not heal in the same way as other epithelial-like cells. Epithelium heals by centripetal migration, with cells at the edge of the wound proliferating and migrating into the injured area. Hertzler in 1919 noted that both large and small peritoneal injuries healed within the same time frame, concluding that the mesothelium could not heal solely by centripetal migration. The exact mechanisms involved in mesothelial regeneration following injury are controversial with a number of proposals suggested to explain the origin of the regenerating cells. This review will examine these proposals and give some insights into the likely mechanisms involved.
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Hjelle, J. Thomas, Marcia A. Miller-Hjelle, and James W. Dobbie. "The Biology of the Mesothelium during Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 15, no. 7_suppl (October 1995): 13–23. http://dx.doi.org/10.1177/089686089501507s03.
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Substantial derangements of mesothelial biology are observed during experimental simulations of dialysis conditions, inferred from the content of human dialysis effluent and visualized by microscopy of human mesothelial biopsies. Canosmotically active solutions be made biocompatible with the osmoregulatory system of the mesothelium? Can the contributions of the mesothelium to host defenses against inflammation and/or infection be supported during CAPD? Do underlying metabolic derangements present in various kidney diseases and end-stage renal disease, regardless of cause, require customized CAPD protocols and solutions? Use of dialysis solutions less directly toxic to the mesothelium is a necessary step toward some day manipulating peritoneal biology by pharmacological and therapeutic modalities.
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Miclăuş, V., A. Mihalca, A. Gal, and C. Cătoi. "Mesothelial metaplasia in European pond turtle, Emys orbicularis (Testudines: Emydidae) infected with Spiroxys contortus (Nematoda: Spirurida)." Helminthologia 50, no. 2 (June 1, 2013): 104–7. http://dx.doi.org/10.2478/s11687-013-0116-4.
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AbstractThe mesothelium consists of a monolayer of specialized epithelial cells that line the surfaces of the peritoneal, pleural, and pericardial cavities. The present study reports mesothelial changes associated with larval stages of the spirurid nematode Spiroxys contortus in a naturally infected European pond turtle. Between 2002 and 2007, eight European pond turtle, Emys orbicularis were brought for necropsy. In one adult male turtle, necropsy revealed the presence of gastric and mesothelial changes associated with gastric infestation with the nematode Spiroxys contortus. Gastrointestinal samples with gross lesions were collected and processed by paraffin technique for further histological examination. Mesothelial cuboidal to columnar or pseudostratified focal progressive metaplasia was observed in visceral coelomic cavity. Intracytoplasmic acidophilic hyaline inclusions were also observed in metaplastic mesothelial cells, most of them being placed to the apical cell’s poles. The significance of our findings is discussed in the light of current knowledge regarding the mesothelial cells.
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Mohammed, Kamal A., Najmunnisa Nasreen, Joyce Hardwick, Carolyn S. Logie, Carolyn E. Patterson, and Veena B. Antony. "Bacterial induction of pleural mesothelial monolayer barrier dysfunction." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (July 1, 2001): L119—L125. http://dx.doi.org/10.1152/ajplung.2001.281.1.l119.
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Pneumonia remains one of the most common infectious causes of mortality. Patients with pneumonia develop parapneumonic effusions with a high neutrophil count as well as high protein concentrations. We hypothesized that pulmonary parenchymal bacterial infection causes a permeability change in the pleural mesothelium by inducing the production of vascular endothelial growth factor (VEGF). Complicated parapneumonic pleural effusions (empyema) have a 19-fold higher VEGF level than pleural fluids secondary to congestive heart failure and a 4-fold higher level than pleural fluids secondary to uncomplicated parapneumonic effusions. We also analyzed the influence of live Staphylococcus aureus on mesothelial barrier function using a model of confluent mesothelial monolayers. There was a significant drop in electrical resistance across S. aureus-infected pleural mesothelial cell (PMC) monolayers. Recombinant VEGF also decreases PMC electrical resistance. Neutralizing antibodies to VEGF significantly inhibited the drop in PMC electrical resistance caused by S. aureus. S. aureusinfection also caused a significant increase in protein leak across confluent mesothelial monolayers. Our results suggest that bacterial pathogens induce VEGF release in mesothelial cells and alter mesothelial permeability, leading to protein exudation in empyema.
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Nasreen, Najmunnisa, Kamal A. Mohammed, Gabriella Galffy, Melissa J. Ward, and Veena B. Antony. "MCP-1 in pleural injury: CCR2 mediates haptotaxis of pleural mesothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 3 (March 1, 2000): L591—L598. http://dx.doi.org/10.1152/ajplung.2000.278.3.l591.
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Pleural injury results in the death of mesothelial cells and denudation of the mesothelial basement membrane. Repair of the mesothelium without fibrosis requires proliferation and migration of mesothelial cells into the injured area. We hypothesized that monocyte chemoattractant protein-1 (MCP-1) induces proliferative and haptotactic responses in pleural mesothelial cells (PMCs) and that the MCP-1 binding receptor CCR2 mediates the pleural repair process. We demonstrate that PMCs exhibited MCP-1-specific immunostaining on injury. MCP-1 induced proliferative and haptotactic responses in PMCs. PMCs express CCR2 in a time-dependent manner. Fluorescence-activated cell sorting analysis demonstrated that interleukin (IL)-2 upregulated CCR2 protein expression in PMCs, whereas lipopolysaccharide (LPS) downregulated the response at the initial period compared with that in resting PMCs. However, the inhibitory potential of LPS was lost after 12 h and showed a similar response at 24 and 48 h. Haptotactic migration was upregulated in PMCs that were cultured in the presence of IL-2. The increased haptotactic capacity of mesothelial cells in the presence of IL-2 correlated with increased CCR2 mRNA expression. PMCs cultured in the presence of LPS showed decreased haptotactic activity to MCP-1. Blocking the CCR2 with neutralizing antibodies decreased the haptotactic response of PMCs to MCP-1. These results suggest that the haptotactic migration of mesothelial cells in response to MCP-1 are mediated through CCR2, which may play a crucial role in reepithelialization of the denuded basement membrane at the site of pleural injury and may thus contribute to the regeneration of the mesothelium during the process of pleural repair.
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Lüdtke, Timo H., Carsten Rudat, Jennifer Kurz, Regine Häfner, Franziska Greulich, Irina Wojahn, Nurullah Aydoğdu, et al. "Mesothelial mobilization in the developing lung and heart differs in timing, quantity, and pathway dependency." American Journal of Physiology-Lung Cellular and Molecular Physiology 316, no. 5 (May 1, 2019): L767—L783. http://dx.doi.org/10.1152/ajplung.00212.2018.
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The mesothelial lining of the lung, the visceral pleura, and of the heart, the epicardium, derive from a common multipotent precursor tissue, the mesothelium of the embryonic thoracic cavity that also contributes to organ-specific mesenchymal cell types. Insight into mesothelial mobilization and differentiation has prevailedin the developing heart while the mesenchymal transition and fate of the visceral pleura are poorly understood. Here, we use the fact that the early mesothelium of both the lung and the heart expresses the transcription factor gene Wt1, to comparatively analyze mesothelial mobilization in the two organs by a genetic cre-loxP-based conditional approach. We show that epicardial cells are mobilized in a large number between E12.5 and E14.5, whereas pleural mobilization occurs only sporadically and variably in few regions of the lung in a temporally highly confined manner shortly after E12.5. Mesothelium-specific inactivation of unique pathway components using a Wt1creERT2line excluded a requirement for canonical WNT, NOTCH, HH, TGFB, PDGFRA, and FGFR1/FGFR2 signaling in the mesenchymal transition of the visceral pleura but indicated a deleterious effect of activated WNT, NOTCH, and HH signaling on lung development. Epicardial mobilization was negatively impacted on by loss of HH, PDGFRA, FGFR1/2 signaling. Epicardial overactivation of WNT, NOTCH, and HH disturbed epicardial and myocardial integrity. We conclude that mesothelial mobilization in the developing lung and heart differs in timing, quantity and pathway dependency, indicating the organ specificity of the program.
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Justet, Aurélien, Audrey Joannes, Valérie Besnard, Joëlle Marchal-Sommé, Madeleine Jaillet, Philipe Bonniaud, Jean Michel Sallenave, et al. "FGF9 prevents pleural fibrosis induced by intrapleural adenovirus injection in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 5 (November 1, 2017): L781—L795. http://dx.doi.org/10.1152/ajplung.00508.2016.
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Fibroblast growth factor 9 (FGF9) is necessary for fetal lung development and is expressed by epithelium and mesothelium. We evaluated the role of FGF9 overexpression on adenoviral-induced pleural injury in vivo and determined the biological effects of FGF9 on mesothelial cells in vitro. We assessed the expression of FGF9 and FGF receptors by mesothelial cells in both human and mouse lungs. Intrapleural injection of an adenovirus expressing human FGF9 (AdFGF9) or a control adenovirus (AdCont) was performed. Mice were euthanized at days 3, 5, and 14. Expression of FGF9 and markers of inflammation and myofibroblastic differentiation was studied by qPCR and immunohistochemistry. In vitro, rat mesothelial cells were stimulated with FGF9 (20 ng/ml), and we assessed its effect on proliferation, survival, migration, and differentiation. FGF9 was expressed by mesothelial cells in human idiopathic pulmonary fibrosis. FGF receptors, mainly FGFR3, were expressed by mesothelial cells in vivo in humans and mice. AdCont instillation induced diffuse pleural thickening appearing at day 5, maximal at day 14. The altered pleura cells strongly expressed α-smooth muscle actin and collagen. AdFGF9 injection induced maximal FGF9 expression at day 5 that lasted until day 14. FGF9 overexpression prevented pleural thickening, collagen and fibronectin accumulation, and myofibroblastic differentiation of mesothelial cells. In vitro, FGF9 decreased mesothelial cell migration and inhibited the differentiating effect of transforming growth factor-β1. We conclude that FGF9 has a potential antifibrotic effect on mesothelial cells.
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Mackay, A. M., R. P. Tracy, and J. E. Craighead. "Cytokeratin expression in rat mesothelial cells in vitro is controlled by the extracellular matrix." Journal of Cell Science 95, no. 1 (January 1, 1990): 97–107. http://dx.doi.org/10.1242/jcs.95.1.97.
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Rat mesothelial cells co-express vimentin and the simple epithelial cytokeratins. While cytokeratins predominate in situ, under most culture conditions vimentin is the major intermediate filament protein of the cells. This loss of cytokeratin production upon culture can be partly prevented by growing mesothelial cells on a basement membrane matrix. However, the basement membrane-promoted persistence of cytokeratin synthesis is not accompanied by expression of cytokeratin G (no. 19), the major acidic cytokeratin of mesothelium in vivo. While cells grown on plastic establish a prominent juxtanuclear assemblage of tonofilaments, those cultured on basement membrane exhibit cytokeratin filaments which are distributed throughout the cytoplasm and attach to neighboring cells at the plasma membrane. This latter pattern resembles that seen in the intact mesothelium. Intermediate filaments are markers of cellular differentiation, but their roles are obscure. The response of cultured mesothelial cells to different growth substrata supports the hypothesis that intermediate filament synthesis is influenced by cellular contact with the extracellular matrix.
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Oku, Teruaki, Kentaro Shimada, Hiroki Kenmotsu, Yusuke Ando, Chisato Kurisaka, Rikio Sano, Makoto Tsuiji, Shinya Hasegawa, Tetsuya Fukui, and Tsutomu Tsuji. "Stimulation of Peritoneal Mesothelial Cells to Secrete Matrix Metalloproteinase-9 (MMP-9) by TNF-α: A Role in the Invasion of Gastric Carcinoma Cells." International Journal of Molecular Sciences 19, no. 12 (December 9, 2018): 3961. http://dx.doi.org/10.3390/ijms19123961.
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It has recently been recognized that inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), upregulate the secretion of matrix metalloproteinase-9 (MMP-9) from cancer cells and thereby promote peritoneal dissemination. In this study, we found that TNF-α also stimulated peritoneal mesothelial cells to secrete MMP-9 as assessed by zymography. MMP-9 gene expression in mesothelial cells induced by TNF-α was confirmed by quantitative RT-PCR analysis. We then utilized the reconstituted artificial mesothelium, which was composed of a monolayer of mesothelial cells cultured on a Matrigel layer in a Boyden chamber system, to examine the effects of TNF-α on carcinoma cell invasion. The transmigration of MKN1 human gastric carcinoma cells through the reconstituted mesothelium was promoted by TNF-α in a dose-dependent manner. The increased MKN1 cell migration was partially inhibited by the anti-α3 integrin antibody, indicating that the invasion process involves an integrin-dependent mechanism. Finally, we observed that the invasion of MMP-9-knockdown MKN1 cells into Matrigel membranes was potentiated by the exogenous addition of purified proMMP-9. These results suggest that TNF-α-induced MMP-9 secretion from mesothelial cells plays an important role in the metastatic dissemination of gastric cancer.
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Kawanishi, Kunio. "Mesothelial cell transplantation: history, challenges and future directions." Pleura and Peritoneum 1, no. 3 (April 24, 2019): 135–43. http://dx.doi.org/10.1515/pp-2016-0014.
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AbstractMesothelial cells line the surface of the pleura, pericardium, peritoneum and internal reproductive organs. One of their main functions is to act as a non-adhesive barrier to protect against physical damage, however, over the past decades their physiological and pathological properties have been revealed in association with a variety of conditions and diseases. Mesothelium has been used in surgical operations in clinical settings, such as omental patching for perforated peptic ulcers and in glutaraldehyde-treated autologous pericardium for aortic valve reconstruction. Various methods for mesothelial cell transplantation have also been established and developed, particularly within the area of tissue engineering, including scaffold and non-scaffold cell sheet technologies. However, the use of mesothelial cell transplantation in patients remains challenging, as it requires additional operations under general anesthesia in order to obtain enough intact cells for culture. Moreover, the current methods of mesothelial cell transplantation are expensive and are not yet available in clinical practice. This review firstly summarizes the history of the use of mesothelial cell transplantation in tissue engineering, and then critically discusses the barriers for the clinical application of mesothelial cell transplantation. Finally, the recent developments in xenotransplantation technologies are discussed to evaluate other feasible alternatives to mesothelial cell transplantation.
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Huang, Huocong, Zhaoning Wang, Yuqing Zhang, Rachana N. Pradhan, Debolina Ganguly, Raghav Chandra, Gilbert Murimwa, et al. "Abstract C078: Mesothelial cell-derived antigen-presenting cancer-associated fibroblasts induce expansion of regulatory T cells in pancreatic cancer." Cancer Research 82, no. 22_Supplement (November 15, 2022): C078. http://dx.doi.org/10.1158/1538-7445.panca22-c078.
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Abstract Recent studies have identified a unique cancer-associated fibroblast (CAF) population termed antigen-presenting CAFs (apCAFs), characterized by the expression of major histocompatibility complex class II molecules, suggesting a function in regulating tumor immunity. Here, by integrating multiple single-cell RNA-sequencing studies and performing robust lineage-tracing assays, we find that apCAFs are derived from mesothelial cells. During pancreatic cancer progression, mesothelial cells form apCAFs by downregulating mesothelial features and gaining fibroblastic features, a process induced by interleukin-1 and transforming growth factor β. apCAFs directly ligate and induce naive CD4+ T cells into regulatory T cells (Tregs) in an antigen-specific manner. Moreover, treatment with an antibody targeting the mesothelial cell marker mesothelin can effectively inhibit mesothelial cell to apCAF transition and Treg formation induced by apCAFs. Taken together, our study elucidates how mesothelial cells may contribute to immune evasion in pancreatic cancer and provides insight on strategies to enhance cancer immune therapy. Citation Format: Huocong Huang, Zhaoning Wang, Yuqing Zhang, Rachana N. Pradhan, Debolina Ganguly, Raghav Chandra, Gilbert Murimwa, Steven Wright, Xiaowu Gu, Ravikanth Maddipati, Sören Müller, Shannon J. Turley, Rolf A. Brekken. Mesothelial cell-derived antigen-presenting cancer-associated fibroblasts induce expansion of regulatory T cells in pancreatic cancer [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C078.
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Louagie, Y., J. C. Schoevaerdts, B. Maldague, C. Remacle, A. Legrand-Monsieur, E. Lavenne-Pardonge, R. Ponlot, and L. Lambotte. "Experimental Inferior Caval Replacement with Mesothelium." Phlebology: The Journal of Venous Disease 2, no. 1 (March 1987): 37–45. http://dx.doi.org/10.1177/026835558700200111.
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Thrombo-resistance of mesothelial grafts was evaluated by replacing the inferior vena cava in 16 dogs. In 10 dogs, treated by antiplatelet aggregation agents, uniform graft thrombosis happened within 15 days. In six other dogs, the addition of an arterio-venous fistula produced conditions of flow (1385 ± 178 ml/min; mean ± s.e.m.) and velocity (17.1 ± 4.5 cm/s) closer to human values and markedly improved the patency rates (four patent over six up to 6 months P < 0.02). Light microscopy and scanning electron microscopy studies performed on the patent grafts showed well preserved mesothelial cells. Mesothelial fibrinolytic activity was 1160 ± 257 tissue activator units/g tissue before and 846 ± 142 activator units/g tissue after implantation (P = n.s.). Prostaglandin synthesis by native mesothelium was respectively 252 ± 103 and 7 ± 3 pg/ml/mg wet tissue/min for 6-keto-PGF1α and TXB2. The synthesis was reduced for 6-keto-PGF1α in the patent grafts but unaltered for TXB2, This work puts forward the suggestion that mesothelium is a promising venous substitute in conditions of high flow.
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Herrick, S. E., and S. E. Mutsaers. "The Potential of Mesothelial Cells in Tissue Engineering and Regenerative Medicine Applications." International Journal of Artificial Organs 30, no. 6 (June 2007): 527–40. http://dx.doi.org/10.1177/039139880703000611.
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Injury to the serosa through injurious agents such as radiation, surgery, infection and disease results in the loss of the protective surface mesothelium and often leads to fibrous adhesion formation. Mechanisms that increase the rate of mesothialisation are therefore actively being investigated in order to reduce the formation of adhesions. These include intraperitoneal delivery of cultured mesothelial cells as well as administration of factors that are known to increase mesothelial proliferation and migration. An exciting alternative that has only recently received attention, is the possible role of mesothelial progenitor cells in the repair and regeneration of denuded serosal areas. Accumulating evidence suggests that such a population exists and under certain conditions is able to form a number of defined cell types indicating a degree of plasticity. Such properties may explain the extensive use of mesothelial cells in various tissue engineering applications including the development of vascular conduits and peripheral nerve replacements. It is likely that with the rapid explosion in the fields of tissue engineering and regenerative medicine, a greater understanding of the potential of mesothelial progenitor cells to repair, replace and possibly regenerate damaged or defective tissue will be uncovered.
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Di Paolo, N., G. Sacchi, L. Vanni, S. Corazzi, V. Pallini, P. Rossi, E. Gaggiotti, and U. Buoncristiani. "Implant of Autologous Mesothelial Cells in Animals and a Peritoneal Dialysis Patient." International Journal of Artificial Organs 12, no. 8 (August 1989): 485–501. http://dx.doi.org/10.1177/039139888901200802.
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Success in culturing human and animal peritoneal mesothelial cells for the purpose of study, led us to determine whether these cells could be autoimplanted in animals and man during peritoneal dialysis in cases of acute and extensive loss of mesothelial surface area. Using an original biopsy technique, we were able to cultivate and characterize from the structural and caryological point of view, human and rabbit peritoneal mesothelial cells. Staphylococcal peritonitis was provoked in 12 rabbits with in-dwelling peritoneal catheters and after 4 days of antibiotic therapy, 6 of them were autoimplanted with cultured mesothelial cells. In the animals sacrificed on the third and sixth days, direct morphological observation and autoradiographic techniques showed that the transplanted cells had taken and revealed a different picture from that in the non-transplanted rabbits. In a 56 year old female diabetic patient, upon insertion of the first peritoneal catheter, a specimen of mesothelial cells was cultured and then frozen. Seven months later after an episode of peritonitis from Candida which dictated removal of the peritoneal catheter, since there was a sufficient number of cultured mesothelial cells and the patient consented, the implant was performed. Peritoneal biopsy by laparoscopy three and six days later showed that the cells had taken. The purpose of the study was merely to show that autoimplant of mesothelium in man and animals is possible.
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Jonjić, N., G. Peri, S. Bernasconi, F. L. Sciacca, F. Colotta, P. Pelicci, L. Lanfrancone, and A. Mantovani. "Expression of adhesion molecules and chemotactic cytokines in cultured human mesothelial cells." Journal of Experimental Medicine 176, no. 4 (October 1, 1992): 1165–74. http://dx.doi.org/10.1084/jem.176.4.1165.
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The mesothelium is a flat epithelial lining of serous cavities that could gate the traffic of molecules and cells between the circulation and these body compartments. The present study was designed to elucidate the capacity of mesothelial cells to express adhesion molecules and chemoattractant cytokines, two fundamental mechanisms of regulation of leukocyte recruitment. Cultured human mesothelial cells express appreciable levels of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and these were increased by in vitro exposure to tumor necrosis factor (TNF), interferon gamma (IFN-gamma), or TNF and IFN-gamma. Interleukin 1 (IL-1) was a less consistent stimulus for adhesion molecule expression in vitro. Unlike endothelial cells, used as a reference cell population, resting or stimulated mesothelial cells did not express E-selectin and ICAM-2, as assessed by flow cytometry. Analysis of VCAM-1 mRNA by reverse transcriptase and polymerase chain reaction using appropriate primers revealed that mesothelial cells expressed both the seven- and the six-Ig domain transcripts, with predominance of the longer species. Monocytes bound appreciably to "resting" and, to a greater extent, to stimulated mesothelial cells. Monocytes exposed to IFN-gamma and lipopolysaccharide, used as prototypic activation signals, showed increased capacity to bind mesothelial cells. Anti-CD18 monoclonal antibody significantly inhibited binding of monocytes to mesothelial cells, and this blocking effect was amplified by anti-very late antigen 4. Mesothelial cells were able to express the chemotactic cytokines IL-8 and monocyte chemotactic protein 1 at the mRNA and protein levels. These results indicate that mesothelial cells can express a set of adhesion molecules (ICAM-1 and VCAM-1) overlapping with, but distinct from, that expressed in vascular endothelium (ICAM-1, ICAM-2, VCAM-1, E-selectin), and that these are functionally relevant for interacting with mononuclear phagocytes. The regulated expression of adhesion molecules and chemotactic cytokines by mesothelial cells is probably important in inflammatory and immune reactions that involve serous cavities, such as the long-known macrophage appearance and disappearance reactions.
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Santamaría, Beatriz, Alvaro Conrado Ucero, Alberto Benito-Martin, Maria Jesús Vicent, Mar Orzáez, Angel Celdrán, Rafael Selgas, Marta Ruíz-Ortega, and Alberto Ortiz. "Biocompatibility Reduces Inflammation-Induced Apoptosis in Mesothelial Cells Exposed to Peritoneal Dialysis Fluid." Blood Purification 39, no. 1-3 (2015): 200–209. http://dx.doi.org/10.1159/000374103.
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Background/Aims: Peritonitis is a major complication that arises out of peritoneal dialysis (PD), leading to death and loss of mesothelium and peritoneal injury, which may impede PD. We studied the combined impact of inflammatory mediators and PD fluids on mesothelial cell death. Methods: Cultured human mesothelial cells. Results: Inflammatory cytokines (TNF-α and interferon-γ) cooperate with bioincompatible PD fluids containing high glucose degradation product (GDP) concentrations to promote mesothelial cell death. Thus, the inflammatory cytokine cocktail induced a higher rate of death in cells cultured in high GDP PD fluid than in low GDP PD fluid or cell culture medium (cell death expressed as % hypodiploid cells: TNF-α and interferon-γ in RPMI: 14.15 ± 1.68, TNF-α and interferon-γ in 4.25% low GDP PD fluid 13.16 ± 3.29, TNF-α and interferon-γ in 4.25% high GDP PD fluid 25.88 ± 2.18%, p < 0.05 vs. the other two groups). BclxL BH4 peptides, Apaf-1 inhibition or caspase inhibition failed to protect from apoptosis induced by the combination of inflammatory cytokines and bioincompatible PD fluids, although they protected from other forms of mesothelial cell apoptosis. Conclusion: Inflammation cooperates with high GDP PD fluids to promote mesothelial cell death, which is resistant to several therapeutic approaches. This information provides a framework for selection of PD fluid during peritonitis.
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Yung, Susan, and Tak Mao Chan. "Pathophysiological Changes to the Peritoneal Membrane during PD-Related Peritonitis: The Role of Mesothelial Cells." Mediators of Inflammation 2012 (2012): 1–21. http://dx.doi.org/10.1155/2012/484167.
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The success of peritoneal dialysis (PD) is dependent on the structural and functional integrity of the peritoneal membrane. The mesothelium lines the peritoneal membrane and is the first line of defense against chemical and/or bacterial insult. Peritonitis remains a major complication of PD and is a predominant cause of technique failure, morbidity and mortality amongst PD patients. With appropriate antibiotic treatment, peritonitis resolves without further complications, but in some PD patients excessive peritoneal inflammatory responses lead to mesothelial cell exfoliation and thickening of the submesothelium, resulting in peritoneal fibrosis and sclerosis. The detrimental changes in the peritoneal membrane structure and function correlate with the number and severity of peritonitis episodes and the need for catheter removal. There is evidence that despite clinical resolution of peritonitis, increased levels of inflammatory and fibrotic mediators may persist in the peritoneal cavity, signifying persistent injury to the mesothelial cells. This review will describe the structural and functional changes that occur in the peritoneal membrane during peritonitis and how mesothelial cells contribute to these changes and respond to infection. The latter part of the review discusses the potential of mesothelial cell transplantation and genetic manipulation in the preservation of the peritoneal membrane.
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Saeed, Anwaar Mohammed, Ammar Ali Alkhazna, Agostino Molteni, Tim Quinn, and Betty Herndon. "Dissecting the link between nanoparticle lung effects and tumor markers with CD24 measurements." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e21085-e21085. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21085.
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e21085 Background: It was postulated that carbon nanoparticles (CN) induced mesothelioma-like changes equal to asbestos in mice. We investigated CN added to human mesothelial cells in culture and reported that CN-induced cell damage to untransformed human mesothelial cells is rapidly followed by secretion of tumor markers like mesothelin and osteopontin. In vivo in animals, our group quantifies CN lung damage by HMGB1, an intranuclear protein released into alveolar lavage after CN exposure. Recent work suggests that the cell surface marker CD24 associates with HMGB1 to blunt lung responses to damage (like CN), but does not blunt cell response to pathogen-released HMGB1. Since CD24 is also a known cancer marker, elevated in many malignancies, we hypothesized that the cellular change elicited by CD24 when coupled with a damage marker would offer a mechanism through which CN could produce –repeated over time—malignant change in exposed human mesothelial cells. Such expression would support our previous research efforts. Methods: Untransformed human mesothelial cells were cultured and then stimulated or not with a CN dose giving 80% cell viability. At 24, 48 & 72 hr cells were fixed and stained with anti-CD 24. Presence of positive stain was photographed and counted. CN exposed and control rat lungs were harvested and frozen at 0.5 hr, 3 hr, 24 hr and 4 weeks. Western blot and immunostaining (with Anti-CD24 antibody and mucin chemical stain) was used to measure CD24 levels. Results: In CN-exposed animals, CD24 was highest at 24 hr. Mucin presence confirms the CD24 staining. Homogenates by Western blot also showed highest CD24 reactivity at 24 hr. In CN-exposed cultured cells, at 48 hr, some anti-CD24 staining was seen and at 72 hr in clusters of hyperproliferating cells, strong CD24 stain was seen. Conclusions: Our data suggest, as shown by a second cellular marker CD24, that the mesothelin upregulation seen in our previous studies indicated a cellular change beyond necrosis. Nanoparticles at a dose producing 20% cell death induce this change in healthy human mesothelial cells in culture.
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Gordillo, Carlos H., Pilar Sandoval, Patricia Muñoz-Hernández, Lucía Pascual-Antón, Manuel López-Cabrera, and José A. Jiménez-Heffernan. "Mesothelial-to-Mesenchymal Transition Contributes to the Generation of Carcinoma-Associated Fibroblasts in Locally Advanced Primary Colorectal Carcinomas." Cancers 12, no. 2 (February 21, 2020): 499. http://dx.doi.org/10.3390/cancers12020499.
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During peritoneal metastasis, cancer cells spread from abdominal solid tumors, disseminate through the peritoneal fluid and attach to and invade through mesothelial cells (MCs) that line the peritoneum. Intestinal adenocarcinomas originating in the mucosa infiltrate the submucosa, muscle layer, and serosa in order to finally colonize the peritoneal cavity. However, the mechanism by which metastatic cells leave the primary tumor and reach the peritoneal cavity has not been previously described. Hence, we investigate whether MCs lining visceral peritoneum, through a mesothelial-to-mesenchymal transition (MMT), are a source of carcinoma-associated fibroblasts (CAFs), which could contribute to cancer progression toward the peritoneal cavity. CAFs detected in biopsies from patients with superficially invasive colorectal cancer differed from locally advanced tumors. An aberrant accumulation of myofibroblasts expressing mesothelial markers was found in the stroma of deeply infiltrative tumors located in the neighborhood of a frequently activated mesothelium. We suggest that MMT is a key event in the early stages of peritoneal dissemination.
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Aroeira, Luiz S., Jesús Loureiro, Guadalupe T. González-Mateo, Vanessa Fernandez-Millara, Gloria del Peso, José Antonio Sánchez-Tomero, Marta Ruiz-Ortega, M. Auxiliadora Bajo, Manuel López-Cabrera, and Rafael Selgas. "Characterization of Epithelial-to-Mesenchymal Transition of Mesothelial Cells in a Mouse Model of Chronic Peritoneal Exposure to High Glucose Dialysate." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 5_suppl (September 2008): 29–33. http://dx.doi.org/10.1177/089686080802805s06.
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Animal models of peritoneal dialysis fluid (PDF) exposure are key tools in the study of mechanisms involved in alterations of the peritoneal membrane and in the design of therapies. We recently developed a mouse model of chronic peritoneal exposure to high glucose dialysate. Herein, we make a sequential analysis of the effects of glucose-based PDF on mouse peritoneal membrane and on mesothelium. We demonstrate that chronic exposure to PDF induces thickness and fibrosis of the peritoneal membrane in a time-dependent manner. We also show that mesothelial cells progressively detach and lose cytokeratin expression. In addition, we demonstrate that some mesothelial cells invade the submesothelial space, where they appear as cytokeratin- and alpha-smooth muscle actin-positive cells. These findings demonstrate that epithelial-to-mesenchymal transition (EMT) of mesothelial cells takes place in mouse peritoneum exposed to PDF, validating this model for the study of effects of drugs on the EMT process as a therapy for peritoneal deterioration.
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Breborowicz, Andrzej, Kostas Sombolos, Helen Rodela, Raymond Ogilvie, Joanne Bargman, and Dimitrios Oreopoulos. "Mechanism of Phosphatidylcholine Action during Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 7, no. 1 (January 1987): 6–9. http://dx.doi.org/10.1177/089686088700700103.
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We studied the effect of phosphatidyl- choline (PDC) (50 mg/L) on the peritoneal ultrafiltration and permeability in vivo and in vitro. Our in vivo studies with normal rabbits confirmed previous observations of increased ultrafiltration mainly by decreasing the reabsorption phase. We observed no effect on glucose absorption rate. In in vitro studies, using isolated section of rabbit's mesentery, phosphatidylcholine increased the permeability of the mesothelium to water, urea and glucose from the vascular to the mesothelial side but not in the opposite direction. Following exposure of the peritoneal membrane to Alcian blue, a positively charged dye, phosphatidylcholine had no effect on mesothelial permeability. Our observations suggest that necessary for the action of phosphatidylcholine is its attachment to the anionic sites of the mesothelium. We speculate that improvement in UF is achieved by diminishing the thickness of the stagnant fluid layers trapped between the microvilli.
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Simon, Marek. "Peritoneal Mesothelium in Vitro: An Electrophysiologic Study." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 16, no. 4 (July 1996): 393–97. http://dx.doi.org/10.1177/089686089601600413.
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Objective In vitro electrophysiologic characterization of the peritoneal mesothelium as a barrier for ion transport during peritoneal dialysis. Design Experiments were performed on rat's mesentery and diaphragm. Electrophysiologic parameters of the isolated tissue were assessed in the modified Ussing system. Results We have shown that there are significant differences between electrophysiological parameters of the parietal and visceral peritoneum. The value of the potential difference across the parietal mesothelium lining the abdominal part of the diaphragm (PDmpt) was 0.26 ± 0.03 mV (mean ± SEM), with a positive charge recorded from the apical side of the mesothelium. Electrical resistance of the mesothelial monolayer (Am t) was mAp t = 13.6 ± 1.3 Ω.cm and 1.4±0.2 Ω.cm for the tissue isolated from the diaphragm and mesentery, respectively. Both the mechanical and chemical procedures used for the preparation of the peritoneal membrane model from the diaphragm have been shown to produce similar values of electrophysiological parameters. Conclusion The electrophysiologic approach presented here may be a useful tool for studies of highly permeable biological membranes such as the peritoneal mesothelium. The mesothelial tissue isolated from the rat diaphragm has been shown to be a suitable model for electrophysiologic studies of the peritoneum as assessed by the values of the PDmpt and Ampt parameters.
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Wilkinson, L., P. De, and C. Bloxham. "Mesothelial reaction in longstanding Crohn’s ileitis simulating papillary mesothelioma." Journal of Clinical Pathology 61, no. 10 (September 26, 2008): 1119–21. http://dx.doi.org/10.1136/jcp.2008.058693.
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Intestinal and extraintestinal complications of Crohn’s disease are well documented. Changes in the connective tissue within the intestinal wall and surrounding tissue including mesenteric fat are characteristically seen in resected and autopsy specimens. A rare and unusually florid mesothelial reaction in the surrounding small bowel serosa of a patient with a 2-year history of Crohn’s ileitis is described. The peritoneal surface of the ileal resection specimen displayed exuberant tubulo-papillary formations of the mesothelium, with superficial invasion of the underlying stroma. The case demonstrates the well-recognised difficult differential diagnosis between a benign mesothelial proliferation and malignant mesothelioma in a novel clinical setting, and the diversity of the extramural manifestations of Crohn's disease.
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Wu, Maoxin, Yuhua Sun, Gan Li, Garrett Desman, Beverly Wang, Joan Gil, and David E. Burstein. "Immunohistochemical Detection of XIAP in Mesothelium and Mesothelial Lesions." American Journal of Clinical Pathology 128, no. 5 (November 2007): 783–87. http://dx.doi.org/10.1309/lx7nfrdxy1jqf9r1.
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Bejarano, P. "Immunohistochemical Detection of XIAP in Mesothelium and Mesothelial Lesions." Yearbook of Pathology and Laboratory Medicine 2009 (January 2009): 65–66. http://dx.doi.org/10.1016/s1077-9108(08)79039-x.
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Hiriart, Emilye, Raymond Deepe, and Andy Wessels. "Mesothelium and Malignant Mesothelioma." Journal of Developmental Biology 7, no. 2 (April 8, 2019): 7. http://dx.doi.org/10.3390/jdb7020007.
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The mesothelium is an epithelial structure derived from the embryonic mesoderm. It plays an important role in the development of a number of different organs, including the heart, lungs, and intestines. In this publication, we discuss aspects of the development of the mesothelium, where mesothelial structures can be found, and review molecular and cellular characteristics associated with the mesothelium. Furthermore, we discuss the involvement of the mesothelium in a number of disease conditions, in particular in the pathogenesis of mesotheliomas with an emphasis on malignant pleural mesothelioma (MPM)—a primary cancer developing in the pleural cavity.
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Dobbie, James w. "Pathogenesis of Peritoneal Fibrosing Syndromes (Sclerosing Peritonitis) in Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 12, no. 1 (January 1992): 14–27. http://dx.doi.org/10.1177/089686089201200105.
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Drawing from diverse sources including epidemiological and clinical data, surgical observations, histopathology, serosal healing responses to fibrin and fibrinolysis, tissue reaction to chronic exposure, and to exo and endotoxins, new information on mesothelial stem cells, autocrine and paracrine influences on their proliferation and collagen synthesis, and the effect of glucose on fibroconnective tissue, we have begun to piece together the pathogenetic jigsaw of fibrosis in continuous ambulatory peritoneal dialysis (CAPD). The reaction of peritoneal mesothelium and stroma to the stress of continual dialysis results in a spectrum of alterations ranging from opacification through a tanned peritoneum syndrome to sclerosing encapsulating peritonitis (SEP). Any agent that causes irritation of the mesothelial layer and induces serositis, or single severe or multiple episodes of peritonitis resulting in mesothelial loss, predisposes the peritoneum to fibroneogenesis. An accurate definition of the histopathological changes of peritoneal thickening is a prerequisite for defining pathogenesis. This paper is the first attempt to create such a framework. It is evident from many areas of study that fibrin deposition and fibrinolysis, hyalinization of the superficial stromal collagen possibly tanned through nonenzymatic glycosylation by dialysate glucose and the proliferative potential of mesothelial stem cells play an important and possibly interdependent role in excessive fibroneogenesis in certain patients on CAPD. Many of the pieces of the jigsaw are obviously still missing, and the picture is most surely incomplete. Nevertheless, the outline of the pathologic and etiologic landscape should now be discernible.
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Gotloib, Lazaro, Abshalom Shostack, Phina Bar-Sella, and Ricardo Cohen. "Continuous Mesothelial Injury and Regeneration during long Term Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 7, no. 3 (July 1987): 148–56. http://dx.doi.org/10.1177/089686088700700307.
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This study reconstructs the whole sequence of mesothelial injury and regeneration in patients on longterm peritoneal dialysis. Our observations indicate that peritoneal dialysis induces a process of continuous mesothelial injury and regeneration. New mesothelial cells seem to originate from wandering mesothelial cells of the peritoneal fluid, as well as from mesothelial cell precursors localized in the sub-mesothelial connective tissue.
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Dobbie, James W., and John K. Lloyd. "Mesothelium Secretes Lamellar Bodies in a Similar Manner to Type II Pneumocyte Secretion of Surfactant." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 9, no. 3 (July 1989): 215–19. http://dx.doi.org/10.1177/089686088900900314.
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In the early 1970s it was found that a specific lipid-fixing technique of tissue preparation for electron microscopy (tannic acid-gluteraldehyde) preserved and thus unmasked distinctive inclusions in Type II pneumocytes which were called lamellar bodies. This discovery was the first crucial step in demonstrating that lamellar bodies were the storage granules from which alveolar surfactant was secreted. In a previous study a comparison between mesothelium and Type II pneumocytes showed close ultrastructural similarities. In the present investigation of normal peritoneal tissue from man, monkey, rabbit and mouse, following primary tannic acidgluteraldehyde fixation and modified embedding procedures similar to those used for lung, examination by transmission electron microscopy demonstrated in all mesothelial cells examined, characteristic lamellar structures similar to those described in Type II pneumocytes. Exocytotic extrusion of lamellar bodies from the apical portion of the mesothelial cell, and the presence of lamellar bodies on the cell surface in a manner identical to that found in Type II pneumocytes was also observed. These findings provide compelling evidence that a process of specialized biosynthesis and secretion of phospholipids similar to that established for Type II pneumocytes also occurs in mesothelial cells.
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Davey, Andrew K., Jessica Hayward, Jean K. Marshall, and Anthony E. Woods. "The Effects of Insufflation Conditions on Rat Mesothelium." International Journal of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/816283.
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Aim. The aim of this investigation was to examine the alterations in the peritoneum after cold dry CO2, heated dry CO2, and humidified heated CO2at pressures equivalent to intraperitoneal pressures used in human laparoscopy.Methods. Eighteen rats were divided into 4 treatment groups—group 1: untreated control; group 2: insufflation with cold dry CO2; group 3: insufflation with heated, dry CO2; group 4: insufflation with heated and humidified CO2. The abdomen was insufflated to 5 mm/Hg (flow rate 50 mL/min) for 2 h. Twelve hours later, tissue samples were collected for analysis by light microscopy (LM) and scanning electron microscopy (SEM).Results. Group 1: no abnormalities were detected. Group 2: specimens revealed an inflammatory response with loss of mesothelium and mesothelial cell nuclei showing lytic change. Cells were rounded with some areas of cell flattening and separation. Group 3: some animals showed little or no alteration, while others had a mild inflammatory response. Mesothelial cells were rounded and showed crenation on the exposed surface. Group 4: specimens showed little change from the control group.Conclusions. The LM results indicate that insufflations with heated, humidified CO2are the least likely to induce mesothelial damage.
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Shidham, Vinod B. "The panorama of different faces of mesothelial cells." Cytojournal 18 (December 6, 2021): 31. http://dx.doi.org/10.25259/cmas_02_02_2021.
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All effusions in serous cavities represent a pathologic processes secondary to inflammatory, neoplastic, hemodynamic, or mechanical/traumatic etiologies. This elicits reactive changes in the extremely sensitive mesothelial cells lining the serosal surfaces. The result is hypertrophy and hyperplasia which lead to broad changes with a wide range of morphological appearances. These reversible alterations may resolve entirely after the recovery of underlying pathology. Under the tertiary care situations, neoplastic effusion specimens are encountered more frequently. Although some non-neoplastic pathologic process may demonstrate a few diagnostic features, cytologic evaluation of malignant effusions usually show diagnostic malignant cells. However, the most versatile mesothelial cells demonstrate a very wide cytomorphological spectrum secondary to reactive challenges. These mesothelial cells are usually referred to as ‘reactive mesothelial cells’. In addition other terms such as reactive mesothelial proliferation, reactive mesothelial hyperplasia, irritated mesothelial cells, activated mesothelial cells, hyperplastic mesothelial cells, hypertrophic mesothelial cells, and proliferative mesothelial cells. Rarely atypical mesothelial cells, although not recommended, is used inadvertently. Although there is a lack of general agreement defining these terms, some of these including atypical mesothelial cells, should not be preferred. With reference to this CMAS series, usually favored term ‘reactive mesothelial cells’ is preferred. The size of reactive mesothelial cells range from 15 to 30 µm (but may be up to 50 µm). These polyhedral cells with variable amount of cytoplasm and enlarged nuclei may show variation in sizes and shapes with conspicuous nucleoli. Bi- and multi-nucleation is frequent. Cohesive groups of mesothelial cells as sheets and three dimensional groups may be present. Some floridly reactive mesothelial cells with hyperchromatic enlarged nuclei with prominent nucleoli and scant cytoplasm may resemble malignant cells. This astonishingly wide morphological spectrum of reactive mesothelial cells is a significant interpretation challenge in effusion fluid cytology. Methodical interpretation approach with appropriate knowledge about this wide spectrum is important aspect in diagnostic cytopathology of effusion fluids.
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Husain, Aliya N. "Mesothelial Proliferations." American Journal of Clinical Pathology 141, no. 2 (February 1, 2014): 152–53. http://dx.doi.org/10.1309/ajcpoi1desu8mthz.
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Wick, Mark R., and Stacey E. Mills. "Mesothelial Proliferations." American Journal of Clinical Pathology 113, no. 5 (May 1, 2000): 619–22. http://dx.doi.org/10.1309/315h-e2ly-qye7-143j.
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Di Paolo, N., G. Sacchi, M. T. Del Vecchio, G. Nicolai, S. Brardi, and G. Garosi. "State of the Art on Autologous Mesothelial Transplant in Animals and Humans." International Journal of Artificial Organs 30, no. 6 (June 2007): 456–76. http://dx.doi.org/10.1177/039139880703000604.
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Sixteen years ago rabbit and human mesothelial cells were successsfully cultured and autoimplanted. The aim of the study was merely to demostrate that mesothelial implant was possible and interesting not only in peritoneal dialysis, but also in the vaster field of medicine and surgery concerning all the mesothelial districts of the body. The aim of this paper is to recollect the steps which have led to autolougous mesothelial transplantation and verify if the tecnique has been validated and adopted by others. Review of the literature published in the last 15 years shows that intraperitoneal transplantation of mesothelial cells has been effective in reducing the formation of peritoneal adhesions, and in remodeling the area of mesothelial denudation. New studies on the mesothelial cell opened the way to costruction of transplantable tissue-engineered artificial peritoneum, to the utilization of mesothelial progenitor cells and to find simple metods to collect autologous mesothelial cells. Finally mesothelial trasnsplantation may represent a new neovascular therapy in the prevention and treatment of ischemic coronaric heart disease.