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12. The role of iron in the pathogenesis of atherosclerosis
- Creator:
- Pavel Kraml
- Format:
- print, bez média, and svazek
- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, železo, železivce, oxidační stres, záněty, ateroskleróza, iron, ironstones, oxidative stress, inflammations, atherosclerosis, macrophages, 14, and 612
- Language:
- English
- Description:
- Ferritin and increased iron stores first appea red on the list of cardiovascular risk factors more than 30 years ago and their causal role in the pathogenesis of atherosclerosis has been heavily discussed since the early 1990s. It seems that besides traditional factors such as hyperlipoprotein emia, hyp ertension, diabetes mellitus, obesity, physical inactivity, smoking and family history, high iron stores represent an additional parameter that could modify individual cardiovascular risk. The role of iron in the pathogenesis of atherosclerosis was origina lly primarily associated with its ability to cataly ze the formation of highly reactive free oxygen radicals and the oxidation of atherogenic lipoproteins. Later, it became clear that the mechanism is more complex. Atherosclerosis is a chronic fibroprolife rative inflammatory process and iron, through increased oxidation stress as well as directly, can control both native and adaptive immune responses. Within the arterial wall, iron affects all of the cell types that participate in the atherosclerotic proces s (monocytes/macrophages, endothelial cells, vascular smooth muscle cells and platelets). Most intracellular iron is bound in ferritin, whereas redox-active iron forms labile iron pool. Pro-inflammatory and anti-inflammatory macrophages within arterial plaque differ with regard to the amount of intracellular iron and most probably with regard to their labile iron pool. Yet, the relation between plasma ferritin and intracellular labile iro n pool has not been fully clarified. Data from population studies document that the consumption of meat and lack of physical activity contribute to increased iron stores. Patients with hereditary h emochromatosis, despite extreme iron storage, do not show i ncreased manifestation of atherosclerosis probably due to the low expression of hepcidin in macrophages., P. Kraml., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
13. Transformation of blood monocytes to multinucleated giant cells in vitro: are there any differences between malignant and nonmalignant states ?
- Creator:
- Munzarová, M. and Zemanová, D.
- Type:
- article, model:article, and TEXT
- Subject:
- cell fusion, monocytes, macrophages, melanoma, breast cancer, and multinucleated giant cells
- Language:
- English
- Description:
- Blood monocytes (BMs) from 139 subjects (70 malignant melanoma patients, 31 breast cancer patients, 38 healthy controls) were cultured for at least 7 days. The formation of multinucleated giant cells (MGCs), which was checked during the whole time of culture, was observed in all cases. By the seventh day MGCs represented 25-50 % and during the second and third month more than 90% of all cells. Lymphokines and/or concanavalin A stimulation (16-34 cases respectively) of BMs was performed as well. This stimulation greatly accelerated MGC formation. There were no differences either in spontaneous or in stimulated fusion between the different groups compared.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
14. Visfatin is actively secreted in vitro from U-937 macrophages, but only passively released from 3T3-L1 adipocytes and HepG2 hepatocytes
- Creator:
- Svoboda, P., Křížová, E., Čeňková, K., Vápenková, K., Jarmila Zídková, Václav Zídek, and Vojtěch Škop
- Format:
- print, bez média, and svazek
- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, nampt, visfatin, active secretion, adipocytes, hepatocytes, macrophages, 14, and 612
- Language:
- English
- Description:
- Visfatin is a multi-functional molecule that can act intracellularly and extracellularly as an adipokine, cytokine and enzyme. One of the main questions concerning visfatin is the mechanism of its secretion; whether, how and from which cells visfatin is released. The objective of this in vitro study was to observe the active secretion of visfatin from 3T3-L1 preadipocytes and adipocytes, HepG2 hepatocytes, U-937, THP-1 and HL-60 monocytes and macrophages. The amount of visfatin in media and cell lysate was always related to the intracellular enzyme, glyceraldehyde-3- phosphate dehydrogenase (GAPDH), to exclude the passive release of visfatin. Visfatin was not found in media of 3T3-L1 preadipocytes. In media of 3T3-L1 adipocytes and HepG2 hepatocytes, the ratio of visfatin to the amount of GAPDH was identical to cell lysates. Hence, it is likely that these cells do not actively secrete visfatin in a significant manner. However, we found that significant producers of visfatin are differentiated macrophages and that the amount of secreted visfatin depends on used cell line and it is affected by the mode of differentiation. Results show that 3T3-L1 adipocytes and HepG2 hepatocytes released visfatin only passively during the cell death. U-937 macrophages secrete visfatin in the greatest level from all of the tested cell lines., P. Svoboda, E. Křížová, K. Čeňková, K. Vápenková, J. Zídková, V. Zídek, V. Škop., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public