Browsing by Subject "Cholesterol"

Now showing 1 - 7 of 7
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    Embryonic stem cells markers are present within rabbit atherosclerotic plaques
    (Murcia : F. Hernández, 2008) Zulli, Anthony; Buxton, Brian F.; Black, M. Jane; Hare, David L.
    Recent evidence suggests that smooth muscle cells within atherosclerotic plaques originate from vascular progenitor cells. We have previously shown that smooth muscle cells and macrophages present within rabbit atherosclerotic plaques are positive for factors of the renin angiotensin and nitric oxide systems as well as the hematopoietic stem-cell marker CD34 and the panleukocyte marker CD45. To explore the idea that these cells are of primitive types, immunohistochemistry was used to identify pluripotent embryonic stem cells (ESC) markers (Oct-4, SSEA1,3,4, TRA1-60, 81) in these plaques and to compare these to intimal thickening. Objective: To immunolocalise ESC markers in rabbit aortic intimal thickening and atherosclerotic plaques. Design: New Zealand White rabbits were fed either a control (Con) diet, 0.5% cholesterol (Chol) or 1% methionine (Meth) for 12 weeks. Animals were perfusion fixed, aortae excised and processed for paraffin. Immunohistochemistry was performed by standard techniques. Results: Oct-4, SSEA 1, 3 and 4, TRA-1-60 and TRA-1-81 were all present within in atherosclerotic plaques. However, some cells were not positive for TRA-1-60 and TRA-1-81. In fact, positive TRA-1-81 macrophages were uncommon, and positive TRA-1-81 smooth muscle cells were rare. Intimal thickening in Meth did not show any TRA-1-81 positive cells Conclusions: Macrophages and smooth muscle cells within atherosclerotic plaques express markers of ESC. These results suggest that cells within these plaques are primitive and might differentiate into other types of cells.
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    Intracellular cholesterol trafficking
    (Murcia : F. Hernández, 1999) Sviridov, D.
    The overall picture of intracellular cholesterol trafficking is very complex. The transfer of cholesterol within the cell depends on the contribution of several trafficking mechanisms. The known elements of cholesterol trafficking machinery include clathrin-coated pits, scavenger receptor type B1, caveolae, phospholipd rafts, Niemann-Pick C disease protein, sterol carrier protein 2, multidrug resistance protein, microsomal triglyceride transfer protein and steroidogenic acute regulation protein. Several pathways of intracellular cholesterol trafficking, for example retroendocytosis and cholesterol absorption in the intestine, are yet to be connected to specific structural elements. The contribution of different pathways depends on cell type, the source and destination of cholesterol and cellular cholesterol content and requirements. Some pathways are found in most, if not all, cell types, while others are associated with the specialized function of a particular cell type, for example, lipoprotein assembly in the liver or intestine and steroid hormone synthesis in steroidogenic tissue. Certain routes of intracellular cholesterol trafficking are heavily backed up by several auxiliary pathways, others entirely depend on a single functional element. In this review we describe the intracellular machinery involved in the intracellular transfer of cholesterol and give an overview of both the general and specialized pathways of intracellular cholesterol trafficking known to date.
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    Microstructural analysis of bile: relevance to cholesterol gallstone pathogenesis
    (Murcia : F. Hernández, 2000) Rubin, M.; Pakula, R.; Konikoff, F.M.
    The study of physical-chemical factors and pathways leading to cholesterol crystallization in bile has important clinical relevance. The major processes in cholesterol gallstone formation can be subdivided into nucleation, formation and precipitation of solid crystals (crystallization), crystal growth, crystal agglomeration and stone growth. A clear understanding of the microstructural events occurring during the earliest stages of these processes in bile is crucial for the identification of factors possibly delaying or preventing precipitation of cholesterol crystals and, therefore, gallstone formation in bile. Detection and characterization of microstructures in native and model biles can be achieved by both direct and indirect techniques. Direct imaging techniques provide more readily interpretable information, but sample preparation problems, particularly for electron microscopy, are a source of artifacts. Moreover, microscopic techniques provide only qualitative data without the possibility to quantitate or to analyse the composition of microstructures. Several indirect techniques have been used to obtain additional microstructural information about nucleating bile. These techniques have the disadvantage of often being model dependent in addition to constraints specific for each method. The systematic, judicious use of a combination of complementary direct and indirect techniques have led to a comprehensive understanding of the various microstructural processes and interactions occurring during bile secretion, flow in the biliary tract and storage in the gallbladder. This forms the basis for our current understanding of cholesterol nucleation, crystallization and gallstone formation.
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    Mitochondrial cholesterol in health and disease
    (Murcia : F. Hernández, 2009) Garcia-Ruiz, Carmen; Mari, Monserrat; Colell, Ana; Morales, Albert; Caballero, Francisco; Montero, Joan; Terrones, Ohiana; Basañez, Gorka; Fernández-Checa, José C.
    Cholesterol is a critical component of biological membranes, which not only plays an essential role in determining membrane physical properties, but also in the regulation of multiple signaling pathways. Cells satisfy their need for cholesterol either by uptake from nutrients and lipoproteins or de novo synthesis from acetyl-CoA. The latter process occurs in the endoplasmic reticulum, where transcription factors that regulate the expression of enzymes involved in the de novo cholesterol synthesis reside. Cholesterol is distributed to different membranes most prominently to plasma membrane, where it participates in the physical organization of specific membrane domains. Mitochondria, however, are considered cholesterol-poor organelles, and obtain their cholesterol load by the action of specialized proteins involved in its delivery from extramitochondrial sources and trafficking within mitochondrial membranes. Although mitochondrial cholesterol fulfills vital physiological functions, such as the synthesis of bile acids in the liver or the formation of steroid hormones in specialized tissues, recent evidence indicates that the accumulation of cholesterol in mitochondria may be a key step in disease progression, including steatohepatitis, carcinogenesis or Alzheimer disease.
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    Sex-dependent effect of liver growth factor on atherosclerotic lesions and fatty liver disease in apolipoprotein E knockout mice
    (Murcia : F. Hernández, 2010) Surra, Joaquin C.; Guillén, Natalia; Barranquero, Cristina; Arbonés Mainar, José M.; Navarro, María A.; Gascón, Sonia; Arnal, Carmen; Godino, Javier; Guzmán, Mario A.; Díaz-Gil, Juan J.; Osada, Jesús
    Objective: Since the hepatic mitogen, liver growth factor (LGF), improves vascular structure and function in a hypertensive rat model and exhibits antioxidant activity, it may play a role in the development of atherosclerosis. Methods: To test this hypothesis, 14 male and 11 female apolipoprotein E (apoE)-deficient mice with a C57BL/6J genetic background were injected intraperitoneally twice a week with 1.7 µg of LGF per mouse for ten weeks. Plasma carbohydrates, inflammatory and lipid parameters, apolipoproteins A-I and A-II and paraoxonase activity were assessed at the end of the experimental period. Histological and chemical analyses of the livers and quantification of aortic atherosclerotic lesions were also carried out. Results: LGF administration changed neither plasma lipid nor inflammatory parameters. ApoA-I and arylesterase activity were not affected by LGF either, while apoA-II decreased significantly in males but not in females. Plasma apoA-II correlated positively with liver fat in males but negatively in females. Atherosclerotic area lesions in males receiving LGF were 25% lower than in control mice. Likewise, a significant reduction of fatty liver disease was also observed in males in association with decreased levels of insulin, leptin and resistin. Conclusion: These results indicate that administration of LGF modulates atherosclerotic lesions in a sex-dependent manner. This effect is independent of plasma cholesterol, triglycerides, IL-6, MCP-1 and TNF-α and is related to a remodelling of HDL particles characterised by a decrease in apoA-II induced by changes in hepatic mRNA expression. Hence, LGF administration could be used as a safe alternative to control fatty liver disease and atherosclerosis in males
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    Student sports achievement: Can it control body mass index (BMI) and cholesterol?
    (Universidad de Murcia, Servicio de Publicaciones, 2024) Wati, Isti Dwi Puspita; Kusnanik, Nining Widyah; Wahjuni, Endang Sri; Samodra, Y Touvan Juni; Sastaman, B Putra; Suryadi, Didi
    The aim of this study was to assess the BMI and cholesterol levels of athletes selected for preparation for the National Sports Week in Indonesia. The study used a quantitative approach through a survey with researchers giving a test and measurement. The subjects used as research samples were all athletes in the sports of Weightlifting, Fencing, Aero Modeling, Bicycle Racing, Billiard, Handball, Badminton, Parachuting, Judo, Karate, Kempo, Muay Thai, Archery, Wall Climbing, Pencak Silat, Petangque, Swimming, Sepak Takraw, Taekwondo, Tarung Derajat, Table Tennis, Boxing, Volly Beach, Wushu. Additionally, following the selection test, a total of 328 athletes were included in the study. Instruments utilized in this study included the Omron Karada Scan HBF-328 scales for weight measurement, and the OneTouch device for cholesterol testing. The data were analyzed using Microsoft Excel and IBM SPSS Statistics version 26. The results revealed that the mean BMI and cholesterol levels were 22.85 and 171.38, respectively. Among the athletes, 11% were categorized as underweight, 63.11% as normal weight, 21.65% as overweight, 2.74% as obese I, 0.91% as obese II, and 0.61% as obese III. In terms of cholesterol levels, 80% were within the normal range, 10% were low, and 10% were high. Non-parametric correlation analysis demonstrated no significant relationship between BMI and cholesterol levels among the athletes, with a significance value of 0.815. This study concluded that the athlete's BMI was normal, as well as the average athlete's cholesterol condition in normal conditions.
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    The effects of Eicosapentaenoic acid on the endothelium of the carotid artery of rabbits on a high-cholesterol diet
    (Murcia : F. Hernández, 2010) Cayli, Sevil; Sati, Leyla; Seval-Celik, Yasemin; Altug Tuncer, M.; Yaymaci, Bengi; Berkman, Zafer; Altug, Tuncay; Demir, Ramazan
    The preventive and therapeutic effects ofEicosapentaenoic acid (EPA) on diet-inducedhyperlipidemia in rabbits have been investigated.Eighteen New Zealand rabbits were randomly dividedinto three groups of 6 subjects each; experimental group-I (EG-I) was administered a cholesterol rich diet,experimental group-II (EG-II) was treated with EPA(300 mg/kg/d) following a cholesterol-rich diet and thecontrol group (CG) had a standard diet. Blood sampleswere collected at day 0 and at the 4th and 12th weeks ofEG-II to obtain serum levels of total cholesterol (TC),high density lipid-cholesterol (HDL-C), low densitylipid-cholesterol (LDL-C) and triglyceride (TG). Fromeach group tissue samples were collected from thecarotid artery for immunohistochemistry and electronmicroscopy. Our results showed that EPA couldsignificantly lower (p<0.001) serum TC, LDL-C, HDL-C and TG levels with a reduction of 35%; 55%; 44% and51%, respectively. Scanning and transmission electronmicroscopy results revealed that endothelial damage wasmore prominent in EG-I when compared to EG-II. Theruptured endothelial lining and damaged cellular surfacewas increased in EG-I when compared to EG-II.Ultrastructural observations showed that after EPAtreatment, the degeneration and cellular surface damageon the endothelium were also decreased. These biochemical and ultrastructural results suggestthat EPA is a potential drug which significantly lowersthe serum lipid profile and partially repairs endothelialdysfunction due to hyperlipidemia