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Journal articles on the topic 'LDL'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 May 2024

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1

Wang, Feng, Wei Wang, Kristiina Wähälä, Herman Adlercreutz, Elina Ikonen, and Matti J. Tikkanen. "Role of lysosomal acid lipase in the intracellular metabolism of LDL-transported dehydroepiandrosterone-fatty acyl esters." American Journal of Physiology-Endocrinology and Metabolism 295, no. 6 (December 2008): E1455—E1461. http://dx.doi.org/10.1152/ajpendo.90527.2008.

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Dehydroepiandrosterone-fatty acyl esters (DHEA-FAE) belong to a unique family of naturally occurring hydrophobic steroid hormone derivatives that are transported in circulating lipoproteins and may act as a source of dehydroepiendrosterone (DHEA) and other biologically active steroid hormones in cells. Here, we studied the metabolic fate of low-density lipoprotein-associated [3H]DHEA-FAE ([3H]DHEA-FAE-LDL) and the possible role of lysosomal acid lipase (LAL) in the hydrolysis of DHEA-FAE in cultured human cells. When HeLa cells were incubated with [3H]DHEA-FAE-LDL, the accumulation of label in the cellular fraction increased with incubation time and could be inhibited by excess unlabeled LDL, suggesting LDL receptor or LDL receptor-related receptor-dependent uptake. During 48 h of chase, decreasing amounts of [3H]DHEA-FAE were found in the cellular fraction, while in the medium increasing amounts of unesterified [3H]DHEA and its two metabolites, [3H]-5α-androstanedione (5α-adione) and [3H]androstenedione (4-adione), appeared. As LDL-cholesteryl ester hydrolysis is dependent on LAL activity, we depleted LAL from HeLa cells using small interfering RNAs and compared the hydrolysis of [3H]DHEA-FAE-LDL and [3H]cholesteryl-FAE-LDL. The results demonstrated a more modest but significant reducing effect on the hydrolysis of [3H]DHEA-FAE compared with [3H]cholesteryl-FAE. Moreover, experiments in LAL-deficient human fibroblasts (Wolman disease patient cells) showed that [3H]DHEA-FAE hydrolysis was not completely dependent on LAL activity. In summary, LDL-transported [3H]DHEA-FAE entered cells via LDL receptor or LDL receptor-related receptor-mediated uptake, followed by intracellular hydrolysis and further metabolism into 5α-adione and 4-adione that were excreted from cells. Although LAL contributed to the deesterification of DHEA-FAE, it was not solely responsible for the hydrolysis.

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2

Vinagre, Carmen G. C., Elisabeth S. Ficker, Claudia Finazzo, Maria J. N. Alves, Katia de Angelis, Maria Claudia Irigoyen, Carlos E. Negrão, and Raul C. Maranhão. "Enhanced removal from the plasma of LDL-like nanoemulsion cholesteryl ester in trained men compared with sedentary healthy men." Journal of Applied Physiology 103, no. 4 (October 2007): 1166–71. http://dx.doi.org/10.1152/japplphysiol.01176.2006.

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The objective of this study was to evaluate the effects of exercise training on plasma removal of a cholesterol-rich nanoemulsion (LDE) that mimics low-density lipoprotein (LDL) lipid structure and binds to LDL receptors. LDE-derived cholesteryl ester plasma kinetics was studied in 24 exercise-trained and 20 sedentary male subjects. LDE labeled with [14C]cholesteryl ester was injected intravenously, and plasma samples were collected over a 24-h period to determine radioisotope decay curves. LDL cholesterol concentration was similar in both groups. Fractional clearance rate (FCR) of the nanoemulsion label was greater in the exercise-trained group compared with the sedentary group (0.138 ± 0.152 and 0.0261 ± 0.023 h−1, respectively). A positive correlation was found ( r = 0.60, P < 0.01) between FCR and peak O2consumption in trained subjects. Circulating oxidized LDL levels were lower in trained subjects compared with the sedentary group (9.0 ± 2.0 and 16.0 ± 3.0 mU/l). LDE was also injected into control and LDL receptor gene knockout mice submitted and not submitted to training. Muscle LDE uptake percentage was increased in the trained mice compared with the untrained mice (1.1 ± 0.8 and 0.2 ± 0.1, respectively, P < 0.0001) in the control group but not in the knockout animals, indicating that the LDL receptor is involved in the increased uptake elicited by exercise. These results show that exercise training increases LDE plasma removal, which in turn suggests that it also increases LDL receptors or LDL receptor activity.

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3

Oravec, Stanislav, K. Gruber, Elisabeth Dostal, and J. Mikl. "LDL ist nicht gleich LDL." Wiener klinisches Magazin 15, no. 3 (June 2012): 32–34. http://dx.doi.org/10.1007/s00740-012-0005-3.

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4

Ebert, James Ray, Miryoung Lee, and Stefan Czerwinski. "LDL-c, LDL-p, and Oxidized-LDL in Overweight Children." Journal of Clinical Lipidology 5, no. 3 (May 2011): 223. http://dx.doi.org/10.1016/j.jacl.2011.03.048.

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5

Levy, Debora, Adriana Aguiar Debes, Andrea Turbuck Celestino, Shirley Schreier, Raul Maranhão, and Sergio Paulo Bydlowski. "Lipid Emulsion as Antisense Oligonucleotides Vector That Inhibits P-Glycoprotein Expression in a Sarcoma Cell Line through LDL Receptor." Blood 112, no. 11 (November 16, 2008): 4633. http://dx.doi.org/10.1182/blood.v112.11.4633.4633.

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Abstract It is well known that antisense oligonucleotides (OAS) are able to inhibit gene expression in a sequence-specific way. The potencial use of an artificial lipid nanoemulsion (LDE) as a vector to carry OAS has been described. LDE was shown to bind 3’-cholesteryl- OAS (C-OAS) and to be internalized into cells through LDL receptors. Here we further explore these findings by examining the capacity of this complex to inhibit MDR-1 gene expression in a sarcoma cell line (MES-DX), which express P-glycoprotein. LDE was prepared as described (Bydlowski et al. ,1995). The capacity of LDE to bind C-OAS was examined by fluorescence spectra analysis using a Hitachi F4500 fluorimeter. Human plasma was obtained from healthy blood donors and LDL, HDL and lipoprotein free serum (LPDS) were separated by sequencial ultracentrifugation. C-OAS/LDE complex was incubated with HDL (apoE donor) before cell experiments were performed. Binding of [3H] LDE/C-OAS complex to LDL receptors from MES-DX cells was studied by competition assay. Two different C-OASs, both complementary to regions flanking the AUG initiation codon were used. Inhibition of MDR-1 gene expression was evaluated by RT-PCR. The binding constant for C-OAS/LDE was 4,2 × 10−3M−1 indicating a high specific capacitiy of conjugation.The C-OAS/LDE complex was shown, by the competition assays and confocal microscopy, to bind to LDL receptors and then to be internalized into cells. Both C-OAS/ LDE complexes strongly inhibited (70% inhibition) the MDR-1 gene expression after 48 hours of cell incubation. This inhibition was not observed when LDE was used alone or complexed with scrambled OAS sequences. The results show that this nanoemulsion binds to cholesteryl-OASs. Moreover, this nanoparticle is an efficient carrier for OAS to target cells expressing LDL receptors. This complex is able to internalize oligonucleotides into cells specifically through the LDL receptor-mediated pathway. The internalized ODN was able to act on nucleic acid sequences as determined by the inhibition of MDR-1 gene expression. Therefore, LDE/C-OAS is promissing nanoparticle complex to be used in gene therapy studies.

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6

Huygen, Lisa P. M., Jan Westerink, Gerben C. Mol, and Remy H. H. Bemelmans. "When LDL Cholesterol Is Not LDL Cholesterol." JACC: Case Reports 4, no. 11 (June 2022): 690–93. http://dx.doi.org/10.1016/j.jaccas.2022.03.009.

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7

Yeang, Calvin, Joseph L. Witztum, and Sotirios Tsimikas. "‘LDL-C’ = LDL-C + Lp(a)-C." Current Opinion in Lipidology 26, no. 3 (June 2015): 169–78. http://dx.doi.org/10.1097/mol.0000000000000171.

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8

Superko, H. Robert. "CHOLESTEROL METABOLISM, LDL, AND THE LDL RECEPTOR." Chest 100, no. 5 (November 1991): 21. http://dx.doi.org/10.1016/s0012-3692(16)33652-2.

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9

Vella, F. "Cholesterol Metabolism, LDL, and the LDL Receptor." Biochemical Education 19, no. 1 (January 1991): 44. http://dx.doi.org/10.1016/0307-4412(91)90161-z.

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10

Scriver, Charles R. "Cholesterol metabolism, LDL and the LDL receptor." Cell 64, no. 3 (February 1991): 485–86. http://dx.doi.org/10.1016/0092-8674(91)90230-v.

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11

Lombarde, Washington, and Neide Maria Michellan Kiouranis. "A ALQUIMIA NOS LIVROS DIDÁTICOS DE QUÍMICA APROVADOS PELO PROGRAMA NACIONAL DO LIVRO DIDÁTICO." Ensino de Ciências e Tecnologia em Revista – ENCITEC 13, no. 3 (December 22, 2023): 301–29. http://dx.doi.org/10.31512/encitec.v13i3.460.

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Considerando a importância da Alquimia e seu contexto histórico, a presente pesquisa teve como objetivo compreender como a Alquimia é explorada nas obras didáticas aprovadas pelo Programa Nacional do Livro Didático (PNLD) de 2018. Trata-se de uma pesquisa de natureza qualitativa. Para análise dos livros didáticos, utilizamos como critério as marcas da historiografia tradicional apontadas por Beltran, Saito e Trindade (2014), e os livros didáticos foram identificados pelas letras LD, seguidas por um código numérico: LD1, LD2, LD3, LD4, LD5, LD6. Pela análise dos livros didáticos, identificaram-se características da perspectiva historiográfica tradicional, consideradas ultrapassadas por Beltran, Saito e Trindade (2014), o que evidencia que, de modo geral, não há importante valorização da nova historiografia da ciência. Verificou-se que, em LD4, a Alquimia não é contemplada em nenhum dos capítulos, enquanto que apenas LD5 apresenta poucos aspectos da antiga historiografia, evidenciando que os autores buscaram inserir a nova historiografia da ciência em sua abordagem. De modo geral, os livros didáticos analisados fazem uma abordagem da Alquimia que carece de informações históricas e ainda é permeada por aspectos da antiga historiografia da ciência.

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12

Hattori, Yuichi, Masaaki Suzuki, Motoo Tsushima, Masami Yoshida, Yoko Tokunaga, Ying Wang, Di Zhao, et al. "Development of approximate formula for LDL-chol, LDL-apo B and LDL-chol/LDL-apo B as indices of hyperapobetalipoproteinemia and small dense LDL." Atherosclerosis 138, no. 2 (June 1998): 289–99. http://dx.doi.org/10.1016/s0021-9150(98)00034-3.

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13

Liu, Mengnan, Gang Luo, Tianzhu Liu, Tingfu Yang, Raoqiong Wang, Wei Ren, Ping Liu, Xiaoling Lai, Hua Zhou, and Sijin Yang. "Zhilong Huoxue Tongyu Capsule Alleviated the Pyroptosis of Vascular Endothelial Cells Induced by ox-LDL through miR-30b-5p/NLRP3." Evidence-Based Complementary and Alternative Medicine 2022 (January 27, 2022): 1–10. http://dx.doi.org/10.1155/2022/3981350.

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Background. Our previous studies have demonstrated a protective role of Zhilong Huoxue Tongyu capsule in atherosclerosis (AS); however, the molecular mechanisms are unclear. Methods. Human coronary artery endothelial cells (HCAECs) were induced with oxidized low-density lipoprotein (ox-LDL) to obtain cellular AS models. Then, the medicated serum of Zhilong Huoxue Tongyu capsule was obtained and used for treatment with ox-LDL-induced HCAECs. The cell viability was detected by CCK-8 assay. Besides, the binding between miR-30b-5p and NLRP3 was determined by the dual-luciferase reporter gene system assay. Furthermore, ox-LDL-induced HCAECs were transfected with miR-30b-5p mimic or miR-30b-5p inhibitor. The pyroptosis of HCAECs was assessed by flow cytometry, LDH content detection, and qRT-PCR assays. Results. 10% medicated serum of Zhilong Huoxue Tongyu capsule was the maximum nontoxic concentration and it was used in subsequent assays. The rate of pyroptosis, LDH content, and the mRNA expression level of pyroptosis-related genes including NLRP3, ASC, Caspase 1, IL-1β, and IL-18 were prominently enhanced after HCAECs were induced by ox-LDL, which were markedly rescued with medicated serum of Zhilong Huoxue Tongyu capsule. In addition, the medicated serum of Zhilong Huoxue Tongyu capsule significantly enhanced the ox-LDL-induced reduction of miR-30b-5p level. NLRP3 could bind to miR-30b-5p and was negatively corrected with miR-30b-5p. Moreover, all the rates of pyroptosis, LDH content, and the mRNA expression levels of pyroptosis-related genes including NLRP3, ASC, Caspase 1, IL-1β, and IL-18 were further observably decreased after ox-LDL-induced HCAECs treated with medicated serum were transfected with miR-30b-5p mimic, while these were significantly rescued with transfection of miR-30b-5p inhibitor. Conclusion. Zhilong Huoxue Tongyu capsule alleviated the pyroptosis of vascular endothelial cells induced by ox-LDL through miR-30b-5p/NLRP3.

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14

Tanishima, K., T. Hayashi, M. Matsushima, and Y. Mochikawa. "Activity of lactate dehydrogenase isoenzymes LD1 and LD2 in serum as determined by using an inhibitor of the M-subunit." Clinical Chemistry 31, no. 7 (July 1, 1985): 1175–77. http://dx.doi.org/10.1093/clinchem/31.7.1175.

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Abstract To measure activities of lactate dehydrogenase (EC 1.1.1.27) isoenzymes LD1 and LD2 in serum, we developed a method involving 1,6-hexanediol as specific inhibitor of the M-subunit. Addition of hexanediol, 0.6 mol/L, to five LD isoenzyme fractions purified from human liver and heart homogenates resulted in complete loss of activities of LD4 and LD5, and partial loss of LD2 and LD3. The activity of LD1, which is composed of the H-subunit only, was not affected. In studying what conditions would allow only the activities of LD1 or LD1 + LD2 to be expressed in serum, we found that the respective activities could be determined by treatment with hexanediol, 0.75 mol/L and 0.55 mol/L, respectively. Results of binding experiments and analytical-recovery tests supported the effectiveness of analyses with this inhibitor in determination of LD1 and LD1 + LD2 activities in serum. Results by this proposed inhibition method correlated well with those by the conventional electrophoretic method for determination of LD1 activity, but LD1 + LD2 activities by the inhibition method were a little less than those by the electrophoretic method, requiring some correction.

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15

TANI, Nobutaka. "Development of Selective LDL Adsorbent and LDL Apheresis System: Immobilized Polyanion as LDL-Specific Adsorbent for LDL Apheresis System." Journal of Japan Atherosclerosis Society 18, no. 2 (1990): 173–81. http://dx.doi.org/10.5551/jat1973.18.2_173.

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16

Uusinarkaus, Kari, Thomas White, Hollye Garner, Deborah Winegar, and Ray Pourfarzib. "Discordance Between LDL Particle Number (LDL-P) and LDL-cholesterol (LDL-C) Among Patients Treated at Two Medical Systems." Journal of Clinical Lipidology 7, no. 3 (May 2013): 239–40. http://dx.doi.org/10.1016/j.jacl.2013.03.019.

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17

Chung, Yeonseok, Hoyong Lim, Young Uk Kim, Hua Sun, Shino Hanabuchi, and Babie Teng. "Proatherogenic conditions promote autoimmune Th17 responses in vivo (P4136)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 191.14. http://dx.doi.org/10.4049/jimmunol.190.supp.191.14.

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Abstract Although patients with atherosclerosis have a higher incidence of systemic autoimmune diseases, the relationship between proatherogenic factors and autoimmune T cell responses is poorly understood. Mice lacking both LDL receptor and apolipoprotein B mRNA editing enzyme (Ldlr-/-Apobec1-/-; LDb) are hyperlipidemic and prone to atherosclerosis. Here, we show that LDb mice exhibit increased IL-17 in circulation as well as in the aortic sinus area, which was attributed to a preferential enhancement of Th17 cells in the secondary lymphoid organs. In addition, the environment within LDb mice was substantially favorable for the Th17 polarization of auto-reactive CD4+ T cells during homeostatic proliferation. In vitro, the addition of oxidized LDL, but not native LDL, promoted dendritic cell-mediated Th17 polarization by triggering IL-6 and IL-1 in a MyD88-dependent fashion. Furthermore, myelin oligodendrocyte glycoprotein (MOG)-reactive CD4+ T cells expanded in the presence of oxidized LDL expressed increased levels of Th17 signature genes, and induced more profound experimental autoimmune encephalitomyelitis (EAE) when transferred into naïve mice. Our findings demonstrate that proatherogenic factors induce the polarization and functional maturation of autoimmune Th17 cells, which may be critical for the pathogenesis of atherosclerosis and other related autoimmune diseases.

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18

Thompson, Gilbert R. "LDL apheresis." Atherosclerosis 167, no. 1 (March 2003): 1–13. http://dx.doi.org/10.1016/s0021-9150(02)00251-4.

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19

Saunier, Vincent, and Henri Portugal. "Cholestérol LDL." EMC - Biologie Médicale 1, no. 1 (January 2006): 1–5. http://dx.doi.org/10.1016/s2211-9698(06)76044-7.

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20

Hawkins, David B., and Donald J. Schum. "LDL Measures." American Journal of Audiology 1, no. 1 (November 1991): 8–10. http://dx.doi.org/10.1044/1059-0889.0101.08.

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21

Menédez, Roberto, Lourdes Arruzazabala, Rosa Más, Armando Del RíO, Ana M. Amor, Rosa M. GonzáLez, Daisy Carbajal, Vivian Fraga, Vivian Molina, and José Illnait. "Cholesterol-lowering effect of policosanol on rabbits with hypercholesterolaemia induced by a wheat starch-casein diet." British Journal of Nutrition 77, no. 6 (June 1997): 923–32. http://dx.doi.org/10.1079/bjn19970090.

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The effect of policosanol, a mixture of high-molecular-weight aliphatic alcohols isolated from sugar-cane wax, on casein-induced hypercholesterolaemia in rabbits was studied. When policosanol was administered by the oral route once daily for 30 d (50mg/kg) the increases in plasma total cholesterol and LDL-cholesterol (LDC-C) were significantly reduced when compared with the control group. The incorporation of 3H2O into sterols in the liver was significantly depressed, suggesting inhibition of hepatic cholesterol biosynthesis. The oral administration of policosanol raised the rate of removal of 125l-labelled LDL from serum. Kinetic parameters calculated following injection of [125I]LDL showed than in casein-fed rabbits, the terminal half-life (t½) was significantly decreased after policosanol treatment. The hepatic LDL-binding activity was increased after policosanol administration which suggested that the enhanced clearance was due, at least in part, to increased receptor-mediated uptake of LDL by the liver. Considered together, these results suggest that policosanol can significantly reduce the increase of plasma LDL-C in rabbits fed on a wheat starch-casein diet by reducing cholesterol biosynthesis in the liver. Such an effect could account for the enhancement of LDL catabolism through the receptor-mediated pathway.

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22

Innerarity, T. L. "STRUCTURAL BIOLOGY: LDL Receptor's β-Propeller Displaces LDL." Science 298, no. 5602 (December 20, 2002): 2337–39. http://dx.doi.org/10.1126/science.1080669.

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23

Benitez, S., C. Bancells, J. Ordonez-Llanos, and J. L. Sanchez-Quesada. "HDL COUNTERACTS INFLAMMATORY PROPERTIES OF ELECTRONEGATIVE LDL (LDL(-))." Atherosclerosis Supplements 9, no. 1 (May 2008): 50. http://dx.doi.org/10.1016/s1567-5688(08)70195-8.

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24

Hamilton, Ryan T., Liana Asatryan, Jon T. Nilsen, Jose M. Isas, Timothy K. Gallaher, Tatsuya Sawamura, and Tzung K. Hsiai. "LDL protein nitration: Implication for LDL protein unfolding." Archives of Biochemistry and Biophysics 479, no. 1 (November 2008): 1–14. http://dx.doi.org/10.1016/j.abb.2008.07.026.

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25

Gupta, Vishal Kumar, Richa Giri, and Saurabh Agrawal. "Biochemical markers as predictors of dengue severity." International Journal of Advances in Medicine 9, no. 2 (January 25, 2022): 89. http://dx.doi.org/10.18203/2349-3933.ijam20220114.

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Background: The objective of this study was to evaluate biochemical markers as predictors of dengue severity clinical outcome, bleeding severity, capillary leakage, supportive therapy requirement and duration of hospital stay.Methods:In this observational study Patients from age more than 15 years with history of acute febrile illness Total 263 confirmed cases (based on the WHO criteria) of DF were included in this study, who have been admitted in our hospital. We measured levels of CK, LDH, AST and ALT with modified liquid-UV tests; semi-quantitative levels of CRP with a colorimetric rapid test; levels of albumin with colorimetric tests; and lipid profiles [cholesterol, triglycerides, Low-density lipoprotein (LDL) and High-density lipo-protein (HDL)] with a liquid-color test. Positive control human samples were included in all tests.Results: We found that TG and LDL-C levels were significantly lower in dengue-positive patients compared to dengue-negative patients, and that LDL-C levels showed greater decreases and thus appeared to drive the reduction in total cholesterol. LDH, CPK, AST and ALT were significantly raised in DSS in compared to DF and other febrile illness. We found that lower total serum cholesterol and LDL-C levels at presentation were associated with subsequent development of DHF/DSS.Conclusions:Assessment of lymphocyte, platelet counts, levels of LDL, TG, CPK, LDH, levels of AST and ALT are very significant and easily available and low-cost biochemical markers for prediction of dengue infection severity.

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26

Hermann, M., and B. Gmeiner. "Altered susceptibility to in vitro oxidation of LDL in LDL complexes and LDL aggregates." Arteriosclerosis and Thrombosis: A Journal of Vascular Biology 12, no. 12 (December 1992): 1503–6. http://dx.doi.org/10.1161/01.atv.12.12.1503.

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27

HERMANN, MARCELA, and BERNHARD GMEINER. "Altered Susceptibility to in Vitro Oxidation of LDL in LDL Complexes and LDL Aggregates." Annals of the New York Academy of Sciences 683, no. 1 Dietary Lipid (June 1993): 363–64. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35734.x.

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28

Li, Ben, Chufan Wang, Peng Lu, Yumeng Ji, Xufeng Wang, Chaoyang Liu, Xiaohu Lu, Xiaohan Xu, and Xiaowei Wang. "IDH1 Promotes Foam Cell Formation by Aggravating Macrophage Ferroptosis." Biology 11, no. 10 (September 23, 2022): 1392. http://dx.doi.org/10.3390/biology11101392.

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A distinctive feature of ferroptosis is intracellular iron accumulation and the impairment of antioxidant capacity, resulting in a lethal accumulation of lipid peroxides leading to cell death. This study was conducted to determine whether inhibiting isocitrate dehydrogenase 1 (IDH1) may help to prevent foam cell formation by reducing oxidized low-density lipoprotein (ox-LDL)-induced ferroptosis in macrophages and activating nuclear factor erythroid 2-related factor 2 (NRF2). Gene expression profiling (GSE70126 and GSE70619) revealed 21 significantly different genes, and subsequent bioinformatics research revealed that ferroptosis and IDH1 play essential roles in foam cell production. We also confirmed that ox-LDL elevates macrophage ferroptosis and IDH1 protein levels considerably as compared with controls. Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, reduced ox-LDL-induced elevated Fe2+ levels, lipid peroxidation (LPO) buildup, lactate dehydrogenase (LDH) buildup, glutathione (GSH) depletion, glutathione peroxidase 4 (GPX4), ferritin heavy polypeptide 1 (FTH1), and solute carrier family 7 member 11 (SLC7A11) protein downregulation. More crucially, inhibiting IDH1 reduced Fe2+ overload, lipid peroxidation, LDH, and glutathione depletion, and elevated GPX4, FTH1, and SLC7A11 protein expression, resulting in a reduction in ox-LDL-induced macrophage ferroptosis. IDH1 inhibition suppressed ox-LDL-induced macrophage damage and apoptosis while raising NRF2 protein levels. We have demonstrated that inhibiting IDH1 reduces ox-LDL-induced ferroptosis and foam cell formation in macrophages, implying that IDH1 may be an important molecule regulating foam cell formation and may be a promising molecular target for the treatment of atherosclerosis.

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29

Tang, Wei-Jun, Chang-Ping Hu, Mei-Fang Chen, Pan-Yue Deng, and Yuan-Jian Li. "Epigallocatechin gallate preserves endothelial function by reducing the endogenous nitric oxide synthase inhibitor level." Canadian Journal of Physiology and Pharmacology 84, no. 2 (February 2006): 163–71. http://dx.doi.org/10.1139/y05-156.

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Asymmetric dimethylarginine (ADMA), the endogenous nitric oxide synthase inhibitor, is thought to be a key factor contributing to endothelial dysfunction. Tea catechins can cause an endothelium-dependent vasorelaxation. The present study examined the effect of epigallocatechin gallate (EGCG), the major component of tea catechins, on endothelial dysfunction induced by native low density lipoprotein (LDL) in rats and oxidized LDL (ox-LDL) in cultured endothelial cells, and whether the protective effect of EGCG is related to reduction of ADMA level. A single injection of LDL (4 mg·kg–1, i.v.) markedly reduced endothelium-dependent relaxation and the serum nitrite/nitrate (NO) level, and increased serum concentrations of ADMA, malondialdehyde (MDA), and tumor necrosis factor-α (TNF-α). EGCG (10 or 50 mg·kg–1, i.p.) significantly attenuated the inhibition of vasodilator response to acetylcholine and the decreased serum nitrite/nitrate level, and reduced the elevated levels of ADMA, MDA, and TNF-α. Exposure of endothelial cells to ox-LDL (100 μg·mL–1) for 24 h markedly increased the medium levels of lactate dehydrogenase (LDH), ADMA, TNF-α, and MDA, and decreased the level of nitrite/nitrate in the medium and the activity of dimethylarginine dimethylaminohydrolase (DDAH) in the endothelial cells. EGCG (10 and 100 μg·mL–1) significantly decreased the levels of LDH, ADMA, TNF-α, and MDA, and increased the level of nitrite/nitrate and the activity of DDAH. These results suggest that EGCG protects endothelial dysfunction induced by native LDL in vivo or by ox-LDL in endothelial cells, and the protective effect of EGCG on the endothelium is related to decrease in ADMA level via increasing of DDAH activity.

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30

Reignier, Arnaud, Émilie Sacchetto, Jean-Benoît Hardouin, Jean-Luc Orsonneau, Didier Le Carrer, Odile Delaroche, and Édith Bigot-Corbel. "Comparison of calculated LDL cholesterol (LDL-C) versus measured LDL cholesterol (LDL-M) and potential impact in terms of therapeutic management." Annales de biologie clinique 72, no. 5 (September 2014): 593–98. http://dx.doi.org/10.1684/abc.2014.0990.

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31

Folse, Henri, Devesh Goswami, Badri Rengarajan, Richard Kahn, Matthew Budoff, Deborah Winegar, and James Otvos. "Using Low-Density Lipoprotein (LDL) Particle Number (LDL-P) versus LDL Cholesterol (LDL-C) to Guide Preventative Therapy for Cardiovascular Disease." Journal of Clinical Lipidology 8, no. 3 (May 2014): 297–98. http://dx.doi.org/10.1016/j.jacl.2014.02.016.

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32

Mehta, Jawahar L., and Dayuan Li. "Facilitative interaction between angiotensin II and oxidised LDL in cultured human coronary artery endothelial cells." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S70—S76. http://dx.doi.org/10.1177/14703203010020011201.

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Background Several studies have shown that angiotensin II (Ang II) and oxidised low-density lipoprotein (ox-LDL) are critical factors in atherosclerosis. In this study, we examined the molecular basis of mutually facilitative interactions between Ang II and ox-LDL in human coronary artery endothelial cells (HCAECs). Methods and results We observed that incubation of cultured HCAECs with Ang II (10-12 to 10-6 M) for 24 hours caused a concentration-dependent increase in the expression of mRNA and protein of a specialised receptor for ox-LDL (LOX-1). These effects of Ang II were completely blocked by pretreatment of HCAECs with candesartan (10-6 M), a specific AT1-receptor blocker, but not by PD 123319 (10-6 M), a specific AT2-receptor blocker. On the other hand, incubation of HCAECs with ox-LDL (10 and 40 µg/ml) for 24 hours progressively upregulated AT1-, but not AT 2-, receptor mRNA and protein. Pretreatment of cells with the anti-oxidant alpha-tocopherol (1—5 x 10-6 M) inhibited the upregulation of AT1-receptor expression induced by ox-LDL (p<0.05). To determine the significance of expression of AT1-receptors and LOX-1, we measured cell injury in response to Ang II and ox-LDL. Incubation of cells with both ox-LDL and Ang II synergistically increased cell injury, measured as cell viability and LDH release, compared with either ox-LDL or Ang II alone (both p<0.05). Alpha-tocopherol, as well as candesartan, attenuated cell injury in response to Ang II and ox-LDL (both p<0.05). Conclusions These observations show that Ang II upregulates a novel endothelial receptor for ox-LDL (LOX-1) gene expression and ox-LDL in turn upregulates Ang II AT 1receptor gene expression. This interaction between Ang II and ox-LDL further augments cell injury in HCAECs. These findings provide basis for the use of AT1-receptor blockers and anti-oxidants in designing therapy for atherosclerosis and myocardial ischaemia.

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33

Masana, Luis. "The Zero-LDL Hypothesis. Towards Extremely Low LDL Concentrations." Revista Española de Cardiología (English Edition) 71, no. 7 (July 2018): 591–92. http://dx.doi.org/10.1016/j.rec.2017.04.009.

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Selwyn, Andrew P. "Antiatherosclerotic effects of statins: LDL versus non-LDL effects." Current Atherosclerosis Reports 9, no. 4 (June 26, 2007): 281–85. http://dx.doi.org/10.1007/s11883-007-0034-3.

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Bardelli, M., M. Bossi, L. Cattin, L. Macaluso, B. Fabris, R. Candido, F. Fischetti, and R. Carretta. "ENDOTHELIAL DYSFUNCTION (ED) IN FAMILIAL HYPERCHOLESTEROLEMIA (FH). ROLE OF THE LDL-CHOLESTEROL (LDL) VARIATIONS AFTER LDL-APHAERESIS (LDL-A) Vs MEDICAL THERAPY." Journal of Hypertension 22, Suppl. 2 (June 2004): S74. http://dx.doi.org/10.1097/00004872-200406002-00252.

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Bardelli, M., M. Bossi, L. Cattin, L. Macaluso, B. Fabris, R. Candido, F. Fischetti, and R. Carretta. "ENDOTHELIAL DYSFUNCTION (ED) IN FAMILIAL HYPERCHOLESTEROLEMIA (FH). ROLE OF THE LDL-CHOLESTEROL (LDL) VARIATIONS AFTER LDL-APHAERESIS (LDL-A) vs MEDICAL THERAPY." Journal of Hypertension 22, Suppl. 2 (June 2004): S87. http://dx.doi.org/10.1097/00004872-200406002-00298.

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NAGANO, Makoto, Hiroaki HATTORI, Tohru EGASHIRA, Hideaki KURATA, Kazuo KONDO, and Hiroshige ITAKURA. "A Simple, Flow Cytometric Assay for Functional LDL Receptor using a Fluorescent-labeled LDL, DiI-LDL." Journal of Japan Atherosclerosis Society 23, no. 4-5 (1995): 263–68. http://dx.doi.org/10.5551/jat1973.23.4-5_263.

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Schultis, HW, H. von Baeyer, H. Neitzel, and E. Riedel. "Functional characteristics of LDL particles derived from various LDL-apheresis techniques regarding LDL-drug-complex preparation." Journal of Lipid Research 31, no. 12 (December 1990): 2277–84. http://dx.doi.org/10.1016/s0022-2275(20)42115-7.

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Maki, Kevin C., Jelani K. Grant, and Carl E. Orringer. "LDL-C Estimation." Journal of the American College of Cardiology 79, no. 6 (February 2022): 542–44. http://dx.doi.org/10.1016/j.jacc.2021.12.005.

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Gerber, Philipp A., Dragana Nikolic, and Manfredi Rizzo. "Small, dense LDL." Current Opinion in Cardiology 32, no. 4 (July 2017): 454–59. http://dx.doi.org/10.1097/hco.0000000000000410.

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Uroić, Valentina. "Prehrana i LDL." Posebna izdanja HAZU. Prilozi za strategiju hrvatskog razvoja 33 (2017): 83–92. http://dx.doi.org/10.21857/94kl4cwxvm.

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Spector, Arthur A., and William G. Haynes. "LDL Cholesteryl Oleate." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 6 (June 2007): 1228–30. http://dx.doi.org/10.1161/atvbaha.107.147082.

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Goldstein, Joseph L., and Michael S. Brown. "The LDL Receptor." Arteriosclerosis, Thrombosis, and Vascular Biology 29, no. 4 (April 2009): 431–38. http://dx.doi.org/10.1161/atvbaha.108.179564.

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Fath, Roland. "Starke LDL-Senkung." MMW - Fortschritte der Medizin 158, no. 14 (August 2016): 73. http://dx.doi.org/10.1007/s15006-016-8603-4.

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Marlovits, Thomas C., Christina Abrahamsberg, and Dieter Blaas. "Soluble LDL Minireceptors." Journal of Biological Chemistry 273, no. 50 (December 11, 1998): 33835–40. http://dx.doi.org/10.1074/jbc.273.50.33835.

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van der Westhuyzen, D. R., A. M. Fourie, G. A. Coetzee, and W. Gevers. "The LDL receptor." Current Opinion in Lipidology 1, no. 2 (April 1990): 128–35. http://dx.doi.org/10.1097/00041433-199004000-00008.

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Moriarty, Patrick M. "LDL-apheresis therapy." Current Treatment Options in Cardiovascular Medicine 8, no. 4 (July 2006): 282–88. http://dx.doi.org/10.1007/s11936-006-0049-z.

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Can, Ümmügülsüm. ".Okside-LDL ve Reseptörü Lektin Benzeri Ox-LDL Reseptör-1." Genel Tip Dergisi 26, no. 4 (December 26, 2016): 121–26. http://dx.doi.org/10.15321/geneltipder.2017.128.

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Konishi, Keiko, Hirokazu Matsubara, and Hisao Sasaki. "Modified LDL acquired from LDL fractions by polyacrylamide gel electrophoresis." SEIBUTSU BUTSURI KAGAKU 46, no. 2 (2002): 115–20. http://dx.doi.org/10.2198/sbk.46.115.

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Hayashi, Tsutomu, Midori Kimura, Kazuyo Watanabe, and Hideharu Ogasawara. "Usefulness of malondialdehyde-modified LDL (MDA-LDL) at health evaluation." Health Evaluation and Promotion 39, no. 2 (2012): 261–66. http://dx.doi.org/10.7143/jhep.39.261.

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