Rozprawy doktorskie na temat „Liver sinusoidal endothelial cell”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 35 najlepszych rozpraw doktorskich naukowych na temat „Liver sinusoidal endothelial cell”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Pełny tekst źródłaCheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Pełny tekst źródłaOwing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life
Akingbasote, J. A. "The potential role of liver sinusoidal endothelial cells in drug-induced liver injury". Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3005113/.
Pełny tekst źródłaO'REILLY, Jennifer. "The role and ultrastructure of the liver sinusoidal endothelial cell in fasting, hepatoxicity, and ageing". Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/10550.
Pełny tekst źródłaRowe, Ian Alston Cooper. "The role of liver sinusoidal endothelial cells in hepatitis C virus infection". Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4123/.
Pełny tekst źródłaMohamad, Mashani. "The Role of the Liver Sinusoidal Endothelial Cells in the Pathophysiology of Insulin Resistance". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15716.
Pełny tekst źródłaBanga, Neal Roop. "Effects of Ischaemia-Reperfusion Injury and Ischaemic Preconditioning on Human Liver Sinusoidal Endothelial Cells". Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515298.
Pełny tekst źródłaKojima, Hidenobu. "Establishment of practical recellularized liver graft for blood perfusion using primary rat hepatocytes and liver sinusoidal endothelial cells". Kyoto University, 2018. http://hdl.handle.net/2433/233836.
Pełny tekst źródłaYagi, Toshikazu. "The protective effects of prostaglandin E1 on sinusoidal endothelial cells in xenogeneic pig liver perfusion". Kyoto University, 1998. http://hdl.handle.net/2433/182254.
Pełny tekst źródłaMiyachi, Yosuke. "Causes of liver steatosis influence the severity of ischemia reperfusion injury and survival after liver transplantation in rats". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263516.
Pełny tekst źródłaFord, Andrew Joseph. "Investigating the Interplay between Inflammation and Matrix Stiffness: Evaluation of Cell Phenotype and Cytoplasmic Stiffness In Vitro". Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/96711.
Pełny tekst źródłaPHD
Yassin, Abdallah [Verfasser], Percy A. [Akademischer Betreuer] Knolle, Percy A. [Gutachter] Knolle i Angelika [Gutachter] Schnieke. "NKT cells crosstalk with liver sinusoidal endothelial cells is triggering induction of polyclonal T-cell and NK cell immunity / Abdallah Yassin ; Gutachter: Percy A. Knolle, Angelika Schnieke ; Betreuer: Percy A. Knolle". München : Universitätsbibliothek der TU München, 2021. http://d-nb.info/1239812590/34.
Pełny tekst źródłaZierow, Johanna [Verfasser], i Jonathan [Akademischer Betreuer] Sleeman. "Investigation of liver sinusoidal endothelial cells - characterisation and application of new transgenic mouse models / Johanna Zierow ; Betreuer: Jonathan Sleeman". Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177252686/34.
Pełny tekst źródłaPasarín, Castellanos Marcos. "Resistència a la insulina i disfunció endotelial sinusoïdal a la malaltia hepàtica per dipòsit de greix". Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/83491.
Pełny tekst źródłaNon-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD incidence is increasing in western societies, paralleling the increase of obesity. The deposit of fat in the hepatocytes leads in some patients to the development of hepatocyte injury, inflammation, fibrosis and cirrhosis, but the mechanisms that govern the progression of liver injury are not well understood. There is not an effective pharmacological treatment for NAFLD. Insulin-resistance, the underlying pathophysiological feature of the metabolic syndrome, is associated with peripheral endothelial dysfunction. However, the sinusoidal endothelium is phenotypically different from the peripheral endothelium, and it is not known whether insulin resistance induces sinusoidal endothelial dysfunction. An adequate sinusoidal endothelial function is required to maintain an anti-inflammatory, antifibrogenic and antithrombotic environment in the liver. We hypothesize in this project that in NAFLD, which is associated with insulin-resistance, there is sinusoidal endothelial dysfunction, and that this is relevant to the development of liver injury. In the first study, we have demonstrated that after 3-days high fat feeding, rats developed steatosis without the presence of inflammation. Insulin resistance was present at the liver vasculature, and specifically, at the liver sinusoidal endothelium. This was accompanied by a reduction of the ability of insulin to phosphorylate eNOS. The conclusions of this first study were that vascular insulin resistance precedes inflammation, and can contribute to the progression of the disease. In the second study we demonstrate that rats fed for one month with a high fat diet presented steatosis without fibrosis or inflammation. This was accompanied by alterations resembling metabolic syndrome, endothelial dysfunction and a decreased liver eNOS and Akt phosphorylation. This was due to functional alterations (and no structural) at the sinusoidal endothelial cells, without phenotypical changes occurring at this level. We concluded that endothelial dysfunction is a primary event that precedes inflammation in a model of NAFLD, and might constitute a useful target for devising new therapies for this disease.
Takeda, Yoshihisa. "Morphologic alteration of hepatocytes and sinusoidal endothelial cells in rat fatty liver during cold preservation and the protective effect of hepatocyte growth factor". Kyoto University, 1999. http://hdl.handle.net/2433/181710.
Pełny tekst źródłaCao, Peter. "Age-related structural changes in the liver of old mice with SIRT1 overexpression in conjunction with NMN supplementation". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16872.
Pełny tekst źródłaHammoutene, Adel. "Rôle de l’autophagie dans les cellules endothéliales du foie dans le développement de la stéatohépatite non alcoolique A defect in autophagy in liver sinusoidal endothelial cells occurs in NASH and promotes inflammation and fibrosis". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB179.
Pełny tekst źródłaBackground and Aims: Non alcoholic steatohepatitis (NASH) is defined as the excessive lipids accumulation in the liver, hepatocellular injury and inflammation with or without fibrosis. NASH has the potential for cirrhosis and hepatocellular carcinoma. Recent studies suggest that microvascular alterations and sinusoidal endothelial dysfunction precede inflammation and fibrosis in NASH. Autophagy is a cellular process by which the dysfunctional cytoplasmic material joins lysosomes for degradation. The role of autophagy in hepatocytes, in hepatic stellate cells and in liver monocyte-macrophages has been studied but nothing is known about the role of autophagy in liver sinusoidal endothelial cells (LSECs) in NASH. The aim of my thesis work was to investigate the potential implication of autophagy in LSECs in NASH and liver fibrosis. Method: (a) Human samples: I used liver biopsies from patient without liver histological abnormalities, with simple steatosis or with NASH to analyze autophagy in LSECs by electron microscopy. (b) Cultured LSECs: I tested the effect of TNFa and IL6 (at concentrations present in the portal venous blood of patients with metabolic syndrome) on autophagy in LSECs exposed to shear stress. I characterized the effect of autophagy deficiency on the phenotype of LSECs by transducing transformed LSECs with a shRNA targeting ATG5. (c) Transgenic mice: I analyzed the effect of a defect in endothelial autophagy on early stages of NASH, by using mice deficient in autophagy specifically in endothelial cells (Atg5lox/lox-VE-CadherinCre), fed a high fat diet (HFD) for 16 weeks, and on advanced stages of liver fibrosis by treating Atg5lox/lox-VE-CadherinCre mice with carbon tetrachloride (CCl4). Results: (a) Human samples: Patients with NASH had twice less LSECs containing autophagic vacuoles than patients without liver histological abnormalities or patients with simple steatosis. (b) Cultured LSECs: The combination of TNFa and IL6 decreased autophagy level in LSECs. This reduction of autophagy involved the inhibition of AMPKa. LSECs deficient in autophagy overexpressed Mcp1 and Rantes genes and VCAM1 protein expression. Deficiency in autophagy in LSECs induced the expression of the endothelial to mesenchymal transition markers a-SMA, Collagen1a1, Collagen1a2 and Tgf-b1. (c) Transgenic mice: As compared to littermate controls, mice deficient in endothelial ATG5 fed a HFD had a more frequent nodular liver surface, a higher liver inflammation (increased liver gene expression of Mcp-1 and Rantes and VCAM1 protein) and more liver fibrosis (increased liver gene expression of Collagen1a2 and Tgf-b1, higher expression a-SMA protein and more collagen deposition). Mice deficient in ATG5 in endothelial cells treated with CCl4 had more liver fibrosis (increased liver gene expression of a-SMA, Collagen1a1, Collagen 1a2 and Tgf-b1 and more collagen deposition). Conclusion: Autophagy is defective in LSECs of patients with NASH. TNFa and IL6 at concentrations present in the portal blood of patients with NASH could be responsible for this defect through the impairment of AMPKa activity. Autophagy defect in LSECs contributes to the development of liver inflammation and fibrosis at early and advanced stages of the disease. Stimulating endothelial autophagy could be an attractive strategy for NASH treatment
Neumann, Katrin. "Modulation der gewebespezifischen Migration von CD4+ T-Zellen durch das Lebersinusendothel". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16587.
Pełny tekst źródłaT-cell immigration into a tissue is controlled by selective interactions with vascular endothelial cells. The present study addressed the question if interactions between liver sinusoidal endothelial cells (LSEC) and CD4+ T cells influence the tissue-specific migration of CD4+ T cells and thus have relevance for the course of specific immune responses. Antigen presentation by cytokine-activated LSEC increased adhesion and transmigration of antigen-specific CD4+ T cells. These results indicate an involvement of LSEC in the inflammation-induced, antigen-specific migration of CD4+ T cells into the liver tissue. Antigen-specific activation of naive CD4+ T cells by LSEC and their supply of retinoic acid induced expression of gut-specific homing receptors on CD4+ T cells. LSEC-activated CD4+ T cells migrated into the intestine of C57BL/6 mice. The findings presented here imply that LSEC induce a gut-specific homing phenotype resulting in migration of liver-activated CD4+ T cells into the intestine. The active supply of chemokines by LSEC via transcytosis and immobilization enhanced transmigration of CD4+ T cells. Administration of an inhibitor of the endothelial chemokine transcytosis during Concanavalin A-induced autoimmune hepatitis suppressed hepatitis and resulted in reduced migration of activated CD4+ T cells into the liver tissue. The data show the impact of LSEC on the chemokine-dependent recruitment of CD4+ T cells into the liver. In the present study the modulation of the tissue-specific migration of CD4+ T cells by LSEC via antigen presentation and supply of chemokines was demonstrated. Thus, additional functional aspects concerning the immunologic functions of the liver were described.
Warren, Alessandra. "Hepatic sinusoidal cells in liver immunology and ageing". Thesis, The University of Sydney, 2005. https://hdl.handle.net/2123/27902.
Pełny tekst źródłaNörenberg, Astrid [Verfasser], i Michael [Akademischer Betreuer] Ott. "Generation of proliferating hepatocytes, liver sinusoidal endothelial cells and stellate cells and establishment of a genotoxicity assay based on proliferating hepatocytes / Astrid Nörenberg. Klinik für Gastroenterologie, Hepatologie und Endokrinologie AG für Experimentelle und Klinische Infektionsforschung der Medizinische Hochschule Hannover. Betreuer: Michael Ott". Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2014. http://d-nb.info/1050006968/34.
Pełny tekst źródłaJohnson, Sarah J. "Sinusoidal cell responses to experimental liver injury". Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320389.
Pełny tekst źródłaMoriga, Takeo. "Protection by vascular endothelial growth factor against sinusoidal endothelial cell damage and apoptosis induced by cold preservation". Kyoto University, 2000. http://hdl.handle.net/2433/151416.
Pełny tekst źródłaKnight, Tamara, i Hartmut Jaeschke. "Peroxynitrite formation and sinusoidal endothelial cell injury during acetaminophen-induced hepatotoxicity in mice". BioMed Central, 2004. http://hdl.handle.net/10150/610125.
Pełny tekst źródłaMasek, Lisa Christina. "The study of adhesive interactions between haemopoietic progenitor cells and bone marrow sinusoidal endothelial cells". Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242854.
Pełny tekst źródłaSchrage, Arnhild. "Interaktion von T-Zellen mit sinusoidalen Endothelzellen der Leber". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2006. http://dx.doi.org/10.18452/15557.
Pełny tekst źródłaThe liver plays a major role for the metabolism, but it is also of general importance for the immune system, e.g. for the deletion of activated T cells or the induction of peripheral tolerance. Under physiological conditions T cells and other leukocytes can be found in the liver, in the sinusoids as well as in the parenchyma. This hepatic accumulation of T cells might be due to immunosurveillance, but it would also be a prerequisite for modulation of T cells by hepatic cells. The present study investigated two different aspects of the interaction of liver sinusoidal endothelial cells (LSEC), the barrier between the sinusoidal lumen and the hepatic parenchyma, and CD4+ T cells. In the first part of the study it could be demonstrated that LSEC support the spontaneous transmigration of CD4+ T cells as well as their chemotaxis to CXCL12 and CXCL9 more efficiently than other endothelial cells. Whereas a direct endothelial activation by chemokines could be excluded the efficient chemokine presentation at the luminal LSEC surface (after abluminal uptake) might be responsible for the enhanced T cell transmigration. The findings suggest that LSEC might be involved in the recruitment of T cells by supporting a rapid transendothelial migration. The second part of the study focused on the characteristics of LSEC in the context of antigen presentation. LSEC were able to prime and expand naïve CD4+ T cells in vitro but less effective than professional APC as proven by weaker expansion of cells, a requirement for higher antigen concentration and the lack of cytokine producing T cells. The “immature effector” phenotype of the CD4+ T cells primed on LSEC was reversible since it could be overcome by restimulation on professional APC. In conclusion these data suggest that antigen presentation by LSEC results in activation but incomplete differentiation of CD4+ T cells.
Legrand, Alain. "Liposomes cibles et vecteurs retroviraux pour le transfert et l'expression du gene de la preproinsuline i de rat dans des cellules eucaryotes". Orléans, 1987. http://www.theses.fr/1987ORLE2011.
Pełny tekst źródłaSun, Yu-Wen, i 孫毓雯. "Study on the Combined Transplantation of Mesenchymal Stem Cell and Liver Sinusoidal Endothelial Cell to Promote Liver Regeneration". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/84sr3g.
Pełny tekst źródła國立陽明大學
臨床醫學研究所
102
Non-parenchymal cells including liver sinusoidal endothelial cell (LSECs), kupffer cell and stellate cell, especially LSECs, have been known to respond to the microenvironment and promote liver regeneration through mediating the secretion levels of cellular secretomes such as hepatocyte growth factor (HGF), Wnt2, transforming growth factors (TGFs), tumour necrosis factor (TNF-α) and interleukin 6 (IL-6). Mesenchymal stem cells (MSCs) not only have multi-differentiation potential but also contribute to tissue regeneration both in vivo and vitro by paracrine signaling and our previous results have shown that MSCs can rescue carbon tetrachloride (CCl4)-induced liver injuries in mice. In this study, we have demonstrated that expression levels of mitogenic genes, WNT2 and HGF in LSEC were significant increased after co-cultured with MSCs and MSC condition medium which are important in liver. In addition, we found that MSC/LSEC co-cultured condition medium can not only promote the proliferation rate of primary hepatocytes but also increase the productions of albumin compare to hepatocyte growth medium. Although the detail mechanism of how MSCs increase the mitogenic marker expressions in LSECs is not clear, our data suggested that MSC can be used as a potential cell-based therapeutic resource in cooperation with LSEC which promotes liver regeneration.
Kim, Andrew. "Organ transplantation and the liver tolerance effect: history, mechanisms, and potential implications for the future of transplant care". Thesis, 2017. https://hdl.handle.net/2144/23827.
Pełny tekst źródłaChen, Shin-Wei, i 陳欣蔚. "The differentiation of liver sinusoidal endothelium cells from human induced pluripotent stem cells". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/49410032614909348064.
Pełny tekst źródła國立臺灣大學
生化科技學系
101
Hemophilia A is the most common type of hemophilia and is also known as factor VIII (FVIII) deficiency. FVIII is an essential blood clotting factor, and its defects result in the formation of fibrin deficient clots, causing bleeding. liver is a major source of FVIII and the liver sinusoidal endothelial cells (LSEC) are endothelial cells (EC) that line the hepatic microvasculature, sinusoids, which are the major cell type of FVIII production. Previous reports showed that transplantation of LSEC improved the hemophilia phenotype of mice deficient for FVIII. Thus, LSEC is expected to be one of the source for cell therapy of Hemophilia A. My research can be divided into two parts, the generation of human induced pluripotent stem cell (hiPSC) and the differentiation toward LSEC, which can express FVIII, from hiPSC. In the first part, I infect c-Myc, Klf4, Oct4, and Sox2 to human somatic cell line HS68 by lentivirus for human iPSC formation. However, the results from analysis of cell surface antigen and mRNA expression showed that there is no complete pluripotent-specific expressed in cells. LSEC is a specified EC which emerged into liver bud at early development stage. In my second part of thesis, on the basis of differentiation from human embryonic stem cell (hESC) toward EC, associated the previous study: the inhibition of TGFβ/activin signaling could generate LESC-like from mouse ESC. I designed the protocol for inducing hiPSC toward LSEC through conditional medium with specific cytokines such as BMP4, ActivinA, bFGF, VEGF and TGFβ receptor inhibitor (Tbr1ki2) at different stages. By adopting 253G1 into embryonic body (EB) form, I used the protocol for LSEC induction.16 days later, about 55%-differentiated cells expressed a LESC marker, stabilin-2, a major hyaluronan clearance receptor, and incorporated FITC-labeled hyaluronan. Most importantly, those cells produced FVIII as evidenced by mRNA expression and protein secretion. In conclusion, FVIII-producing LSEC can be derived from human iPS cells and those cells may be an excellent source for cell therapy of hemophilia and the application of regeneration medicine.
Bleau, Christian. "Rôle des cellules endothéliales dans l’immunité innée précoce induite lors d’infections par des coronavirus murins". Thèse, 2015. http://hdl.handle.net/1866/13913.
Pełny tekst źródłaEndothelial cells (EC) act as a physical barrier against invasion by pleiotropic blood borne viruses but their contribution in innate antiviral defense is poorly known. Dysfunctions in blood-brain barrier EC (BMECs) and liver sinusoidal EC (LSECs) have been reported in viral neuropathologies and hepatitis, suggesting that loss of ECs integrity may contribute to the pathogenesis. Mouse hepatitis coronaviruses (MHV), differing in their ability to induce severe to subclinical hepatitis and neurological diseases and / or their tropism for ECs, are relevant viral models to study the consequences of EC infection in viral pathogenesis. Following hematogenous infection, the MHV3 serotype, the most virulent MHV, induces fulminant hepatitis, characterized by severe inflammatory response, followed by neurological damage whereas the less virulent MHV-A59 serotype induces milder hepatitis but does not invade the central nervous system (CNS). In addition, MHV3, in contrast to MHV-A59, shows ability to induce TLR2-dependent cytokine response. The attenuated MHV3 variants, 51.6-MHV3 and YAC-MHV3, are characterized by a weak tropism for LSECs and induce moderated and subclinical hepatitis respectively. Given the importance of LSECs in hepatic tolerance and the elimination of circulating pathogens, it has been postulated that the severity of hepatitis and inflammatory response induced by MHVs correlates with infection and alterations in vascular and tolerogenic properties of LSECs. Hepatic inflammatory disorders may result from differential activation of TLR2, rather than other TLRs and helicases, according to serotypes. Moreover, given the role of BMECs in preventing CNS infections, it has been postulated that secondary cerebral invasion by coronaviruses is related to infection of BMECs and subsequent breakdown of the blood-brain barrier (BBB). Through in vitro and in vivo infections of isolated BMECs, LSECs or mice with the different MHVs, we demonstrated, first, that in vitro productive infection of LSECs by the highly virulent MHV3 serotype, in contrast to 51.6- et YAC-MHV3 variants, altered their production of vasoactive factors and overthrew their intrinsic tolerogenic properties by promoting inflammatory cytokines and chemokines production. These disturbances were reflected in vivo by an uncontrolled inflammatory response and a deregulation of intrahepatic leukocyte recruitment, favoring viral replication and liver damages. We demonstrated, using TLR2 KO mice and LSECs treated with siRNA for TLR2 that the abnormal inflammatory response induced by MHV3 depended in part on preferential induction and activation of TLR2 by the virus on the surface of hepatic cells. Moreover, the severity of the primary viral replication in the liver and disorders in intrahepatic leucocyte recruitment induced by MHV3, but not by MHV-A59 and 51.6-MHV3, correlated with a subsequent brain invasion at the BBB level. Such invasion was related to productive infection of BMECs and subsequent IFN--dependent disruption of tight junction proteins occludin, VE-cadherin and ZO-1, resulting in an increase of BBB permeability and further viral entry into the CNS. Overall, the results of this study highlight the importance of structural and functional integrity of LSECs and BMECs during acute viral infections by MHVs to limit liver damages associated with viral-induced exacerbation of inflammatory response and prevent brain invasion by MHVs following viral spread through the bloodstream. They also reveal a new worsening role for TLR2 in the evolution of acute viral hepatitis paving the way for new therapies targeting TLR2-induced inflammatory activity.
Papadimitriou, Minas N. B. "Adhesion of murine RAW117 lymphoma cells to hepatic sinusoidal endothelial cells: Study of surface molecule interactions under flow and effect of cyclooxygenase and lipoxygenase inhibitors". Thesis, 2000. http://hdl.handle.net/1911/19545.
Pełny tekst źródłaHsiao, Yu-Ling, i 蕭玉翎. "Pathological effects of antibodies against dengue virus nonstructural protein 1 in liver damage and endothelial cell activation". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/20832160480205379025.
Pełny tekst źródła國立成功大學
微生物暨免疫學研究所
91
Dengue virus (DV) infection causes dengue fever or severe life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). However, the pathogenesis of DHF/DSS is still not well understood. Previous studies in our laboratory showed that the AST and ALT, but not BUN, in mouse sera increased after either active immunization with DV nonstructural protein 1 (NS1) or passive administration with anti-DV NS1 antibodies (Abs). Furthermore, anti-DV NS1 Abs could bind to mouse vessel endothelium in inferior vena. In this study, we investigate the potential pathogenic role of anti-DV NS1 Abs in the damaged organs. Mice actively immunized with DV NS1 protein revealed the presence of anti-DV NS1 Abs on vessel endothelium in the liver. However, in the kidney, mice actively immunized with DV NS1 protein, JEV NS1 protein or PBS show similar binding patterns. Studies using organ sections from normal mice showed that anti-DV NS1 Abs, but not anti-JEV NS1 Abs, could directly bind to vessel endothelium in the liver sections. However, no specific cross-reaction of anti-DV NS1 Abs with mouse kidney vessel endothelium. Interestingly, gross and histological examinations revealed tissue damage with the presence of macrophage infiltration in the liver of NS1-immunized mice. We speculate that anti-DV NS1-induced endothelial cell dysfunction might result in liver tissue damage, at least in part, by infiltrated cells. Previous in vitro studies in our laboratory showed immune activation including cytokine and chemokine production in endothelial cells after treatment with anti-DV NS1 Abs. In this study, we demonstrated the involvement of upstream regulator NF-kB in immune activation by EMSA. After treatment with NF-kB inhibitor pyrrolidine dithiocarbamate, the expressions of IL-6、IL-8 and MCP-1 which could be stimulated by anti-DV NS1 Abs were inhibited. Taken together, endothelial cell damage and abnormal activation after stimulation by anti-DV NS1 Abs have been examined both in vivo and in vitro. These results imply the involvement of anti-DV NS1 Abs in the pathogenesis of DV infection.
Hu, Shu-Bauh, i 胡淑寶. "Effects of Interferon-α on Vascular Endothelial Growth Factor and E-cadherin Expression in Liver Cancer Cell Lines". Thesis, 2004. http://ndltd.ncl.edu.tw/handle/27512200453751108473.
Pełny tekst źródła高雄醫學大學
藥學研究所碩士在職專班
92
Purpose: Vascular endothelial growth factor(VEGF) and E-cadherin have been examined and taken for indicators of angiogenesis and metastasis respectively. In our study, we evaluated the in vitro effects of IFN-α treatment on the tumorigenicity of liver cancer cell lines. From the changes of the expression of VEGF and E-cadherin, we expected to evaluate the prognostic markers. Materials and Methods: Two well differentiated (Hep G2, Hep 3B) and one poor differentiated (SK-Hep I) human liver cancer lines were used. Cells were incubated with Interferon-α to evaluate their metastatic potential. Hep G2, SK-Hep-I cells were incubated with IFN-α for different concentrations (5000 unit/ml; 1000 unit/ml) and different periods(3;6 days) of time. Then, the VEGF protein expression was assayed by ELISA test in those culture media. The Hep 3B cells were treated with fresh medium, that contained 1000, 5000, 20000 unit/ml INF-α. It were incubated for 3 days. After that, E-cadherin expression changes was confirmed by Western blotting and Immunocytochemistry. All three cell lines, treated with INF-α, their survival rates were measured by cell counting and MTT test . Results: In the angiogenesis study, both in group A(5000 unit/ml; 3days)and group B(1000 unit/ml, 6days), the VEGF protein expression was down-regulated by IFN-α. In Group A, the VEGF protein expression were, in Hep G2 (no IFN-α:124.4, with IFN-α: 76.8),and in SK-Hep-I (no IFN-α: 44.5, with IFN-α: 30.0). In Group B, VEGF protein expression were, in Hep G2 (no IFN-α: 225.5, with IFN-α:151.4) and SK-Hep-I (no IFN-α: 74.1, with IFN-α: 53.4). In the cell invasion study, Western blotting and Immunocytochemistry showed that E-cadherin expression were up-regulated by the increasing concentration of IFN-α. The declined cell number counts and survival rates of all three cell lines showed antiproliferative activity of IFN-α. Conclusion: IFN-α confers its antitumor activity, at least in part, by its antiangiogenic activity, which results from decreased VEGF expression, and by anti-invasive activity, which results from elevated E-cadherin expression and antiproliferative activity on cancer cell lines. The results may help us to design the treatment protocol and to define the chemopreventive role of IFN-α. Key words:Interferon-α,Angiogenesis,Invasion,Metastasis,VEGF,E-cadherin
Lightstone, Noam S. "Design of a Bioreactor to Mimic Hemodynamic Shear Stresses on Endothelial Cells in Microfluidic Systems". Thesis, 2014. http://hdl.handle.net/1807/65572.
Pełny tekst źródłaBurns, C. J., E. Fantino, A. K. Powell, Steven D. Shnyder, Patricia A. Cooper, S. Nelson, C. Christophi i in. "The microtubule depolymerizing agent CYT997 causes extensive ablation of tumor vasculature in vivo". 2011. http://hdl.handle.net/10454/5902.
Pełny tekst źródła