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Veena B Antony - One of the best experts on this subject based on the ideXlab platform.

  • wilms tumor 1 wt1 regulates pleural Mesothelial Cell plasticity and transition into myofibroblasts in idiopathic pulmonary fibrosis
    The FASEB Journal, 2014
    Co-Authors: Suman Karki, Jason S Zolak, Ranu Surolia, Thomas D Hock, Purusotham Guroji, Ryan Duggal, Victor J Thannickal, Veena B Antony
    Abstract:

    Pleural Mesothelial Cells (PMCs), which are derived from the mesoderm, exhibit an extraordinary capacity to undergo phenotypic changes during development and disease. PMC transformation and trafficking has a newly defined role in idiopathic pulmonary fibrosis (IPF); however, the contribution of Wilms' tumor 1 (Wt1)-positive PMCs to the generation of pathognomonic myofibroblasts remains unclear. PMCs were obtained from IPF lung explants and healthy donor lungs that were not used for transplantation. Short hairpin Wt1-knockdown PMCs (sh Wt1) were generated with Wt1 shRNA, and morphologic and functional assays were performed in vitro. Loss of Wt1 abrogated the PMC phenotype and showed evidence of Mesothelial-to-mesenchymal transition (MMT), with a reduced expression of E-cadherin and an increase in the profibrotic markers α-smooth muscle actin (α-SMA) and fibronectin, along with increased migration and contractility, compared with that of the control. Migration of PMCs in response to active transforming growth factor (TGF)-β1 was assessed by live-Cell imaging with 2-photon microscopy and 3D imaging, of Wt1-EGFP transgenic mice. Lineage-tracing experiments to map the fate of Wt1+ PMCs in mouse lung in response to TGF-β1 were also performed by using a Cre-loxP system. Our results, for the first time, demonstrate that Wt1 is necessary for the morphologic integrity of pleural membrane and that loss of Wt1 contributes to IPF via MMT of PMCs into a myofibroblast phenotype.—Karki, S., Surolia, R., Hock, T. D., Guroji, P., Zolak, J. S., Duggal, R., Ye, T., Thannickal, V., J., Antony, V. B. Wilms' tumor 1 (Wt1) regulates pleural Mesothelial Cell plasticity and transition into myofibroblasts in idiopathic pulmonary fibrosis.

  • pleural Mesothelial Cell expression of c c monocyte chemotactic peptide and c x c interleukin 8 chemokines
    American Journal of Respiratory Cell and Molecular Biology, 1995
    Co-Authors: Veena B Antony, Jeffrey W. Hott, Steven W. Godbey, Steven L Kunkel, Marie D Burdick, Robert M Strieter
    Abstract:

    The arrival of inflammatory phagocytic Cells, namely neutrophils and mononuclear phagocytes, in the pleural space is a hallmark of pleural inflammation. It is probable that the temporal arrival of Cells is mediated via the release of chemotactic cytokines by activated Mesothelial Cells. We hypothesized that human pleural Mesothelial Cells activated by bacterial endotoxin lipopolysaccharide (LPS), interleukin-1 beta (IL-1 beta), or tumor necrosis factor-alpha (TNF-alpha) release Cell-specific chemokines from the C-C and C-X-C family of chemokines, specifically monocyte chemoattractant protein 1 (MCP-1) and IL-8. We evaluated supernatants of stimulated Mesothelial Cells for biologic chemotactic activity for monocytes and neutrophils and quantitative antigenic protein levels for MCP-1 and IL-8. Expression of the proteins at mRNA level was tested via Northern blot analysis. We found that responses to LPS were significantly higher (P less than 0.05) than control supernatants of unstimulated Mesothelial Cells. Responses to IL-1 beta and TNF-alpha were significantly greater than those to LPS. Neutralization studies with specific rabbit anti-MCP-1 and IL-1 antibody demonstrated significant decreases in bioactivity for MCP-1 and IL-8, indicating that Mesothelial Cell-derived MCP-1 and IL-8 play a significant role in the chemotactic activity seen in stimulated Mesothelial Cell supernatants. On specific enzyme-linked immunosorbent assay testing, stimulated Mesothelial Cells produced significantly more MCP-1 and IL-8 when stimulated with IL-1 beta or TNF-alpha as compared to LPS. mRNA expression for MCP-1 peaked within 2 to 4 h following stimulation and was noted as early as 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Mesothelial Cell modulation of pleural repair: thrombin stimulated Mesothelial Cells release prostaglandin E2.
    Prostaglandins Leukotrienes and Essential Fatty Acids, 1994
    Co-Authors: Jeffrey W. Hott, Steven W. Godbey, Veena B Antony
    Abstract:

    Abstract Repair of an injured pleura without fibrosis not only requires a re-establishment of the normal pleural Mesothelial monolayer but also a downregulation of the inflammatory response, including inhibition of fibroblast proliferation and collagen synthesis. However, the role of the Mesothelial Cell in regulating these processes in the pleural space remains underfined. We therefore hypothesized that Mesothelial Cells, stimulated by thrombin, release prostaglandin E 2 PGE 2 , which is capable of inhibiting fibroblast proliferation. In vitro rat visceral Mesothelial Cells were exposed to thrombin and PGE 2 levels in the supernatant were measured using a competitive radioimmunoassay. Our results demonstrated that Mesothelial Cells produce PGE 2 in a dose- and time-dependent manner. In addition, both anti-thrombin 3 and indomethacin completely blocked the PGE 2 released. Finally, conditioned media from thrombin-stimulated Mesothelial Cells inhibited fibroblast [ 3 H]thymidine incorporation. These results demonstrate that the Mesothelial Cell is capable of contributing to the repair process of pleural injury by the release of a local factor such as PGE 2 .

  • Mesothelial Cell Response to Pleural Injury: Thrombin-induced Proliferation and Chemotaxis of Rat Pleural Mesothelial Cells
    American Journal of Respiratory Cell and Molecular Biology, 1992
    Co-Authors: Jeffrey W. Hott, Jae A. Sparks, Steven W. Godbey, Veena B Antony
    Abstract:

    Injury to the pleura ultimately results in either repair with fibrosis or repair without fibrosis and a reestablishment of the normal Mesothelial monolayer. The role of the Mesothelial Cell, and of local mediators, in these repair processes remains essentially undefined. In order for repair without fibrosis to occur, Mesothelial Cells, in response to local mediators, must be capable of migration and/or proliferation to cover the injured and denuded mesothelium. We hypothesized that rat pleural Mesothelial Cells were capable of both chemotaxis and proliferation in response to thrombin. In an in vitro assay, Mesothelial Cells demonstrated directed migration in response to a known chemoattractant, formylmethionylleucylphenylalanine. In addition, Mesothelial Cells demonstrated chemotaxis in a dose-dependent manner in response to thrombin, with a maximal response at a concentration of 10−8 M. Finally, this chemotaxis was blocked by a specific blocker of thrombin, antithrombin 3. Thrombin also stimulated mesoth...

Teruo Okano - One of the best experts on this subject based on the ideXlab platform.

  • Therapeutic Applications of Mesothelial Cell Sheets
    Therapeutic Apheresis and Dialysis, 2014
    Co-Authors: Kunio Kawanishi, Kosaku Nitta, Masayuki Yamato, Teruo Okano
    Abstract:

    Mesothelial Cells are an integral part of the peritoneum and play an important role in maintaining its structural and functional properties. In recent years a number of studies on Mesothelial Cells have been performed to evaluate the localization, secretional properties and the ability of regeneration and transdifferentiation of these Cells. They are also involved in the repair of the peritoneum damage following surgery or peritonitis. Mesothelial Cells produce several cytokines, growth factors and extraCellular matrix components, possessing anti-inflammatory and immunomodulatory properties. Based on previous research, Cell sheet engineering has made it possible to transplant Cells that retain the Cells' function, and stacking different Cells in layers has also become possible. Arranging blood vessels between the Cell layers is a problem when stacking Cells in layers. Whether adequate blood flow can be obtained for the Cell layers to survive long-term is the difference between success and failure. Mesothelial Cell transplantation for peritoneal regeneration needs to be performed under conditions in which the surface area of the visceral peritoneum is large and the Mesothelial Cell damage area is small. In this article we explain Cell sheet engineering as one of the technologies for transplanting Cells with a variety of interCellular adhesion and Cell membrane molecules maintained intact, and its application to peritoneal regeneration.

  • Mesothelial Cells from tunica vaginalis, a practical source for Mesothelial transplantation.
    The International Journal of Artificial Organs, 2007
    Co-Authors: Touko Asano, Masayuki Yamato, Ryoji Takazawa, Kazunori Kihara, Teruo Okano
    Abstract:

    Transplantation of Mesothelial Cells is used to repair peritoneum that is damaged by surgery, peritonitis, and peritoneal dialysis. The largest obstacle for clinical application of Mesothelial Cell transplantation is the lack of a reliable source of Mesothelial Cells. So far, they are isolated from omentum, mesentery, parietal wall and ascites. Procedures used to obtain Mesothelial Cells from the omentum or mesentery are invasive, however, especially in pre-operative situations. Sufficient amounts of ascites for aspiration can not be obtained under physiological conditions. We have developed a novel method of isolating Mesothelial Cells from the tunica vaginalis. The tunica vaginalis originates from the peritoneum and descends into the scrotum along with the testis during fetal development. This region provides a source of Mesothelial Cells that is convenient to approach and free from abdominal complications. Transplantation of autologous Mesothelial Cells that were isolated from tunica vaginalis was effective in preventing post-operative adhesions. In this review, we summarize Mesothelial Cell transplantation trials and describe the method of isolating Mesothelial Cells form the tunica vaginalis. Mesothelial Cell transplantation might be widely accepted for clinical use in the near future.

  • transplantation of an autologous Mesothelial Cell sheet prepared from tunica vaginalis prevents post operative adhesions in a canine model
    Tissue Engineering, 2006
    Co-Authors: Touko Asano, Masayuki Yamato, Ryoji Takazawa, Ryo Takagi, Yasumasa Iimura, Hitoshi Masuda, Kazunori Kihara, Teruo Okano
    Abstract:

    Post-operative adhesions often cause severe complications such as bowel obstruction and abdominopelvic pain. Previously, we reported that transplantation of a Mesothelial Cell sheet is effective for preventing adhesion in rat model. We also proposed a new technique for harvesting autologous Mesothelial Cells from tunica vaginalis without intra-abdominal maneuvers. In this study, we examined whether an autologous Mesothelial Cell sheet can prevent post-operative peritoneal adhesions in a canine adhesion model. Mesothelial Cells were isolated from the tunica vaginalis of male beagles. Isolated Cells were cultured on fibrin gel. We named this construct the "Mesothelial Cell sheet." Animals underwent surgery to induce peritoneal adhesion formation and were then transplanted with the Mesothelial Cell sheets (sheet group, n = 4), fibrin gel (fibrin group, n = 4), or no materials (sham group, n = 4). Four weeks after the transplantation, we evaluated adhesion formation and scored adhesion levels. The abdominal w...

  • Mesothelial Cell sheets cultured on fibrin gel prevent adhesion formation in an intestinal hernia model
    Tissue Engineering, 2005
    Co-Authors: Ryoji Takazawa, Masayuki Yamato, Teruo Okano, Yukio Kageyama, Kazunori Kihara
    Abstract:

    In the present study, we examined a novel technique to prevent adhesion formation in a rat intestinal hernia model with Mesothelial Cell sheets cultured on fibrin gel. Mesothelial Cells were obtained from isologous rats by enzymatic disaggregation of mesentery and cultured on fibrin gel. Electron microscopy revealed that these cultured Cells form contiguous monolayer Cell sheets with well-developed microvilli. These tissue-engineered constructs were grafted in vivo to an intestinal hernia model that results in regular surgical adhesions without treatment. Five days postgrafting, rats were sacrificed. Adhesion formation was not observed in rats grafted with the constructs, whereas severe adhesions were observed in all control rats. Constructs seeded with Mesothelial Cells isolated from EGFP-transgenic rats clearly revealed that grafted Mesothelial Cells remained at the host tissue site even after fibrin scaffold degradation. These Cells developed more abundant microvilli in vivo than those in vitro. These ...

Aron Chakera - One of the best experts on this subject based on the ideXlab platform.

  • analysis of early Mesothelial Cell responses to staphylococcus epidermidis isolated from patients with peritoneal dialysis associated peritonitis
    PLOS ONE, 2017
    Co-Authors: Aron Chakera, Amanda L Mcguire, Kieran T Mulroney, Christine F Carson, Ramesh Ram, Grant Morahan
    Abstract:

    The major complication of peritoneal dialysis (PD) is the development of peritonitis, an infection within the abdominal cavity, primarily caused by bacteria. PD peritonitis is associated with significant morbidity, mortality and health care costs. Staphylococcus epidermidis is the most frequently isolated cause of PD-associated peritonitis. Mesothelial Cells are integral to the host response to peritonitis, and subsequent clinical outcomes, yet the effects of infection on Mesothelial Cells are not well characterised. We systematically investigated the early Mesothelial Cell response to clinical and reference isolates of S. epidermidis using primary Mesothelial Cells and the Mesothelial Cell line Met-5A. Using an unbiased whole genome microarray, followed by a targeted panel of genes known to be involved in the human antibacterial response, we identified 38 differentially regulated genes (adj. p-value < 0.05) representing 35 canonical pathways after 1 hour exposure to S. epidermidis. The top 3 canonical pathways were TNFR2 signaling, IL-17A signaling, and TNFR1 signaling (adj. p-values of 0.0012, 0.0012 and 0.0019, respectively). Subsequent qPCR validation confirmed significant differences in gene expression in a number of genes not previously described in Mesothelial Cell responses to infection, with heterogeneity observed between clinical isolates of S. epidermidis, and between Met-5A and primary Mesothelial Cells. Heterogeneity between different S. epidermidis isolates suggests that specific virulence factors may play critical roles in influencing outcomes from peritonitis. This study provides new insights into early Mesothelial Cell responses to infection with S. epidermidis, and confirms the importance of validating findings in primary Mesothelial Cells.

  • Staphylococcus epidermidis Mesothelial array and RT2 data
    2017
    Co-Authors: Aron Chakera
    Abstract:

    Changes in Mesothelial Cell gene expression following treatment with Staphylococcus epidermidis species.

Matthew B. Grisham - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of rat pleural Mesothelial Cell nitric oxide synthesis by transforming growth factor-β1
    Inflammation, 1996
    Co-Authors: Michael W. Owens, Shawn A. Milligan, Matthew B. Grisham
    Abstract:

    Pleuritis is a common initial clinical manifestation of tuberculosis. It is associated with an accumulation of a variety of cytokines in the pleura and pleural fluid. We have recently shown that these proinflammatory cytokines induce the pleural Mesothelial Cell to produce large amounts of nitric oxide, a nitrogen intermediate that has been shown to have a tuberculocidal effect. TGF- β has also been found in situ in tuberculous effusions and pleural tissues and is thought to suppress the immune response and promote tissue repair. This study examined the effects of TGF- β on cytokine-induced NO synthesis by rat pleural Mesothelial Cells in vitro. Results demonstrated that TGF- β significantly inhibited NO synthesis and that this inhibition was associated with a proportionate decrease in iNOS mRNA and iNOS protein. Suppression of pleural Mesothelial Cell NO synthesis by TGF- β may be important in the pathogenesis of tuberculous pleuritis.

Nicholas Topley - One of the best experts on this subject based on the ideXlab platform.

  • biocompatibility of bicarbonate buffered peritoneal dialysis fluids influence on Mesothelial Cell and neutrophil function
    Kidney International, 1996
    Co-Authors: Nicholas Topley, Davender Kaur, Meryl M Petersen, Achim Jorres
    Abstract:

    Biocompatibility of bicarbonate buffered peritoneal dialysis fluids: Influence on Mesothelial Cell and neutrophil function. The present study compares the effects of lactate and bicarbonate buffered PDF on human neutrophil (PMN) and human peritoneal Mesothelial Cell (HPMC) viability and function. Acute exposure of PMN to lactate buffered PDF at pH 5.5 (CAPD 2, 1.5% and CAPD 3, 4.25% glucose) resulted in significant reductions in Cellular ATP levels, the phagocytosis of serum treated zymosan (STZ) and respiratory burst activation (CL). Exposure of PMN to bicarbonate buffered PDF (BIC 20, 1.5% glucose and BIC 30, 4.25% glucose both at pH 7.2) had no significant effect on Cell viability or the CL response. Phagocytosis was, however, depressed significantly more following exposure to BIC 30 than BIC 20. PMN Cellular ATP levels and phagocytosis were significantly better in Cells exposed to BIC 30 than to CAPD 3 at pH 7.4 ( P = 0.043 for both). Pre-exposure of HPMC to CAPD 2, CAPD 3 or BIC 30 for 30minutes resulted in a significant reduction in Cellular ATP content compared to control medium. Pre-exposure to BIC 20 did not result in a reduction in HPMC ATP levels. HPMC synthesis of IL-6 was unaffected by 15 or 30minutes pre-exposure to BIC 20 or BIC 30, in contrast pre-exposure to CAPD 2 or CAPD 3 for 15 or 30minutes resulted in a significant reduction in stimulated IL-6 synthesis (24.5 ± 3.01 and 32.3 ± 5.0 vs. 43.9 ± 10 pg/ µ g Cell protein in M199, N =6; P = 0.02). Neutralization of the pH of CAPD 2 and CAPD 3 resulted in normalization of HPMC IL-6 secretion. Analysis of IL-6 mRNA expression in control, BIC 20 and 30 pre-treated HPMC subsequently stimulated with IL-1 β revealed no differences in the expression of the IL-6 specific 465 base pair transcripts. The improved Cellular function in bicarbonate buffered PDF indicates potentially improved host defence status and preservation of the peritoneal membrane in CAPD patients.

  • effect of lactate buffered peritoneal dialysis fluids on human peritoneal Mesothelial Cell interleukin 6 and prostaglandin synthesis
    Kidney International, 1995
    Co-Authors: Janusz Witowski, Nicholas Topley, Achim Jorres, Tomasz Liberek, G A Coles, John D Williams
    Abstract:

    Effect of lactate-buffered peritoneal dialysis fluids on human Mesothelial Cell interleukin-6 and prostaglandin synthesis. The present study focused on the evaluation of constitutive and cytokine-stimulated human peritoneal Mesothelial Cell (HPMC) IL-6 and 6-keto-PGF1α, release following pre-exposure to peritoneal dialysis fluid (PDF). Exposure of HPMC to PDF pH 5.2 resulted in a time-dependent increase in Cell cytotoxicity [as assessed by lactate dehydrogenase (LDH) release] and concomitant inhibition of constitutive and IL-1β stimulated IL-6 and 6-keto-PGF1α synthesis. After 15 minutes of exposure to PDF constitutive and IL-1β stimulated IL-6 release were reduced by 32.0 ± 9.7% and 76.0 ± 7.4% (N = 6, P

  • human peritoneal Mesothelial Cell prostaglandin synthesis induction of cyclooxygenase mrna by peritoneal macrophage derived cytokines
    Kidney International, 1994
    Co-Authors: Nicholas Topley, Meryl M Petersen, Ruth Mackenzie, Andreas Neubauer, Eleni Stylianou
    Abstract:

    Human peritoneal Mesothelial Cell prostaglandin synthesis: Induction of cyclooxygenase mRNA by peritoneal macrophage-derived cytokines. Increasing evidence suggests that the Mesothelial Cell contributes to the control of inflammation in both the normal and inflamed peritoneal cavity. The present study examines the regulation of prostaglandin production by human peritoneal Mesothelial Cells (HPMC) following stimulation with peritoneal macrophage-conditioned medium and the cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). IL-1β and TNF-β stimulated significant release of prostaglandin above background levels in a time and dose dependent manner. Stimulation of HPMC with IL-1β (500 pg/ml) or TNF-α (100 pg/ml) for 24 hours resulted in the release of 24.5 ± 4.3 (N = 11) (z = 3.40, P 1α /µg Cellular protein, respectively. Pretreatment of HPMC with dexamethasone (10 -6 to 10 -9 M) inhibited both constitutive and cytokine stimulated prostaglandin synthesis in a dose dependent manner. Both PMO-CM and PMO-S. epi CM stimulated 6-keto-PGF 1α and PGE 2 synthesis by HPMC in a time and dose dependent manner (PMO-S. epi CM >> PMO-CM). Co-incubation of HPMC with PMO-S. epi CM in the presence of anti-IL-1β and/or anti-TNF-α antibody, interleukin-1 receptor antagonist or soluble TNF receptor (TNF p75) significantly reduced the capacity of these supernatants to stimulate prostaglandin synthesis. Exposure of HPMC to cytokines or PMO-S. epi CM resulted in the time dependent increase in the levels of both Cox-1 and Cox-2 mRNA as assessed by RT/PCR analysis with the greatest increase being seen for Cox-2. These data demonstrate specific stimulation of eicosanoid metabolism in HPMC by peritoneal macrophage derived cytokines, indicating the possible importance of these mediators in the activation of intraperitoneal prostaglandin synthesis. HPMC prostaglandins might act as important pro/anti-inflammatory mediators contributing to a cytokine network in the peritoneal cavity during CAPD peritonitis.