Bibliografías temáticas / Liver sinusoidal endothelial cell

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Literatura académica sobre el tema "Liver sinusoidal endothelial cell"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 21 de febrero de 2023

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Artículos de revistas sobre el tema "Liver sinusoidal endothelial cell"

Couvelard, A., JY Scoazec, MC Dauge, AF Bringuier, F. Potet, and G. Feldmann. "Structural and functional differentiation of sinusoidal endothelial cells during liver organogenesis in humans." Blood 87, no. 11 (June 1, 1996): 4568–80. http://dx.doi.org/10.1182/blood.v87.11.4568.bloodjournal87114568.

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During fetal life, human liver sinusoids, which differentiate between 4 and 12 weeks of gestation from capillaries of the septum transversum, must support an important hematopoietic function and acquire the structural and functional characteristics of adult sinusoids. To gain insight into their differentiation process, we studied the expression of (1) markers of continuous endothelia, absent from adult sinusoidal endothelial cells (PECAM-1, CD34, and 1F10); (2) functional markers of adult sinusoidal endothelial calls (CD4, 1CAM-1, CD32, and CD14); and (3) extracellular matrix components (laminin, tenascin, fibronectin, and thrombospondin) in 37 fetuses of different gestational ages. We identified two successive differentiation events. (1) An early structural differentiation, occurring from 5 to 12 weeks of gestation, was characterized by the loss of continuous endothelial cell markers and a reduction in the perisinusoidal amount of laminin and in the deposition of tenascin, fibronectin, and thrombospondin; at the end of this process, fetal liver sinusoids present structural characteristics comparable to those of the sinuses in adult hematopoietic bone marrow. (2) A later functional differentiation was characterized by the acquisition of the markers of adult sinusoidal endothelial cells, initiating at 10 weeks of gestation and completed by 20 weeks of gestation; this process likely contributes to adapt liver sinusoids to the specific functions of the adult hepatic tissue.

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Maretti-Mira, Ana, and Laurie DeLeve. "Liver Sinusoidal Endothelial Cell: An Update." Seminars in Liver Disease 37, no. 04 (November 2017): 377–87. http://dx.doi.org/10.1055/s-0037-1617455.

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AbstractThis update focuses on two main topics. First, recent developments in our understanding of liver sinusoidal endothelial cell (LSEC) function will be reviewed, specifically elimination of blood-borne waste, immunological function of LSECs, interaction of LSECs with liver metastases, LSECs and liver regeneration, and LSECs and hepatic fibrosis. Second, given the current emphasis on rigor and transparency in biomedical research, the update discusses the need for standardization of methods to demonstrate identity and purity of isolated LSECs, pitfalls in methods that might lead to a selection bias in the types of LSECs isolated, and questions about long-term culture of LSECs. Various surface markers used for immunomagnetic selection are reviewed.

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Tee, Jie, Li Ng, Hannah Koh, David Leong, and Han Ho. "Titanium Dioxide Nanoparticles Enhance Leakiness and Drug Permeability in Primary Human Hepatic Sinusoidal Endothelial Cells." International Journal of Molecular Sciences 20, no. 1 (December 21, 2018): 35. http://dx.doi.org/10.3390/ijms20010035.

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Liver sinusoidal endothelial cells (LSECs) represent the permeable interface that segregates the blood compartment from the hepatic cells, regulating hepatic vascular tone and portal pressure amidst changes in the blood flow. In the presence of pathological conditions, phenotypic changes in LSECs contribute to the progression of chronic liver diseases, including the loss of endothelial permeability. Therefore, modulating LSECs offers a possible way to restore sinusoidal permeability and thereby improve hepatic recovery. Herein, we showed that titanium dioxide nanoparticles (TiO2 NPs) could induce transient leakiness in primary human hepatic sinusoidal endothelial cells (HHSECs). Interestingly, HHSECs exposed to these NPs exhibited reduced protein kinase B (Akt) phosphorylation, an important protein kinase which regulates cell attachment. Using a 3D co-culture system, we demonstrated that TiO2 NPs diminished the attachment of HHSECs onto normal human hepatic cell LO2. To further illustrate the significance of leakiness in liver sinusoids, we showed that NP-induced leakiness promoted Sunitinib transport across the HHSEC layer, resulting in increased drug uptake and efficacy. Hence, TiO2 NPs have the potential to modulate endothelial permeability within the specialized sinusoidal endothelium, especially during events of fibrosis and occlusion. This study highlighted the possible use of inorganic NPs as a novel strategy to promote drug delivery targeting the diseased liver.

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Cogger, Victoria Carroll, Mashani Mohamad, Samantha Marie Solon-Biet, Alistair M. Senior, Alessandra Warren, Jennifer Nicole O'Reilly, Bui Thanh Tung, et al. "Dietary macronutrients and the aging liver sinusoidal endothelial cell." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 9 (May 1, 2016): H1064—H1070. http://dx.doi.org/10.1152/ajpheart.00949.2015.

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Fenestrations are pores within the liver sinusoidal endothelial cells (LSECs) that line the sinusoids of the highly vascularized liver. Fenestrations facilitate the transfer of substrates between blood and hepatocytes. With pseudocapillarization of the hepatic sinusoid in old age, there is a loss of fenestrations. LSECs are uniquely exposed to gut-derived dietary and microbial substrates delivered by the portal circulation to the liver. Here we studied the effect of 25 diets varying in content of macronutrients and energy on LSEC fenestrations using the Geometric Framework method in a large cohort of mice aged 15 mo. Macronutrient distribution rather than total food or energy intake was associated with changes in fenestrations. Porosity and frequency were inversely associated with dietary fat intake, while fenestration diameter was inversely associated with protein or carbohydrate intake. Fenestrations were also linked to diet-induced changes in gut microbiome, with increased fenestrations associated with higher abundance of Firmicutes and reduced abundance of Bacteroidetes. Diet-induced changes in levels of several fatty acids (C16:0, C19:0, and C20:4) were also significantly inversely associated with fenestrations, suggesting a link between dietary fat and modulation of lipid rafts in the LSECs. Diet influences fenestrations and these data reflect both the key role of the LSECs in clearing gut-derived molecules from the vascular circulation and the impact these molecules have on LSEC morphology.

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Enomoto, Katsuhiko, Yuji Nishikawa, Yasufumi Omori, Takuo Tokairin, Masayuki Yoshida, Naoto Ohi, Takuya Nishimura, Youhei Yamamoto, and Qinchang Li. "Cell biology and pathology of liver sinusoidal endothelial cells." Medical Electron Microscopy 37, no. 4 (December 2004): 208–15. http://dx.doi.org/10.1007/s00795-004-0261-4.

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Wang, Lin, Xiangdong Wang, Guanhua Xie, Lei Wang, Colin K. Hill, and Laurie D. DeLeve. "Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats." Journal of Clinical Investigation 122, no. 4 (April 2, 2012): 1567–73. http://dx.doi.org/10.1172/jci58789.

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Pitas, R. E., J. Boyles, R. W. Mahley, and D. M. Bissell. "Uptake of chemically modified low density lipoproteins in vivo is mediated by specific endothelial cells." Journal of Cell Biology 100, no. 1 (January 1, 1985): 103–17. http://dx.doi.org/10.1083/jcb.100.1.103.

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Acetoacetylated (AcAc) and acetylated (Ac) low density lipoproteins (LDL) are rapidly cleared from the plasma (t1/2 approximately equal to 1 min). Because macrophages, Kupffer cells, and to a lesser extent, endothelial cells metabolize these modified lipoproteins in vitro, it was of interest to determine whether endothelial cells or macrophages could be responsible for the in vivo uptake of these lipoproteins. As previously reported, the liver is the predominant site of the uptake of AcAc LDL; however, we have found that the spleen, bone marrow, adrenal, and ovary also participate in this rapid clearance. A histological examination of tissue sections, undertaken after the administration of AcAc LDL or Ac LDL (labeled with either 125I or a fluorescent probe) to rats, dogs, or guinea pigs, was used to identify the specific cells binding and internalizing these lipoproteins in vivo. With both techniques, the sinusoidal endothelial cells of the liver, spleen, bone marrow, and adrenal were labeled. Less labeling was noted in the ovarian endothelia. Uptake of AcAc LDL by endothelial cells of the liver, spleen, and bone marrow was confirmed by transmission electron microscopy. These data suggest uptake through coated pits. Uptake of AcAc LDL was not observed in the endothelia of arteries (including the coronaries and aorta), veins, or capillaries of the heart, testes, kidney, brain, adipose tissue, and duodenum. Kupffer cells accounted for a maximum of 14% of the 125I-labeled AcAc LDL taken up by the liver. Isolated sinusoidal endothelial cells from the rat liver displayed saturable, high affinity binding of AcAc LDL (Kd = 2.5 X 10(-9) M at 4 degrees C), and were shown to degrade AcAc LDL 10 times more effectively than aortic endothelial cells. These data indicate that specific sinusoidal endothelial cells, not the macrophages of the reticuloendothelial system, are primarily responsible for the removal of these modified lipoproteins from the circulation in vivo.

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Koch, Philipp-Sebastian, Ki Hong Lee, Sergij Goerdt, and Hellmut G. Augustin. "Angiodiversity and organotypic functions of sinusoidal endothelial cells." Angiogenesis 24, no. 2 (March 21, 2021): 289–310. http://dx.doi.org/10.1007/s10456-021-09780-y.

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Abstract‘Angiodiversity’ refers to the structural and functional heterogeneity of endothelial cells (EC) along the segments of the vascular tree and especially within the microvascular beds of different organs. Organotypically differentiated EC ranging from continuous, barrier-forming endothelium to discontinuous, fenestrated endothelium perform organ-specific functions such as the maintenance of the tightly sealed blood–brain barrier or the clearance of macromolecular waste products from the peripheral blood by liver EC-expressed scavenger receptors. The microvascular bed of the liver, composed of discontinuous, fenestrated liver sinusoidal endothelial cells (LSEC), is a prime example of organ-specific angiodiversity. Anatomy and development of LSEC have been extensively studied by electron microscopy as well as linage-tracing experiments. Recent advances in cell isolation and bulk transcriptomics or single-cell RNA sequencing techniques allowed the identification of distinct LSEC molecular programs and have led to the identification of LSEC subpopulations. LSEC execute homeostatic functions such as fine tuning the vascular tone, clearing noxious substances from the circulation, and modulating immunoregulatory mechanisms. In recent years, the identification and functional analysis of LSEC-derived angiocrine signals, which control liver homeostasis and disease pathogenesis in an instructive manner, marks a major change of paradigm in the understanding of liver function in health and disease. This review summarizes recent advances in the understanding of liver vascular angiodiversity and the functional consequences resulting thereof.

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Gibert-Ramos, Albert, David Sanfeliu-Redondo, Peio Aristu-Zabalza, Ana Martínez-Alcocer, Jordi Gracia-Sancho, Sergi Guixé-Muntet, and Anabel Fernández-Iglesias. "The Hepatic Sinusoid in Chronic Liver Disease: The Optimal Milieu for Cancer." Cancers 13, no. 22 (November 15, 2021): 5719. http://dx.doi.org/10.3390/cancers13225719.

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The liver sinusoids are a unique type of microvascular beds. The specialized phenotype of sinusoidal cells is essential for their communication, and for the function of all hepatic cell types, including hepatocytes. Liver sinusoidal endothelial cells (LSECs) conform the inner layer of the sinusoids, which is permeable due to the fenestrae across the cytoplasm; hepatic stellate cells (HSCs) surround LSECs, regulate the vascular tone, and synthetize the extracellular matrix, and Kupffer cells (KCs) are the liver-resident macrophages. Upon injury, the harmonic equilibrium in sinusoidal communication is disrupted, leading to phenotypic alterations that may affect the function of the whole liver if the damage persists. Understanding how the specialized sinusoidal cells work in coordination with each other in healthy livers and chronic liver disease is of the utmost importance for the discovery of new therapeutic targets and the design of novel pharmacological strategies. In this manuscript, we summarize the current knowledge on the role of sinusoidal cells and their communication both in health and chronic liver diseases, and their potential pharmacologic modulation. Finally, we discuss how alterations occurring during chronic injury may contribute to the development of hepatocellular carcinoma, which is usually developed in the background of chronic liver disease.

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Zhang, Xingqin, Yi Chen, Liqun Tang, Yunhai Zhang, Pengkai Duan, Lei Su, and Huasheng Tong. "The liver sinusoidal endothelial cell damage in rats caused by heatstroke." European Journal of Inflammation 16 (January 2018): 205873921879432. http://dx.doi.org/10.1177/2058739218794328.

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This study was designed to explore whether liver sinusoidal endothelial cells (SECs) play a pathological role in liver injury of heatstroke (HS) in rats. An HS rat model was prepared in a pre-warmed incubator. Rats were randomized into four groups: HS-sham group (SHAM group), the 39°C group, the 42°C group, and the HS group. The serum concentrations of SEC injury biomarkers including hyaluronic acid (HA), von Willebrand factor (vWF), thrombomodulin (TM), were measured. Plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and endothelium-derived vasoactive substances including endothelin-1 (ET-1) and nitric oxide (NO) were determined using a commercially available kit. Hepatic tissues were obtained for histopathological examination, electron microscopy examination, immunohistochemistry, and reverse transcription polymerase chain reaction (PCR) analysis. Our study team found increased levels of plasma ALT/AST during the course of HS. We were also able to detect microcirculation changes and inflammatory injury of the liver (especially in the sinusoidal areas). In addition, markers of SEC injury were significantly elevated. Thrombosis-related markers including vWF and TF expression levels were significantly upregulated and TM levels downregulated. Furthermore, imbalance between ET-1 and NO levels were detected. In conclusion, damage of SECs could result in microcirculation disturbances and pro-inflammatory injury in the liver during HS, which could prove to be a potential pathogenic mechanism of liver injury in HS.

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Tesis sobre el tema "Liver sinusoidal endothelial cell"

Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Owing 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

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Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells." University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Doctor of Philosophy(PhD) Owing 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

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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/.

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Liver sinusoidal endothelial cells (LSEC) constitute a unique population of endothelial cells with specialised liver-specific morphologic features and functions. LSEC are the only endothelial cells with fenestrations and which lack an organised basement membrane. They are involved in hepatic stellate cell (HSC) quiescence, endocytosis of small particles, selective transfer of substances from the blood, in the hepatic sinusoid, to the parenchymal cells and in liver regeneration. As the group of cells that form the inner lining of the capillaries of the liver sinusoids, and being the first to be in contact with blood-borne particles, pathogens, and xenobiotics, they are prone to the deleterious effects of these. The aims of this thesis were to investigate the unique features of human liver sinusoidal endothelial cells (HLSEC) in comparison with endothelial cells from other vascular beds, evaluate the sensitivities of HLSEC to a range of hepatotoxic drugs, including small-molecule receptor tyrosine kinase inhibitors (RTKIs), such as regorafenib, and to explore the role of HLSEC in a triculture human liver microtissue. Results obtained from this study showed that HLSEC expressed phenotypic features of vascular and lymphatic endothelial cells, particularly vascular endothelial growth factor receptor 2 (VEGFR-2) which could be activated by VEGF-A to stimulate cell proliferation, migration and tubular morphogenesis. HLSEC also expressed functional VEGFR-3. Transcriptomic analysis indicated that HLSEC expressed specialised genes, such as plasmalemma vesicle associated protein (PLVAP), that support its liver-specific structure and functions. HLSEC were more sensitive to a range of small-molecule receptor tyrosine kinase inhibitors than other hepatic cells. (primary human hepatocytes [PHH] and human hepatic fibroblasts [HHF]) and endothelial cells from other vascular beds (human dermal microvascular endothelial cells and human dermal lymphatic endothelial cells). Regorafenib inhibited the activation of VEGFR-2 thereby abrogating cell proliferation, migration, tubular morphogenesis as well as upregulation of angiocrine factors involved in liver regeneration following activation by vascular endothelial growth factor A (VEGF-A). Regorafenib also caused a disruption of cytoskeletal structure of HLSEC and induced apoptosis via activation of caspase 3. Triculture liver microtissues formed with PHH, HLSEC and HHF were vascularised with higher expression of liver-specific drug-metabolising enzymes in comparison with the same combination of cells cultured as a monolayer. However, metabolic competence of triculture liver microtissues was significantly lower than in their monoculture counterparts (consisting of PHH only). This study has further confirmed the uniqueness of HLSEC as a specialised endothelial cell adapted to its anatomical role, which could respond to a range growth factors to initiate endothelial cell-specific functions. It has also been demonstrated that HLSEC are a direct target of hepatotoxic drugs. Triculture liver microtissues generated with PHH, HLSEC and HHF showed less metabolic competence than their PHH-only counterparts. Future studies need to investigate the role of RTKIs in vascular toxicity using in vivo models of sinusoidal obstruction syndrome (SOS) and liver regeneration. Finally, it would be informative to investigate the possibility of identifying HLSEC-specific biomarkers of liver toxicity.

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O'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.

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The majority of liver studies focus on the hepatocyte however the work of this thesis investigates the vital role of the liver sinusoidal endothelial cell (LSEC). LSECs line the liver sinusoids forming a protective barrier between the blood and hepatocytes. The LSEC cytoplasm resembles a sieve, perforated with thousands of transcellular pores of approximately 50-150 nm in diameter called fenestrations, and is underlined by a very sparse extracellular matrix. This facilitates the virtually unimpeded passage of fluid and substances smaller than fenestrations from the blood such as drugs and nutrients, and size-dependent filtration of lipoproteins, to and from hepatocytes. Fenestrations are dynamic structures, in that their size and number can be modulated by hormones, drugs, hepatotoxins, and diseases. Reduction of LSEC fenestration size and number (defenestration) is associated with ageing and pathological states, and is also a cause of hyperlipidemia and reduced drug clearance, thus changes in LSEC morphology can affect the entire organism. This thesis aims to broaden knowledge of the role and ultrastructure of the LSEC in physiological and toxicological states by investigating: whether there is fenestration modulation during fasting that could facilitate increased nutrient exchange between the blood and hepatocytes; whether changes to LSEC ultrastructure during acetaminophen hepatotoxicity are consistent with exacerbation of liver injury and/or with the facilitation of liver regeneration after severe necrosis; whether a substance that targets the LSEC could have a therapeutic benefit in acetaminophen hepatotoxicity by protecting the microvasculature from damage; whether isolation and culture of LSECs from ageing rats maintain the ageing (defenestrated) phenotype, and thus whether it is a valid method to study therapeutic substances in vitro that could reverse defenestration-related ailments associated with normal ageing.

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Rowe, 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/.

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Hepatitis C virus (HCV) infection is a major cause of global morbidity, causing chronic liver injury that can progress to cirrhosis and hepatocellular carcinoma. The liver is a large and complex organ containing multiple cell types, including hepatocytes, sinusoidal endothelial cells (LSEC), stellate cells, Kupffer cells and biliary epithelial cells. Hepatocytes are the major reservoir supporting HCV replication, however, the role of non-‐parenchymal cells in the viral lifecycle remain largely unexplored. Endothelial cell hepatocyte co-‐cultures were established to study the role of LSEC in HCV biology. Vascular endothelial growth factor (VEGF-‐A) regulated transcripts were profiled by microarray to identify factors modulating HCV replication. The initial studies indicated that rather than transmitting HCV to permissive hepatocytes LSEC were protective in HCV infection. Co-‐culture of epithelial and endothelial cell showed that LSEC limit hepatocyte permissivity to HCV infection via cell contact-‐dependent mechanisms and by the expression of soluble mediator(s) that are regulated by VEGF-‐A. Transcript analysis identified LSEC expression of bone morphogenetic protein 4 (BMP4), a novel proviral molecule that is negatively regulated by VEGF-‐A via a VEGF receptor-‐2 (VEGFR-‐2) MAPK dependent pathway. Consistent with the in vitro data I observed increased BMP4 expression and reduced VEGFR-‐2 activation in inflamed liver tissue. These studies show a novel role for LSEC and BMP4 in HCV infection and highlight BMP4 as a new therapeutic target for treating liver disease.

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Mohamad, 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.

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Ageing is associated with increased prevalence of metabolic syndrome, as well as impaired glucose metabolism, hyperinsulinemia and insulin resistance. The mechanism underlying these associations is poorly understood and is likely to be complex and multifactorial. The liver is the key target for insulin action and while the endothelium has been shown to influence insulin activity in muscle and fat, the role of the liver sinusoidal endothelium on the action of insulin in the liver is unknown. The liver sinusoidal endothelium is unique: it is perforated with transcellular pores called fenestrations that facilitate unimpeded passage of substrates between blood and hepatocytes. A constellation of age-related morphological changes in the liver sinusoidal endothelium known as pseudocapillarisation have been described in various species including rats, baboons and humans. During ageing, the liver sinusoidal endothelium thickens, there is basement membrane deposition, and the fenestrations are significantly reduced in size and number (defenestration). Age-related pesudocapillarisation has been shown previously to impede the transfer of lipoproteins and medications across the hepatic sinusoidal endothelium. This thesis tests the hypothesis that changes in the ageing liver contribute to age-related insulin resistance, with alterations of the liver sinusoidal endothelial cell leading to age-related impairment of insulin action and insulin resistance/glucose metabolism. This work aims to improve the understanding of the effects of ageing processes in the liver on insulin action and glucose metabolism. It investigates the role of age-related pseudocapillarisation and the acutely induced poloxamer 407 (P407) model of defenestration in hepatic disposition of insulin and glucose metabolism. This thesis also investigates the effect of P407 on the relationship between membrane rafts and fenestrations in SKHep1 cells, a cell line of liver endothelial origin and isolated LSECs. Finally, the effects of dietary macronutrients and calorie intake on fenestrations in old age are examined. The work contained in this thesis aims to examine the role of age-related pseudocapillarisation in one of the major causes of age-related disease and disability, insulin resistance. In doing so it explores the potential mechanisms involved in these changes and how we may alter the progression of ageing through nutritional intervention.

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Banga, 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.

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Kojima, 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.

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Yagi, 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.

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Miyachi, 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.

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Más fuentes

Libros sobre el tema "Liver sinusoidal endothelial cell"

Morgan, Glyn. Correlation of donor nutritional status with sinusoidal lining cell viability and liver function in the rat. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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Lalor, Patricia, Leo A. van Grunsven, and Thomas Huser, eds. Roles of Liver Sinusoidal Endothelial Cells in Liver Homeostasis and Disease. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-794-8.

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Charles, Balabaud, and Bioulac-Sage Paulette, eds. Sinusoids in human liver: Health and disease : editors, Paulette Bioulac-Sage, Charles Balabaud. Rijswijk, The Netherlands: Kupffer Cell Foundation, 1988.

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Claire Maureen Barbara.* Holloway. Sinusoidal lining cell damage: the critical injury in cold preservation of liver allografts in the rat. 1991.

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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.

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Capítulos de libros sobre el tema "Liver sinusoidal endothelial cell"

Kmieć, Zbigniew. "Sinusoidal Endothelial Cells." In Cooperation of Liver Cells in Health and Disease, 13–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56553-3_3.

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Hilscher, Moira B., Robert C. Huebert, and Vijay H. Shah. "Hepatic sinusoidal endothelial cells." In Signaling Pathways in Liver Diseases, 73–84. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118663387.ch5.

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Huebert, Robert C., and Vijay H. Shah. "Hepatic Sinusoidal Endothelial Cells." In Signaling Pathways in Liver Diseases, 79–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_5.

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DeLeve, Laurie D. "Vascular Liver Disease and the Liver Sinusoidal Endothelial Cell." In Vascular Liver Disease, 25–40. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-8327-5_2.

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Fujiwara, Kenji, and Satoshi Mochida. "Sinusoidal Endothelial Cells in Liver Regeneration." In Liver Diseases and Hepatic Sinusoidal Cells, 114–23. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_8.

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Shakado, Satoshi, Shotaro Sakisaka, Kazunori Noguchi, Michio Sata, and Kyuichi Tanikawa. "Angiogenesis of Cultured Rat Sinusoidal Endothelial Cells." In Liver Diseases and Hepatic Sinusoidal Cells, 124–27. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_9.

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Wisse, E., F. Braet, D. Luo, D. Vermijlen, M. Eddouks, M. Konstandoulaki, C. Empsen, and R. B. de Zanger. "Endothelial Cells of the Hepatic Sinusoids: A Review." In Liver Diseases and Hepatic Sinusoidal Cells, 17–53. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_2.

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Okanoue, Takeshi, Shinichi Sakamoto, Takashi Mori, Yoshihiko Sawa, Hikoharu Kanaoka, Kenichi Nishioji, and Yoshito Itoh. "Role of Sinusoidal Endothelial Cells in Alcoholic Liver Disease." In Liver Diseases and Hepatic Sinusoidal Cells, 190–98. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_15.

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Ohira, Hiromasa, Takato Ueno, Kyuichi Tanikawa, and Reiji Kasukawa. "Changes in Adhesion Molecules of Sinusoidal Endothelial Cells in Liver Injury." In Liver Diseases and Hepatic Sinusoidal Cells, 91–100. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_6.

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Oda, Masaya, Hiroaki Yokomori, and Yoshitaka Kamegaya. "Roles of Sinusoidal Endothelial Cells in the Local Regulation of Hepatic Sinusoidal Blood Flow—Involvement of Endothelins and Nitric Oxide." In Liver Diseases and Hepatic Sinusoidal Cells, 141–55. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_11.

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Actas de conferencias sobre el tema "Liver sinusoidal endothelial cell"

Kang, Young Bok (Abraham), Joseph Cirillo, Siddhartha Rawat, Michael Bouchard, and Hongseok (Moses) Noh. "Layered Hepatocytes and Endothelial Cells on a Transwell Membrane: Toward Engineering the Liver Sinusoid." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-89413.

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This paper presents a novel liver model platform that mimics the liver sinusoid, a functional unit of the liver where most liver activities occur. A key component of the current liver model is a layered co-culture of primary rat hepatocytes (PRH) and primary rat liver sinusoidal endothelial cells (LSEC) or a bovine aortic endothelial cells (BAEC) as an alternative. Poly-dimethylsiloxane (PDMS) microchannels were fabricated and attached to transwell membranes that contain submicroscale pores. Cells were cultured either on one side or on both sides of the transwell membrane, and in both cases cells formed confluent layers. A thin matrigel coating or micro porous membrane was applied between the two cell layers in order to mimic the Space of Disse. We used three different methods to check cell viability: recombinant adenovirus expressing green fluorescent protein, mito-tracker red to stain live mitochondria, and an expression plasmid expressing red fluorescent protein (RFP). It was shown that PRH retained normal morphology and remained viable for about 3 days with BAEC in the PDMS microchannel, about 57 days with BAEC on the transwell, and about 39 days with primary LSEC on the transwell. Preliminary observation suggests that there is formation of structures between hepatocytes that appear similar to bile canaliculi when PRH are co-cultured with endothelial cells. The layered co-culture system seems to be a promising method to generate accurate liver models.

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El-Maarri, Osman, Muhammad Ahmer Jamil, Heike Singer, Rawya Al-Rifai, and Johannes Oldenburg. "Molecular Profiling of Fetal and Adult Liver Sinusoidal Endothelial Cells: A F8 Secreting Cell." In Hamburger Hämophilie Symposion Hamburg, Germany. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1721572.

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McNerney, G. P., W. Hubner, V. C. Cogger, D. L. Thompson, C. I. Oie, L. D. DeLeve, P. McCourt, et al. "Structured illumination microscopy applications towards liver sinusoidal endothelial cell fenestrations and HIV-1 cell-to-cell transmission." In 2010 Asia Communications and Photonics Conference and Exhibition (ACP 2010). IEEE, 2010. http://dx.doi.org/10.1109/acp.2010.5682515.

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Gottwick, Cornelia, Daria Krzikalla, LígiaMargaridaMarques Mesquita, Federica Mancini, Marco Fanzutti, Reinaldo Digigow, AnsgarW Lohse, Antonella Carambia, and Johannes Herkel. "Liver fibrosis does not impair tolerance induction by liver sinusoidal endothelial cells in vivo." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740793.

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Gottwick, C., A. Carambia, R. Digigow, M. Şeleci, D. Mungalpara, M. Heine, FA Schuran, et al. "Nanoparticle-mediated peptide delivery to liver sinusoidal endothelial cells protects from CD8 T cell-driven cholangitis." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402201.

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Harrison, R. "HUMAN HEPATIC ENDOTHELIAL CELLS AND HEPATOCYTES IN CULTURE: MORPHOLOGICAL FEATURES, AND PRODUCTION OF VON WILLEBRAND FACTOR AND FIBRINOGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643350.

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Liver cells were derived from cadaveric organ donors. Pieces of human liver 5 to 50 grams were minced, washed, and incubated in collagenase at 37 degrees C. After washing, the cell suspension was plated into culture vessels that had been briefly pre-treated with an extract derived from human liver. A mixed population of liver cells, including endothelial cells, hepatocytes, and Kupffer cells, attached within hours. At the end of 2 to 3 weeks there developed clusters of densely packed cells of two types. The most numerous cells were initially fusiform but grew as a monolayer even when densely packed. As density increased they assumed a polygonal form; cells with this morphological appearance stained immunocytochemically for von Willebrand factor antigen. They were relatively small and resembled cells derived from human umbilical vein except that the cytoplasm was more filmy in appearance. The second prominent cell type was significantly larger and likewise replicated to form clusters. These large cells sometimes contained multiple nuclei, exhibited a relatively low nuclear to cytoplasmic ratio, and immunocytochemically stained for human fibrinogen. A more distinct nuclear membrane and prominent nucleoli were characteristics of hepatocytes that were useful light microscopically in distinguishing these cells from sinusoidal endothelial cells. Ultrastructurally, endothelial cells were characterized by small size, holes in and among the cells that probably were the in vitro analogue of fenestrae, and numerous Weibel-Palade bodies in the cytoplasm, which otherwise was relatively bland. Hepatocytes, by contrast, had an active appearing cytoplasm containing more organelles. Canaliculi and typical tight junctions formed between adjacent hepatocytes. Levels of vWF and fibrinogen increased in a time dependent manner in media overlying this mixed population of cells. Human factor VIII has not yet been detected in the media overlying these mixed cells derived from human liver, and factor VIII antigen has not yet been demonstrable immunocytochemically in either cell type.

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Colucci, S., S. Hammad, S. Altamura, O. Marques, A. Dropmann, NK Horvat, K. Müdder, K. Gould, S. Dooley та MU Muckenthaler. "Liver sinusoidal endothelial cells suppress BMP2 production in response to TGFβ pathway activation". У Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733619.

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Slater, John H., Shailendra Jain, Robin N. Coger, and Charles Y. Lee. "The Effects of Shear Stress on Endothelial Cells at Hypothermic Temperatures." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33705.

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Hypothermic machine perfusion preservation (MPP) has proven to be a successful technique for hypothermic kidney storage, however this technology has not successfully been applied to the liver. Recent research has indicated that the endothelial cells lining the liver sinusoids display rounding phenomena during MPP that is not fully understood. In order to gain a better understanding of endothelial cell shear stress response and the factors that induce rounding, a temperature-controlled micro-shear chamber has been designed and fabricated. The micro-shear chamber has been used to apply shear stresses, corresponding to those imposed during MPP, to rat liver primary endothelial cell cultures in order to form an understanding of how these stresses affect endothelial cell morphology. The chamber allows for the application of shear stresses ranging from 0.2 ± .01 dynes/cm2 to 2.3 ± 0.3 dynes/cm2, corresponding to what occurs during MPP.] Twenty-four hour in vitro experiments with shear stresses ranging from 0 to 1.49 dynes/cm2 at 4 °C were conducted in order to replicate in vivo conditions of the liver during hypothermic MPP. It has been demonstrated that endothelial cell rounding increases with increasing shear and can be prevented by utilizing low flow rates.

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Butola, Ankit, David A. Coucheron, Karolina Szafranska, Azeem Ahmad, Hong Mao, Jean-Claude Tinguely, Peter McCourt, et al. "Quantitative phase imaging and on-chip nanoscopy for 3D imaging of liver sinusoidal endothelial cells." In Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/dh.2022.w4a.2.

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We present a highly spatially sensitive quantitative phase microscopy system integrated with on-chip nanoscopy to visualize 3D morphology of liver sinusoidal endothelial cells (LSECs). We used the system to obtain 3D morphology of LSEC by using chip-based nanoscopy for lateral super-resolution, and QPM for mapping nanoscale thickness.

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