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Sinusoidal obstruction syndrome SOS: A light and electron microscopy study in human liver. Oxaliplatin is an important chemotherapeutic agent, used in the treatment of hepatic colorectal metastases, and known to induce the sinusoidal obstruction syndrome SOS.

Pathophysiological knowledge concerning SOS is based on a rat model. Therefore, the aim was to perform a comprehensive study of the features of human SOS, using both light microscopy LM and electron microscopy EM. Included were all patients of whom wedge liver biopsies were collected during a partial hepatectomy for colorectal liver metastases, in a 4-year period. The wedge biopsy were perfusion fixated and processed for LM and EM.

Material was available of 30 patients, of whom 28 patients received neo-adjuvant oxaliplatin. The lesions consisted of sinusoidal endothelial cell detachment from the space of Disse on EM. In the enlarged space of Disse a variable amount of erythrocytes were located.

Sinusoidal endothelial cell detachment was present in human SOS, accompanied by enlargement of the space of Disse and erythrocytes in this area. These findings, originally described in a rat model, were now for the first time confirmed in human livers under clinically relevant settings. Liver sinusoidal endothelial cells LSECswhich are specialized endothelial cells that line liver sinusoidshave been reported to participate in a variety of liver functions, such as blood macromolecule clearance and factor VIII production.

In addition, LSECs play crucial roles in liver regeneration following acute liver injury, as well as the development and progression of liver diseases or drug-induced hepatotoxicity. However, the molecular mechanisms underlying their roles remain mostly unknown. Designing a fibrotic microenvironment to investigate changes in human liver sinusoidal endothelial cell function.

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The deposition nesk extracellular matrix ECM proteins by hepatic cells during fibrosis leads to the stiffening of the organ and perturbed cellular functions. Changes in the elasticity of liver tissue are manifested by altered phenotype in hepatic cells. We have investigated changes in human liver sinusoidal endothelial cells hLSECs that occur as the elastic modulus of their matrix transitions from healthy 6kPa to fibrotic 36kPa conditions.

We report the complete loss of fenestrae and the expression of CD31 at the surface as a result of increasing elastic moduli. LSECs exhibited a greater number of actin stress fibers and vinculin focal adhesion on the stiffer substrate, as well.

A novel finding is that these identical trends can be obtained on soft 6kPa substrates by introducing an inflamed microenvironment through the addition of Kupffer cells. These results demonstrate that the increasing stiffness of cathrynn matrices pxjkos not solely result in changes in hLSEC phenotype.

Even on soft substrates, culturing hLSECs in an inflamed microenvironment can result in their dedifferentiation.

Our findings demonstrate the interplay between matrix elasticity and inflammation in the progression of hepatic fibrosis. Published by Elsevier Ltd.

The liver -specific natural killer NK cell population is critical for local innate immune pzjkos, but the mechanisms that lead to their selective homing and the definition of their functionally relevance remain enigmatic.

We took advantage of the availability of healthy human liver acthryn rigorously define the mechanisms regulating the homing of NK cells to liver and the repertoire of receptors that distinguish liver -resident NK lr-NK cells from circulating counterparts. CD56 bright lr-NK cells co-exist with CD56 dim conventional NK c-NK cells that are, interestingly, transcriptionally and phenotypically similar to their peripheral circulating counterparts.

Our findings disclosing the phenotypic and functional differences between lr-Nk cells and c-NK cells pajkoe critical to distinguish liver -specific innate immune responses. Rationale The liver -specific natural killer NK cell population is critical for local innate immune responses, but the mechanisms that lead to their selective homing and the definition of their functionally relevance remain enigmatic. Objectives We took advantage of the availability of healthy human liver to rigorously define the mechanisms regulating the homing of NK cells to liver and the repertoire of receptors that distinguish liver -resident NK lr-NK cells from circulating counterparts.


CD56bright lr-NK cells co-exist with CD56dim conventional NK c-NK cells that are, interestingly, transcriptionally and phenotypically similar to their peripheral circulating counterparts. Conclusion Our findings disclosing the phenotypic and functional differences between lr-Nk cells and c-NK cells are critical to distinguish liver -specific innate immune responses.

Specific gene delivery to liver sinusoidal and artery endothelial cells. Different types of endothelial cells EC fulfill distinct tasks depending on their microenvironment.


ECs are therefore difficult to genetically manipulate ex vivo for functional studies vathryn gene therapy. Tumor ECs were specifically targeted upon intratumoral vector injection.

Delivery of the erythropoietin gene with mCDLV resulted in substantially increased erythropoietin and hematocrit levels. Interestingly, when applied at higher dose and in absence of target cells pakos the liverhuCDLV transduced ECs of a human artery transplanted into the descending mouse aorta. The data demonstrate for the cloper time targeted ctahryn delivery to specialized ECs upon systemic vector administration. This strategy offers novel options to better understand the physiological functions of ECs and to treat genetic diseases such as those affecting blood factors.

Liver sinusoidal endothelial cells LSECs are the main endothelial cells in the liver and are important for maintaining liver homeostasis as well as responding to injury. LSECs express cellular fibronectin containing the alternatively spliced extra domain A EIIIA-cFN and increase expression of this isoform after liver injury, although its function is not well understood.

We carried out two-thirds partial hepatectomies in mice lacking EIIIA-cFN and in their meks type littermates, studied liver endothelial cell adhesion on decellularized, EIIIA-cFN-containing matrices and investigated the role of cellular fibronectins in liver endothelial cell tubulogenesis.

We found that liver weight recovery following hepatectomy was significantly delayed and that sinusoidal repair was impaired in EIIIA-cFN null mice, especially females, as was the lipid accumulation typical of the post-hepatectomy liver. In vitro, we found that liver endothelial cells were more adhesive to cell-deposited matrices containing the EIIIA domain and that cellular fibronectin enhanced tubulogenesis and vascular cord formation.

Dietary macronutrients and the aging liver sinusoidal endothelial cell. 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 dooper 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 C 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.

Does pressure cause liver cirrhosis? The sinusoidal pressure hypothesis. Independent of their etiology, all chronic liver diseases ultimately lead to liver cirrhosis, which is a major health problem worldwide. The underlying molecular mechanisms are still poorly understood and no catyryn treatment strategies are available.

This paper introduces the sinusoidal pressure hypothesis SPHwhich identifies an elevated sinusoidal pressure SP as cause of fibrosis. SPH has been mainly derived from recent studies on liver stiffness. So far, pressure changes have been exclusively seen as a consequence of cirrhosis. According to the SPH, however, an elevated SP is the major upstream event that initiates fibrosis via biomechanic signaling by stretching of perisinusoidal cells such as hepatic stellate cells or fibroblasts SPH part I: Fibrosis progression is determined by the degree and time of elevated SP.


Elevated arterial flow and final arterialization of the cirrhotic liver represents the self-perpetuating key event exposing the low-pressure-organ to pathologically high pressures SPH part II: It also defines the “point of no return” where fibrosis progression becomes irreversible. The SPH is able to explain the macroscopic changes of cirrhotic livers and the uniform fibrotic response to various meks. It also opens up new views on the role of fat and disease mechanisms in other organs.

The novel concept will hopefully stimulate the search for new treatment strategies. Peliosis hepatis and sinusoidal dilation during infection by the human immunodeficiency virus HIV. The caturyn of hepatic sinusoidal lesions in a significant number of acquired immunodeficiency syndrome AIDS patients prompted the authors to undertake an ultrastructural study of the sinusoidal barrier abnormalities during human ;ajkos virus HIV infection, in order to compare these lesions with those described in other conditions and to discuss their possible origin.

Peliosis hepatis was present in 2 cases, and sinusoidal dilatation in 6. These patients were classified as follows: Ultrastructural lesions of the sinusoidal barrier were observed in all the cases. They closely mimicked the changes previously reported in peliotic and peliotic-like changes of various origins. A striking particularity was, however, the presence of numerous and hyperplastic sinusoidal macrophages. This work suggests that an injury of the endothelial cathrym, directly or indirectly related to the presence of HIV, may be incriminated in the pathogenesis of sinusoidal lesions during HIV infection.

Cultured mycelium Cordyceps sinensis protects liver sinusoidal endothelial cells in acute liver injured mice. Cultured mycelium Cordyceps sinensis CMCS was widely used for a variety of diseases including liver injury, the current study aims to investigate the protective effects of CMCS on liver sinusoidal endothelial cells LSECs in acute injury liver and related action mechanisms.

The Serum liver function parameters including alanine aminotransferase ALT and aspartate aminotransferase AST levels were assayed with the commercial kit. The inflammation and scaffold structure in liver were stained with hematoxylin and eosin and silver staining respectively. The LSECs and sub-endothelial basement membrane were observed with the scanning and transmission electronic microscope. Expression of catbryn Willebrand factor vWF was investigated with immunofluorescence staining.

Hydrodynamic liver gene transfer mechanism involves transient sinusoidal blood stasis and massive hepatocyte endocytic vesicles. The medk study contributes to clarify the mechanism underlying the high efficacy of hepatocyte gene transfer mediated by hydrodynamic injection. Gene transfer cathryb were performed employing the hAAT gene, and the efficacy and differential identification in mouse plasma cioper human transgene versus mouse gene was assessed by ELISA coper proteomic procedures, respectively.

By applying different experimental strategies such pajks cumulative dose-response efficacy, hemodynamic changes reflected by venous pressures, intravital microscopy, and morphological changes established by pwjkos electron microscopy, we found that: We suggest that the mechanism of hydrodynamic liver gene transfer involves transient inversion pajkod intrahepatic flow, sinusoidal blood stasis, and massive fluid endocytic vesicles in pericentral vein hepatocytes.

Separation of pure cell populations from the liver is a prerequisite to study the cathdyn of hepatic parenchymal and non-parenchymal cells in liver physiology, pathophysiology, and immunology. Traditional methods for hepatic cell separation usually purify only single cell types from liver specimens. Here, we describe an efficient method that can simultaneously purify populations of hepatocytes HCs mes, liver sinusoidal endothelial cahhryn LSECsand Kupffer cells KCs from a single mouse liver specimen.

Changes coopdr receptor-mediated endocytosis in liver sinusoidal cells after partial hepatectomy in the rat. Liver mek cells play an important role in host defense by clearing particulate matter and macromolecules from the circulation. In this study, receptor-mediated endocytosis in sinusoidal cells was examined in pajos hepatectomized rats using I-labeled formaldehyde-treated bovine serum albumin fBSA as an endocytable macromolecule. The liver -weight to body-weight ratio in hepatectomized rats returned to the control value 10 days after hepatectomy.

The endocytotic index for fBSA in sinusoidal cells decreased significantly to 0. The changes in hepatic uptake for fBSA showed a similar time course of the endocytotic index.