oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Hepatic stellate cells may be potential effectors of platelet activating factor induced portal hypertension  [cached]
Yan Chen, Chun-Ping Wang, Yin-Ying Lu, Lin Zhou, Shu-Hui Su, Hong-Jun Jia, Yong-Yi Feng, Yong-Ping Yang
World Journal of Gastroenterology , 2008,
Abstract: AIM: To determine platelet activating factor (PAF) receptor expression in cirrhotic hepatic stellate cells.METHODS: Hepatic stellate cells, isolated from the livers of control and CCl4-induced cirrhotic rats, were placed in serum-free medium after overnight culture. We determined the PAF receptor in hepatic stellate cells by saturation binding technique and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR), and the effects of PAF and its antagonist BN52021 on prostaglandin E2 (PGE2) release by stellate cells.RESULTS: Scatchard analysis indicated the presence of PAF receptor with dissociation constant (Kd) of 4.66 nmol/L and maximum binding capacity (Bmax) of 24.65 fmol/μg in cirrhotic stellate cells. Compared with the control, the maximum PAF binding capacity increased significantly (Bmax: 24.65 ± 1.96 fmol/μg. DNA, R = 0.982 vs 5.74 ± 1.55 fmol/μg. DNA, R = 0.93; P < 0.01), whereas receptor affinity had no significant difference (Kd of 4.66 ± 0.33 nmol/L for the cirrhosis and 3.51 ± 0.26 nmol/L for the control; P > 0.05). Consistent with the receptor binding data, the mRNA expression of PAF receptor was increased significantly in cirrhotic stellate cells. PAF in a concentration-dependent manner induced PGE2 synthesis in cirrhotic hepatic stellate cells, but the effects were blocked significantly by BN52021.CONCLUSION: Cirrhosis sensitizes hepatic stellate cells to PAF by elevating its receptor level and hepatic stellate cells maybe potential effectors of PAF induced portal hypertension.
Distribution of Hepatic Myofibroblasts and Type I and III Collagen in Rat Liver Cirrhosis Induced by Thioacetamide
Poonkhum,Raksawan; Pradidarcheep,Wisuit; Nilbu-Nga,Somneuk; Chaunchaiyakul,Suwadee;
International Journal of Morphology , 2011, DOI: 10.4067/S0717-95022011000200033
Abstract: thioacetamide (taa) can induce various types of cirrhosis in the rat, including bridging fibrosis, biliary fibrosis, perisinusoidal/pericellular fibrosis and centrilobular fibrosis, in which different populations of hepatic myofibroblasts (mfs) are involved. the hepatic mfs can be classified into 3 groups: (a) portal/septal mfs; (b) activated hepatic stellate cell myofibroblasts (hsc/mfs); and (c) interface myofibroblasts (if/mfs). the present study was carried out to examine the morphology and localization of hepatic mfs in relation to the distribution of type i and iii collagen in rat cirrhotic livers. immunohistochemistry to a-smooth muscle actin was employed to demonstrate the morphology and localization of the subpopulations of hepatic mfs. the distribution of type i and iii collagen was investigated by using specific antibodies. portal and septal mfs were windmill in shape and localized around tributaries of the portal and hepatic veins where type i and iii collagen was accumulated. hsc/mfs with arachnoid in shape were localized in the spaces of disse and spaces between neighboring hepatocytes where type i collagen was formed. if/mfs showed arachnoid shapes and distributed along the margin of fibrous septa where type i collagen was condensed. mfs with polygonal shapes were also found around the wall of hepatic sinusoids, margin of fibrous septa and around the portal tract. they were probably transitional cells to the mature mfs. our data suggest that each subpopulation of hepatic mfs shows characteristic morphology and localization, which correlates with localization of type i and/or type iii collagen.
Octreotide decreases portal pressure: Hepatic stellate cells may play a pivotal role
Y Zhai, J Zhang, H Shang, S Lu, M Wang, H You, J Jia, H Ding
African Journal of Biotechnology , 2010,
Abstract: The aim of this study is to elucidate the effects of different dosages of octreotide on portal pressure in cirrhotic patients and to investigate the mechanism of activated human hepatic stellate cells (HSCs) on octreotide. Thirty-one (31) hepatitis B-related cirrhotic patients were randomly assigned to receive treatment with a 50 (group A, n = 12) or a 25 ìg/h infusion of octreotide for 72 h (group B, n = 14); the control group C (n = 5) received conventional treatment. Dynamic portal pressure was directly measured via a portal vein catheter. To study the cellular mechanism of octreotide, the expression of SSTRs 1-5 in LX-2, an HSC line, was examined by immunostaining and RT-PCR. Intracellular Ca2+ in LX2 was measured by laser scanning confocal microscopy (LSCM). The protein and mRNA levels in all five subtypes of SSTRs were positively expressed in LX-2. Octreotide led to an immediate two-fold drop in intracellular Ca2+ (P < 0.01). Portal pressure, in both groups A and B, decreased significantly (mean, - 20.6%) after octreotide infusion. Octreotide decreased portal pressure in cirrhotic patients by inhibiting HSC contractility by decreasing intracellular Ca2+ concentration via stimulation of all SSTRs on HSCs.
Morphological characterisation of portal myofibroblasts and hepatic stellate cells in the normal dog liver
Jooske IJzer, Tania Roskams, Ronald F Molenbeek, Ton Ultee, Louis C Penning, Jan Rothuizen, Ted SGAM van den Ingh
Comparative Hepatology , 2006, DOI: 10.1186/1476-5926-5-7
Abstract: In the formalin-fixed and paraffin embedded normal canine liver vimentin showed staining of hepatic fibroblasts, probably including MF in portal areas and around hepatic veins; however, HSC were in general negative. Desmin proved to react with both portal MF and HSC. A unique feature of these HSC was the positive immunostaining for alpha-smooth muscle actin (α-SMA) and muscle-specific actin clone HHF35 (HHF35), also portal MF stained positive with these antibodies. Synaptophysin and glial fibrillary acidic protein (GFAP) were consistently negative in the normal canine liver. In a frozen chronic hepatitis case (with expected activated hepatic MF and HSC), HSC were negative to synaptophysin, GFAP and NCAM. Transmission electron microscopy (TEM) immunogold labelling for α-SMA and HHF35 recognized the positive cells as HSC situated in the space of Disse.In the normal formalin-fixed and paraffin embedded canine liver hepatic portal MF and HSC can be identified by α-SMA, HHF35 and to a lesser extent desmin immunostaining. These antibodies can thus be used in further studies on hepatic fibrosis. Synaptophysin, GFAP and NCAM do not seem suitable for marking of canine HSC. The positivity of HSC for α-SMA and HHF35 in the normal canine liver may eventually reflect a more active regulation of hepatic sinusoidal flow by these HSC compared to other species.Hepatic fibrosis is a common outcome of hepatic injury in both man and dog. Depending on the primary site of injury the fibrosis may be restricted to the portal areas as in most biliary diseases or may be present in the hepatic parenchyma as seen in chronic hepatitis and cirrhosis. Chronic hepatitis is often diagnosed in pet-dogs. Treatment provides only limited results and the underlying mechanism of fibrosis is unclear. Activated fibroblasts which develop myofibroblasts (MF) characteristics play an essential role in hepatic fibrogenesis [1]. Three different MF-like cells have been described in rat and man based on location a
Liver cirrhosis and hepatic stellate cells
Brand?o, Daniel Ferracioli;Ramalho, Leandra Naira Zambelli;Ramalho, Fernando Silva;Zucoloto, Sérgio;Martinelli, Ana de Lourdes Candolo;Castro e Silva, Orlando de;
Acta Cirurgica Brasileira , 2006, DOI: 10.1590/S0102-86502006000700013
Abstract: the cirrhosis represents the final stage of several chronic hepatic diseases and it is characterized by the presence of fibrosis and morphologic conversion from the normal hepatic architecture into structurally abnormal nodules. in the evolution of the disease there is loss of the normal vascular relationship and portal hypertension. there are also regenerative hepatocelular alterations that become more prominent with the progression of the disease. the liver transplantation continues to be the only therapeutic option in cases of disease in terminal phase. the hepatic stellate cells (hsc) are perisinusoidal cells that store vitamin a and produce growth factors, citocins, prostaglandins and other bioactive substances. they can suffer an activation process that convert them to cells with a phenotype similar to myofibroblasts. when activated, they present increased capacity of proliferation, mobility, contractility and synthesis of collagen and other components of extracelular matrix. they possess cytoplasmic processes adhered to sinusoids and can affect the sinusoidal blood flow. hsc are important in pathogenesis of fibrosis and portal hypertension.
Role of hepatic stellate cells (HSCs) in the development of hepatic fibrosis in cats with polycystic kidney disease (PKD)
Aleksi?-Kova?evi? Sanja,Kukolj V.,Kurelju?i? B.,Marinkovi? D.
Acta Veterinaria , 2010, DOI: 10.2298/avb1004391a
Abstract: Hepatic stellate cells (HSCs) play a significant role in hepatic fibrogenesis. In the following study we described the distribution of cells that express alpha-smooth muscle actin (α-SMA) and desmin in the cat liver with various degrees of fibrosis, as well as the significance of hepatic stellate cells and portal myofibroblasts in the genesis of fibrosis in cats with polycistic kidney disease. Liver samples from 15 necropsied Persian cats were examined microscopically, using H&E and Masson-trichrom methods and immunohistology for α-SMA and desmin. Liver fibrosis was confirmed in cats with terminal stage of chronic cholangiohepatitis and it was characterized by connective tissue septa which divide the liver parenchyma into irregular lobuli. Inflammation in the cat liver is connected with the activation of periductal myofibroblasts. The intensity of immunopositivity of perisinusoidal HSCs to α-SMA and desmin varied depending on the degree of fibrosis and was the strongest in livers of cats with cirrhosis.
Up-regulation of uPARAP/Endo180 during culture activation of rat hepatic stellate cells and its presence in hepatic stellate cell lines from different species
Seyed A Mousavi, Marita S F?nhus, Trond Berg
BMC Cell Biology , 2009, DOI: 10.1186/1471-2121-10-39
Abstract: This study investigates the expression of uPARAP/Endo180 protein and messenger RNA in primary rat hepatic stellate cell (HSC) cultures. The results show that uPARAP/Endo180 protein is not expressed in freshly isolated HSCs or during the first few days of culture while the cells still display quiescent features. In contrast, uPARAP/Endo180 protein is expressed early during HSC activation when cells are transdifferentiated into myofibroblast-like cells. Very low levels of uPARAP/Endo180 mRNA are detectable during the first days of culture but uPARAP/Endo180 mRNA is strongly up-regulated with increasing time in culture. Moreover, endocytic uptake of denatured collagen increases as transdifferentiation proceeds over time and correlates with increased expression of uPARAP/Endo180. Finally, analysis of uPARAP/Endo180 expression in four hepatic stellate cell lines from three different species showed that all these cell lines express uPARAP/Endo180 and are able to take up denatured collagen efficiently.These results demonstrate that uPARAP/Endo180 expression by rat HSCs is strongly up-regulated during culture activation and identify this receptor as a feature common to culture-activated HSCs.The urokinase plasminogen activator receptor associated protein (uPARAP)/Endo180 (also known as CD280; referred to hereafter as Endo180) is an endocytic receptor which together with the mannose receptor, the M-type phospholipase A2 receptor and the dendritic cell receptor DEC-205 constitutes the mannose receptor family of C-type lectins [1-3]. Endo180 was discovered as a constitutively recycling receptor of unknown function with a molecular mass of 180 kDa [4], and subsequently identified as a transcript of a gene encoding a novel member of the mannose receptor family of C-type lectins [5]. It was later recognized as a collagen-binding receptor and was referred to as urokinase plasminogen activator (uPA) receptor (uPAR) associated protein (uPARAP) because of its ability to form a ternar
Intercellular Adhesive Structures Between Stellate Cells – An Analysis in Cultured Human Hepatic Stellate Cells  [cached]
Imai Katsuyuki,Sato Mitsuru,Sato Takeya,Kojima Naosuke
Comparative Hepatology , 2004, DOI: 10.1186/1476-5926-2-s1-s13
Abstract: To investigate whether or not hepatic stellate cells can form intercellular junctions with each other, we cultured human stellate cells (LI90) on different kinds of substrata. Intercellular junctions were detected between these cultured stellate cells by transmission electron microscopy (TEM). The molecular components of the intercellular adhesive structures were identified by immunofluorescence microscopy. Immunofluorescence for cadherin and catenins was detected at the adhesion sites between the cultured stellate cells. Thus, the intercellular junctions were indicated to be adherens junctions at the molecular level. The junctions developed in the cultured stellate cells irrespective of the type of substratum. These data suggest that the junctional formation between the stellate cells occurs in vivo as well as in vitro.
Immunohistochemical analysis of α-SMA and GFAP expression in liver stellate cells  [PDF]
Tomanovi? Nada,Bori?i? Ivan,Bra?anac Dimitrije
Vojnosanitetski Pregled , 2006, DOI: 10.2298/vsp0606553t
Abstract: Background/Aim. Liver stellate cells play an important role in hepatic fibrosis, and its progression to cirrhosis. These cells show immunoreactivity with different monoclonal antibodies amongst which the commonest are α-smooth muscle actin (α-SMA) and glial fibrillary acid protein (GFAP). The aim of this study was to analyze stellate cell immunoreactivity for α-SMA and GFAP in tissue sections showing the signs of chronic viral B-hepatitis and compare it with those without histopathological changes. Methods. We included 12 tissue samples showing chronic viral B hepatitis in the different stages of fibrosis and 7 tissue samples showing no histopathological changes. Immunohistochemical staining was performed using the streptavidinbiotin method. Results. There was a regular presence of α-SMA immunoreactivity in tissue sections without histopathological changes in the portal tracts and also in liver parenchyma, while GFAP expression was noted in the periportal cavity. Tissue sections with the signs of chronic viral B hepatitis displayed very strong α-SMA expression in the portal tracts. A statistical analysis showed a positive correlation between the degree of liver fibrosis and α-SMA expression along the fibrous septa, whereas a negative correlation between the degree of liver fibrosis and α-SMA expression was present in the portal zone. Conclusion. This study showed the existance of two different stellate cell subpopulations in liver tissue. Differentiation between them was possible on the basis of SMA/GFAP expression.
Patogénesis de la hipertensión portal
Monta?o-Loza, Aldo;Meza-Junco, Judith;
Revista de investigación clínica , 2005,
Abstract: it is now well established that portal hypertension is not a purely mechanical phenomenon. primary hemodynamic alterations develop in the hepatic and systemic circulatory systems; these alterations in combination with mechanical factors contribute to the development of portal hypertension. in the hepatic circulation, these hemodynamic alterations are characterized by vasoconstriction and impaired hepatic vasodilatory responses, whereas in the systemic circulation, particularly in the splanchnic bed, vessels are hyperemic with increased flow. thus, an increase in intrahepatic resistance in conjunction with increased portal venous inflow, mediated through splanchnic dilation, contributes to the development of portal hypertension. the ensuing development of elevated flow and transmural pressure through collateral vessels from the hypertensive portal vasculature into the lower pressure systemic venous circulation accounts for many of the complications, such as bleeding esophageal varices, observed with portal hypertension. the importance of the primary vascular origin of portal hypertension is emphasized by the utility of current therapies aimed at reversing these hemodynamic alterations, such as nitrates, which reduce portal pressure through direct intrahepatic vasodilatation, and fi blockers and octreotide, which reduce splanchnic vasodilatation and portal venous inflow. new evidence concerning relevant molecular mechanisms of contractile signaling pathways in hepatic stellate cells and the complex regulatory pathways of vasoactive molecules in liver endothelial cells makes a better understanding of these processes essential for developing further experimental therapies for portal hypertension. this article examines the current concepts relating to cellular mechanism that underlie the hemodynamic alterations that characterize and account for the development of portal hypertension.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.