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Artículos de revistas 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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1

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 (lamin

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2

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 select

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3

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 ind

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4

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 co

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5

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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6

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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7

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 rapi

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8

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, compos

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9

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 communicat

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10

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 subst

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11

DeLeve, Laurie D. "Liver sinusoidal endothelial cells and liver regeneration." Journal of Clinical Investigation 123, no. 5 (May 1, 2013): 1861–66. http://dx.doi.org/10.1172/jci66025.

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12

Xie, Guanhua, Steve S. Choi, Wing-Kin Syn, Gregory A. Michelotti, Marzena Swiderska, Gamze Karaca, Isaac S. Chan, Yuping Chen, and Anna Mae Diehl. "Hedgehog signalling regulates liver sinusoidal endothelial cell capillarisation." Gut 62, no. 2 (February 23, 2012): 299–309. http://dx.doi.org/10.1136/gutjnl-2011-301494.

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13

Tong, Chun-Fang, Yan Zhang, Shou-Qin Lü, Ning Li, Yi-Xin Gong, Hao Yang, Shi-Liang Feng, Yu Du, Dan-Dan Huang та Mian Long. "Binding of intercellular adhesion molecule 1 to β2-integrin regulates distinct cell adhesion processes on hepatic and cerebral endothelium". American Journal of Physiology-Cell Physiology 315, № 3 (1 вересня 2018): C409—C421. http://dx.doi.org/10.1152/ajpcell.00083.2017.

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Flowing polymorphonuclear neutrophils (PMNs) are forced to recruit toward inflamed tissue and adhere to vascular endothelial cells, which is primarily mediated by the binding of β2-integrins to ICAM-1. This process is distinct among different organs such as liver and brain; however, the underlying kinetic and mechanical mechanisms regulating tissue-specific recruitment of PMNs remain unclear. Here, binding kinetics measurement showed that ICAM-1 on murine hepatic sinusoidal endothelial cells (LSECs) bound to lymphocyte function-associated antigen-1 (LFA-1) with higher on- and off-rates but low

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14

Natarajan, Vaishaali, Edward N. Harris, and Srivatsan Kidambi. "SECs (Sinusoidal Endothelial Cells), Liver Microenvironment, and Fibrosis." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4097205.

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Liver fibrosis is a wound-healing response to chronic liver injury such as alcoholic/nonalcoholic fatty liver disease and viral hepatitis with no FDA-approved treatments. Liver fibrosis results in a continual accumulation of extracellular matrix (ECM) proteins and paves the way for replacement of parenchyma with nonfunctional scar tissue. The fibrotic condition results in drastic changes in the local mechanical, chemical, and biological microenvironment of the tissue. Liver parenchyma is supported by an efficient network of vasculature lined by liver sinusoidal endothelial cells (LSECs). These

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15

Zhang, Chunqing, Juren Zu, Hengmei Shi, Jiyong Liu, and Chengyong Qin. "The Effect of Ginkgo biloba Extract (EGb 761) on Hepatic Sinusoidal Endothelial Cells and Hepatic Microcirculation in CCl4 Rats." American Journal of Chinese Medicine 32, no. 01 (January 2004): 21–31. http://dx.doi.org/10.1142/s0192415x04001692.

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It has been shown that Ginkgo biloba Extract (EGb 761) increases peripheral and cerebral blood flow and microcirculation and improves myocardial ischemia reperfusion injury. This study was designed to investigate the effect of EGb 761 on hepatic endothelial cells and hepatic microcirculation. Sixty male Wister rats were divided into normal, carbon tetrachloride ( CCl 4) and EGb groups, and were given normal saline, CCl 4 and CCl 4 plus EGb 761, respectively, for 10 weeks. Samples were taken from the medial lobe of the rat livers ten weeks later. Hepatic sinusoidal endothelial cells and other p

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16

Serra, Monica, Michela Marongiu, Antonella Contini, Toshio Miki, Erika Cadoni, Ezio Laconi, and Fabio Marongiu. "Evidence of Amniotic Epithelial Cell Differentiation toward Hepatic Sinusoidal Endothelial Cells." Cell Transplantation 27, no. 1 (January 2018): 23–30. http://dx.doi.org/10.1177/0963689717727541.

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Amniotic epithelial cells (AECs) represent a useful and noncontroversial source for liver-based regenerative medicine, as they can differentiate into hepatocytes upon transplantation into the liver. However, the possibility that AECs can differentiate into other liver cell types, such as hepatic sinusoidal endothelial cells (HSECs), has never been assessed. In order to test this hypothesis, rat- and human-derived AECs (rAECs and hAECs, respectively) were subjected to endothelial cell tube formation assay in vitro. Moreover, to evaluate differentiation in vivo, the retrorsine (RS) model of live

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17

Kabarriti, R., H. Zhou, J. V. Vainshtein, S. Saha, R. Hannan, N. Thawani, A. Alfieri, S. Kalnicki, and C. Guha. "Transplantation of Liver Sinusoidal Endothelial Cells Repairs HIR Induced Hepatic Endothelial Cell Damage." International Journal of Radiation Oncology*Biology*Physics 78, no. 3 (November 2010): S41. http://dx.doi.org/10.1016/j.ijrobp.2010.07.131.

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18

Speilberg, L., Ø. Evensen, and B. H. Dannevig. "A Sequential Study of the Light and Electron Microscopic Liver Lesions of Infectious Anemia in Atlantic Salmon (Salmo salar L.)." Veterinary Pathology 32, no. 5 (September 1995): 466–78. http://dx.doi.org/10.1177/030098589503200503.

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The present study describes light and electron microscopic changes in the liver of Atlantic salmon during the development of infectious salmon anemia (ISA). Atlantic salmon postsmolts weighing 80-100 g were infected by intraperitoneal injections, and liver samples were collected sequentially between day 0 and day 25 post infection (p.i.), with time intervals of 3-4 days. At each collection time, livers from five infected fish and two control fish were examined. Changes involving the perisinusoidal macrophages were observed by transmission electron microscopy, from day 4 p.i. Large vacuoles, co

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19

Kermani, Pouneh, Anita Ramnarain, Raul Catena, Zu-Lin Chen, Barbara Hempstead, Sidney Strickland, and Karen-Sue B. Carlson. "Laminin Expression Is Necessary for Maintenance of the Vascular Hematopoietic Niche." Blood 118, no. 21 (November 18, 2011): 217. http://dx.doi.org/10.1182/blood.v118.21.217.217.

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Abstract Abstract 217 Laminins are heterotrimeric proteins that are the backbone for all basal laminas. They provide structural support, points for focal adhesion, and biochemical feedback for nearby cells. Laminins are found in many tissues, including bone marrow and lymphoid organs, and are detected in the discontinuous basal lamina of sinusoidal blood vessels. Laminin g1 is the predominant gamma subunit found in the bone marrow and lymphoid tissues. Here we show that the continuous expression of laminin in adulthood is necessary for viability of the vascular hematopoietic niche (sinusoidal

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20

Liu, Songling, and Don C. Rockey. "Cicletanine stimulates eNOS phosphorylation and NO production via Akt and MAP kinase/Erk signaling in sinusoidal endothelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 2 (July 15, 2013): G163—G171. http://dx.doi.org/10.1152/ajpgi.00003.2013.

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The function of the endothelial isoform of nitric oxide synthase (eNOS) and production of nitric oxide (NO) is altered in a number of disease states. Pharmacological approaches to enhancing NO synthesis and thus perhaps endothelial function could have substantial benefits in patients. We analyzed the effect of cicletanine, a synthetic pyridine with potent vasodilatory characteristics, on eNOS function and NO production in normal (liver) and injured rat sinusoidal endothelial cells, and we studied the effect of cicletanine-induced NO on stellate cell contraction and portal pressure in an in viv

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21

McDonald, Braedon, Lisheng Zhuo, Koji Kimata, and Paul Kubes. "Activation of TLR4 on endothelium alone initiates neutrophil adhesion within the liver microcirulation during endotoxemia (102.22)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 102.22. http://dx.doi.org/10.4049/jimmunol.186.supp.102.22.

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Abstract During sepsis and endotoxemia, neutrophils are recruited to the liver where they cause tissue damage and vascular dysfunction. We have previously reported that neutrophils adhere within sinusoids of the endotoxemic liver via interactions between neutrophil CD44 and endothelial hyaluronan. In this study, we aimed to characterize the cellular sentinels that detect circulating LPS via TLR4 and the pathways leading to initiation of neutrophil adhesion via CD44-hyaluronan interactions. Intravital microscopy of bone marrow chimeric mice revealed that TLR4 expression by non-bone marrow deriv

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22

Brougham-Cook, Aidan, Hannah R. C. Kimmel, Chase P. Monckton, Daniel Owen, Salman R. Khetani, and Gregory H. Underhill. "Engineered matrix microenvironments reveal the heterogeneity of liver sinusoidal endothelial cell phenotypic responses." APL Bioengineering 6, no. 4 (December 1, 2022): 046102. http://dx.doi.org/10.1063/5.0097602.

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Fibrosis is one of the hallmarks of chronic liver disease and is associated with aberrant wound healing. Changes in the composition of the liver microenvironment during fibrosis result in a complex crosstalk of extracellular cues that promote altered behaviors in the cell types that comprise the liver sinusoid, particularly liver sinusoidal endothelial cells (LSECs). Recently, it has been observed that LSECs may sustain injury before other fibrogenesis-associated cells of the sinusoid, implicating LSECs as key actors in the fibrotic cascade. A high-throughput cellular microarray platform was u

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23

Zhang, J. X., M. Bauer, and M. G. Clemens. "Vessel- and target cell-specific actions of endothelin-1 and endothelin-3 in rat liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 2 (August 1, 1995): G269—G277. http://dx.doi.org/10.1152/ajpgi.1995.269.2.g269.

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We studied the sinusoidal and extrasinusoidal constrictor response of hepatic microcirculation to endothelin-1 (ET-1) and endothelin-3 (ET-3) and the possible role of Ito cells vs. Kupffer cells or endothelial cells in mediating this response, using isolated rat livers under high-power intravital microscopy. Rats were pretreated by injection of 2.6 x 10(8) fluorescent latex beads (1 micron) intravenously to label Kupffer cells. Three hours later livers were isolated and perfused before and during the infusion of 1 nM ET-1 or ET-3 with or without the endothelin type A (ETA) receptor antagonist

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24

FRENOY, J., S. MAGNUSSON, E. TURPIN, and T. BERG. "Interaction of ricin with sinusoidal endothelial rat liver cells." Cell Biology International Reports 14 (September 1990): 248. http://dx.doi.org/10.1016/0309-1651(90)91091-h.

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25

de Haan, Willeke, Cristina Øie, Mohammed Benkheil, Wouter Dheedene, Stefan Vinckier, Giulia Coppiello, Xabier López Aranguren, et al. "Unraveling the transcriptional determinants of liver sinusoidal endothelial cell specialization." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (April 1, 2020): G803—G815. http://dx.doi.org/10.1152/ajpgi.00215.2019.

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Liver sinusoidal endothelial cells (LSECs) are the first liver cells to encounter waste macromolecules, pathogens, and toxins in blood. LSECs are highly specialized to mediate the clearance of these substances via endocytic scavenger receptors and are equipped with fenestrae that mediate the passage of macromolecules toward hepatocytes. Although some transcription factors (TFs) are known to play a role in LSEC specialization, information about the specialized LSEC signature and its transcriptional determinants remains incomplete. Based on a comparison of liver, heart, and brain endothelial cel

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26

Werner, Melanie, Stefan Schefczyk, Martin Trippler, Juergen W. Treckmann, Hideo A. Baba, Guido Gerken, Joerg F. Schlaak, and Ruth Broering. "Antiviral Toll-like Receptor Signaling in Non-Parenchymal Liver Cells Is Restricted to TLR3." Viruses 14, no. 2 (January 24, 2022): 218. http://dx.doi.org/10.3390/v14020218.

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The role of non-parenchymal liver cells as part of the hepatic, innate immune system in the defense against hepatotropic viruses is not well understood. Here, primary human Kupffer cells, liver sinusoidal endothelial cells and hepatic stellate cells were isolated from liver tissue obtained after tumor resections or liver transplantations. Cells were stimulated with Toll-like receptor 1–9 ligands for 6–24 h. Non-parenchymal liver cells expressed and secreted inflammatory cytokines (IL6, TNF and IL10). Toll-like receptor- and cell type-specific downstream signals included the phosphorylation of

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27

Knolle, Percy A., and Dirk Wohlleber. "Immunological functions of liver sinusoidal endothelial cells." Cellular & Molecular Immunology 13, no. 3 (April 4, 2016): 347–53. http://dx.doi.org/10.1038/cmi.2016.5.

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Rieder, H., K.-H. Meyer zum Büschenfelde, and G. Ramadori. "Functional spectrum of sinusoidal endothelial liver cells." Journal of Hepatology 15, no. 1-2 (May 1992): 237–50. http://dx.doi.org/10.1016/0168-8278(92)90042-n.

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29

Parrow, Nermi L., and Robert E. Fleming. "Liver sinusoidal endothelial cells as iron sensors." Blood 129, no. 4 (January 26, 2017): 397–98. http://dx.doi.org/10.1182/blood-2016-12-754499.

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Klenerman, Paul, and Narayan Ramamurthy. "Liver Sinusoidal Endothelial Cells: An Antiviral “Defendothelium”." Gastroenterology 148, no. 2 (February 2015): 288–91. http://dx.doi.org/10.1053/j.gastro.2014.12.010.

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31

DeLeve, Laurie D. "Liver sinusoidal endothelial cells in hepatic fibrosis." Hepatology 61, no. 5 (March 23, 2015): 1740–46. http://dx.doi.org/10.1002/hep.27376.

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32

Jarnagin, W. R., D. C. Rockey, V. E. Koteliansky, S. S. Wang, and D. M. Bissell. "Expression of variant fibronectins in wound healing: cellular source and biological activity of the EIIIA segment in rat hepatic fibrogenesis." Journal of Cell Biology 127, no. 6 (December 15, 1994): 2037–48. http://dx.doi.org/10.1083/jcb.127.6.2037.

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We have examined the cell-specific expression of two fibronectin isoforms, EIIIA and EIIIB, during experimental hepatic fibrosis induced by ligation of the biliary duct. AT the mRNA level, EIIIA and EIIIB were undetectable in normal liver but expressed early injury, preceding fibrosis. The cellular sources of these changes were determined by fractionating the liver at various time points after bile duct ligation into its constituent cell populations and extracting RNA from the fresh isolates. EIIIA-containing fibronectin mRNA was undetectable in normal sinusoidal endothelial cells but increase

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33

Balaphas, Alexandre, Jeremy Meyer, Remo Perozzo, Magali Zeisser-Labouebe, Sarah Berndt, Antoine Turzi, Pierre Fontana, Leonardo Scapozza, Carmen Gonelle-Gispert та Leo Bühler. "Platelet Transforming Growth Factor-β1 Induces Liver Sinusoidal Endothelial Cells to Secrete Interleukin-6". Cells 9, № 5 (25 травня 2020): 1311. http://dx.doi.org/10.3390/cells9051311.

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The roles and interactions of platelets and liver sinusoidal endothelial cells in liver regeneration are unclear, and the trigger that initiates hepatocyte proliferation is unknown. We aimed to identify the key factors released by activated platelets that induce liver sinusoidal endothelial cells to produce interleukin-6 (IL-6), a cytokine implicated in the early phase of liver regeneration. We characterized the releasate of activated platelets inducing the in vitro production of IL-6 by mouse liver sinusoidal endothelial cells and observed that the stimulating factor was a thermolabile protei

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Colucci, Silvia, Sandro Altamura, Matthias Hentze, and Martina U. Muckenthaler. "Sensing of Liver Iron Content Requires Cell-Cell Communication between Hepatocytes and Liver Sinusoidal Endothelial Cells." Blood 134, Supplement_1 (November 13, 2019): 432. http://dx.doi.org/10.1182/blood-2019-125586.

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The liver stores iron and senses systemic and tissue iron availability. Hepatocytes control iron homeostasis by producing the peptide hormone hepcidin that controls dietary iron absorption and iron release from intracellular stores. Recent data challenged the exclusive role of hepatocytes in controlling iron levels. Indeed, liver sinusoidal endothelial cells (LSECs) increase BMP2 and BMP6 levels in response to iron, which control hepcidin expression in a paracrine manner. However the molecular mechanism(s) of how BMPs respond to iron levels remain unknown. We established primary murine LSEC cu

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Vats, Ravi, Ziming Li, Eun-Mi Ju, Rikesh K. Dubey, Tomasz W. Kaminski, Simon Watkins, and Tirthadipa Pradhan-Sundd. "Intravital imaging reveals inflammation as a dominant pathophysiology of age-related hepatovascular changes." American Journal of Physiology-Cell Physiology 322, no. 3 (March 1, 2022): C508—C520. http://dx.doi.org/10.1152/ajpcell.00408.2021.

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Aging is the most significant risk factor for the majority of chronic diseases, including liver disease. The cellular, molecular, and pathophysiological mechanisms that promote age-induced hepatovascular changes are unknown due to our inability to visualize changes in liver pathophysiology in live mice over time. We performed quantitative liver intravital microscopy (qLIM) in live C57BL/6J mice to investigate the impact of aging on the hepatovascular system over a 24-mo period. qLIM revealed that age-related hepatic alterations include reduced liver sinusoidal blood flow, increased sinusoidal

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Ezhilarasan, Devaraj. "Endothelin-1 in portal hypertension: The intricate role of hepatic stellate cells." Experimental Biology and Medicine 245, no. 16 (August 13, 2020): 1504–12. http://dx.doi.org/10.1177/1535370220949148.

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Portal hypertension is one of the most important cirrhosis-associated complications of chronic liver disease, leading to significant morbidity and mortality. After chronic liver injury, hepatic stellate cells reside in the perisinusoidal space activted and acquire a myofibroblast-like phenotype. The activated hepatic stellate cells act as both sources as well as the target for a potent vasoconstrictor endothelin-1. Activation of hepatic stellate cells plays a vital role in the onset of cirrhosis by way of increased extracellular matrix production and the enhanced contractile response to vasoac

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37

Ribera, Jordi, Montse Pauta, Pedro Melgar-Lesmes, Bernat Córdoba, Anna Bosch, Maria Calvo, Daniel Rodrigo-Torres, et al. "A small population of liver endothelial cells undergoes endothelial-to-mesenchymal transition in response to chronic liver injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 5 (November 1, 2017): G492—G504. http://dx.doi.org/10.1152/ajpgi.00428.2016.

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Rising evidence points to endothelial-to-mesenchymal transition (EndMT) as a significant source of the mesenchymal cell population in fibrotic diseases. In this context, we hypothesized that liver endothelial cells undergo EndMT during fibrosis progression. Cirrhosis in mice was induced by CCl4. A transgenic mouse expressing a red fluorescent protein reporter under the control of Tie2 promoter (Tie2-tdTomato) was used to trace the acquisition of EndMT. Sinusoidal vascular connectivity was evaluated by intravital microscopy and high-resolution three-dimensional confocal microscopy. A modest but

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Yokomori, Hiroaki. "New insights into the dynamics of sinusoidal endothelial fenestrae in liver sinusoidal endothelial cells." Medical Molecular Morphology 41, no. 1 (March 2008): 1–4. http://dx.doi.org/10.1007/s00795-007-0390-7.

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Meyer, Jeremy, Stéphanie Lacotte, Philippe Morel, Carmen Gonelle-Gispert, and Léo Bühler. "An optimized method for mouse liver sinusoidal endothelial cell isolation." Experimental Cell Research 349, no. 2 (December 2016): 291–301. http://dx.doi.org/10.1016/j.yexcr.2016.10.024.

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40

Romayor, Irene, Joana Márquez, Aitor Benedicto, Alba Herrero, Beatriz Arteta, and Elvira Olaso. "Tumor DDR1 deficiency reduces liver metastasis by colon carcinoma and impairs stromal reaction." American Journal of Physiology-Gastrointestinal and Liver Physiology 320, no. 6 (June 1, 2021): G1002—G1013. http://dx.doi.org/10.1152/ajpgi.00078.2021.

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Tumor DDR1 acts as a key factor during the desmoplastic response surrounding hepatic colorectal metastasis. Hepatic sinusoidal cell-derived soluble factors stimulate tumor DDR1 activation. DDR1 modulates matrix remodeling to promote metastasis in the liver through the interaction with hepatic stromal cells, specifically liver sinusoidal endothelial cells and hepatic stellate cells.

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41

Kostallari, Enis, and Vijay H. Shah. "Angiocrine signaling in the hepatic sinusoids in health and disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 2 (August 1, 2016): G246—G251. http://dx.doi.org/10.1152/ajpgi.00118.2016.

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The capillary network irrigating the liver is important not only for nutrient and oxygen delivery, but also for the signals distributed to other hepatic cell types necessary to maintain liver homeostasis. During development, endothelial cells are a key component in liver zonation. In adulthood, they maintain hepatic stellate cells and hepatocytes in quiescence. Their importance in pathobiology is highlighted in liver regeneration and chronic liver diseases, where they coordinate paracrine cell behavior. During regeneration, liver sinusoidal endothelial cells induce hepatocyte proliferation and

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42

Sun, Xinghui, and Edward N. Harris. "New aspects of hepatic endothelial cells in physiology and nonalcoholic fatty liver disease." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1200—C1213. http://dx.doi.org/10.1152/ajpcell.00062.2020.

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The liver is the central metabolic hub for carbohydrate, lipid, and protein metabolism. It is composed of four major types of cells, including hepatocytes, endothelial cells (ECs), Kupffer cells, and stellate cells. Hepatic ECs are highly heterogeneous in both mice and humans, representing the second largest population of cells in liver. The majority of them line hepatic sinusoids known as liver sinusoidal ECs (LSECs). The structure and biology of LSECs and their roles in physiology and liver disease were reviewed recently. Here, we do not give a comprehensive review of LSEC structure, functio

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43

Wang, Lin, Xiangdong Wang, Lei Wang, Jenny D. Chiu, Gijs van de Ven, William A. Gaarde, and Laurie D. DeLeve. "Hepatic Vascular Endothelial Growth Factor Regulates Recruitment of Rat Liver Sinusoidal Endothelial Cell Progenitor Cells." Gastroenterology 143, no. 6 (December 2012): 1555–63. http://dx.doi.org/10.1053/j.gastro.2012.08.008.

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44

Neubauer, Katrin, Thomas Wilfling, Andreas Ritzel, and Giuliano Ramadori. "Platelet-endothelial cell adhesion molecule-1 gene expression in liver sinusoidal endothelial cells during liver injury and repair." Journal of Hepatology 32, no. 6 (June 2000): 921–32. http://dx.doi.org/10.1016/s0168-8278(00)80096-3.

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45

Dini, L., A. Lentini, G. D. Diez, M. Rocha, L. Falasca, L. Serafino, and F. Vidal-Vanaclocha. "Phagocytosis of apoptotic bodies by liver endothelial cells." Journal of Cell Science 108, no. 3 (March 1, 1995): 967–73. http://dx.doi.org/10.1242/jcs.108.3.967.

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Using electron microscopy and cytofluorimetry we studied the role of carbohydrate-specific recognition systems in the interaction of apoptotic bodies with normal and interleukin 1-activated sinusoidal endothelial cells. Microfluorimetric observation of liver tissue sections revealed octadecylrhodamine B-labelled apoptotic body binding to the sinusoidal wall of mouse liver, when they were injected intraportally. Plate-scanning cytofluorimetry demonstrated that about 20–25% of Acridine Orange-labelled apoptotic bodies could adhere specifically to cultured endothelial cells after 15 minutes of in

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46

Hutchins, Noelle, Joshua Borgerding, Chun-Shiang Chung, and Alfred Ayala. "Liver sinusoidal endothelial cells undergo apoptosis during sepsis, leading to organ dysfunction. (54.13)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 54.13. http://dx.doi.org/10.4049/jimmunol.186.supp.54.13.

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Abstract Sepsis is the leading cause of death in critically ill patients, and treatment options are limited. Our laboratory studies polymicrobial sepsis in murine models, and uses the liver as a model organ to investigate the disease’s pathophysiology. The liver, characterized as an immune tolerant organ, is susceptible to septic induced inflammation. We have previously reported that there is a twofold increase in the number of liver CD8+ T cells, 24 hours following cecal ligation and puncture (CLP—a surgical procedure that generates sepsis in mice). Since activated T lymphocytes must transver

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47

Feng, Ya-xing, Wei Li, Xu-dong Wen, Ning Zhang, Wei-hui Liu, and Zhan-yu Yang. "Sinusoidal Endothelial Cell Progenitor Cells Promote Tumour Progression in Patients with Hepatocellular Carcinoma." Stem Cells International 2020 (November 28, 2020): 1–12. http://dx.doi.org/10.1155/2020/8819523.

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Objective. As sinusoidal endothelial cell progenitor cells (SEPCs) play a significant role in liver regeneration, it is necessary to elucidate whether SEPCs participate in tumour progression of hepatocellular carcinoma (HCC). Methods. A total of 45 patients with primary HCC who underwent liver resection were included in this study. The liver tumours were removed from the patients, and partial tissues were prepared to identify SEPCs through double staining of CD133/CD45 and CD133/CD31 at the same location. Blood samples were collected to examine liver function parameters and tumour markers. The

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48

Gudapati, Shweta, Tomasz W. Kaminski, Ravi Vats, Prithu Sundd, and Tirthadipa Pradhan-Sundd. "A Dedifferentiated Sinusoidal Endothelium Impacts Liver-Directed Gene Transfer in Hemophilia-a Mice." Blood 138, Supplement 1 (November 5, 2021): 3981. http://dx.doi.org/10.1182/blood-2021-152905.

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Abstract Hemophilia A is an X-linked recessive bleeding disorder that affects 1 in 5000 males and is caused by procoagulant factor VIII deficiency. Affected people are at danger of spontaneous bleeding into organs, which can be fatal and lead to persistent damage. Current therapy includes intravenous infusion of FVIII protein concentrate which carries the danger of transmitting blood-borne diseases. As a result of recent advancements in liver-directed gene transfer, gene therapy based innovative strategy for treating hemophilia has emerged. In patients with severe hemophilia B, intravenous inf

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Frenzel, C., J. Wasielica, J. Herkel, and A. W. Lohse. "637 Murine liver sinusoidal endothelial cells suppress T cell activation by dendritic cells." Journal of Hepatology 44 (April 2006): S236. http://dx.doi.org/10.1016/s0168-8278(06)80637-9.

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50

Konkle, BA, SJ Schuster, MD Kelly, K. Harjes, DE Hassett, M. Bohrer, and M. Tavassoli. "Plasminogen activator inhibitor-1 messenger RNA expression is induced in rat hepatocytes in vivo by dexamethasone." Blood 79, no. 10 (May 15, 1992): 2636–42. http://dx.doi.org/10.1182/blood.v79.10.2636.2636.

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Abstract Plasminogen activator inhibitor-1 (PAI-1), the major physiologic inhibitor of tissue plasminogen activator (tPA), plays a crucial role in the regulation of fibrinolysis. Both hepatocytes and endothelial cells have been implicated as major sources of plasma PAI-1. To study the relative contribution of these cell types to hepatic PAI-1 production, we have separated hepatocytes and hepatic sinusoidal endothelial cells by fractionation of freshly isolated rat livers using metrizamide density gradients and centrifugal elutriation. In untreated animals, PAI-1 messenger RNA (mRNA) was detect

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