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1

Role of adiponectin - a protein secreted by adipose tissue in preventing atherosclerosis

100%
Karbowska J., Brzezinski M., Kochan Z.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 5
579-591
EN
Adiponectin is an adipocyte-specific secretory protein, which seems to play a protective role in different models of vascular injury. Adiponectin infiltrates in the subendothelial space of injured vascular walls and suppresses the expression of adhesion molecules on endothelial cells, thus inhibiting the inflammatory processes that occur during the early phases of atherosclerosis. Adiponectin also suppresses lipid accumulation in macrophages and macrophage-to-foam cell transformation. The ability of adiponectin to act as an anti-inflammatory and anti-atherogenic factor has made this novel adipocytokine a promising therapeutic tool for the future.
2

From accuracy in protein synthesis to cardiovascular disease: the role of homocysteine

100%
Jakubowski H.
Biotechnologia
|
2002
|
issue 3
39-52
EN
The non-protein amino acid homocysteine (Hcy) enters the first step of protein synthesis and forms an aminoacyl-tRNA synthetase-bound homocysteinyl adenylate (Hcy-AMP). Direct incorporation of Hcy into tRNA and protein is prevented by editing activities of aminoacyl-tRNA synthetases that convert Hcy-AMP into Hcy thiolactone. Editing of Hcy occurs in all cell types investigated, including human. S-Nitrosylation of Hcy prevents its editing by MetRS and allows formation of S-nitroso-Hcy-tRNAMet, as well as incorporation of Hcy into proteins at positions specified by methionine codons. This provides an example of how the genetic code can be expanded by invasion of the metionine coding pathway by Hcy. Hcy can also be incorporated into protein post-translationally by a facile reaction of Hcy thiolactone with ?-amino groups of protein lysine residues. Hcy is present in human blood proteins, such as hemoglobin, serum albumin, and ?-globulins. Hcy thiolactonase, a component of high-density lipoprotein, minimizes protein N-homocysteinylation. Incorporation of Hcy into protein provides plausible chemical mechanism by which elevated levels of Hcy contribute to human cardiovascular disease.
3

Do changes in iron metabolism contribute to the acceleration of the atherosclerosis process?

100%
Formanowicz D.
Biotechnologia
|
2011
|
issue 2
180-192
EN
There are several risk factors whose association with atherosclerosis, a chronic disease with complicated etiology, is well established, including age, gender, smoking, lipids metabolism disorders, diabetes mellitus, obesity and reduced physical activity. Surprisingly, many cardiovascular related deaths occur in individuals without standard risk factors, so it has been suggested that these cases must be the result of other factors, previously not taken into account. This phenomenon resulted in the development of research focused on finding new risk factors. In 1981, Sullivan first postulated the so-called 'iron hypothesis', suggesting that the regular menstrual iron loss, rather than other known effects of estrogen, protects women against coronary heart disease. It is widely believed at present, that iron is an essential catalyst in the oxidation and oxidative modification of low-density lipoprotein cholesterol which appears to be one of the pivotal steps in the early phase of the formation of the atherosclerotic plaque. Thus, iron depletion through menstrual loss might reduce oxidative stress and beneficially affect atherogenesis. Stored iron appears to be essential in the process of atherogenesis which is strictly required for normal cellular metabolism but also serves as a reservoir from which toxic-active iron can be liberated under atherogenic stimuli and result in lipid peroxidation. In this process, two pathways i.e., iron homeostasis metabolic pathway and metabolic pathways involving proinflammatory cytokines are closely interconnected. In human monocytes, these cytokines also increase the uptake of non-transferrin-bound iron, via the stimulation of divalent metal transporter- 1 synthesis and cause iron retention by down-regulating ferroportin synthesis. It has been found recently that iron depositions are prominent in human atherosclerosis lesions. It can therefore be concluded that the results of scientific research, particularly those of the last ten years, provide a strong pathological basis to support the role of iron metabolism alterations in vascular damage and in the progression of atherosclerosis process.
4

Rethinking oxidized low-density lipoprotein, its role in atherogenesis and the immune responses associated with it

100%
Shaw P. X.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
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vol. 52
|
issue 4
225-239
EN
Atherosclerosis is a chronic inflammatory disease, resulting from hyperlipidemia and a complex interplay of many environmental, metabolic, and genetic risk factors. The unregulated macrophage uptake of cholesterol and lipids through modified forms of lowdensity lipoprotein (LDL), such as ?OxLDL', transforms macrophages into 'foam cells' to form the initial morphological lesion (the fatty streak). The modification of LDL not only enhances its uptake by macrophages, but also changes the natural structures of these otherwise ubiquitous molecules to generate a variety of modified lipids and proteins that represent highly immunogenic neo-determinants. For example, in ApoE?/? mice, autoantibody titers to epitopes on OxLDL are correlated with the extent of atherosclerosis. Similarly, oxidative stress on cellular membranes could also give rise to ?oxidation-specific' epitopes and common autoantibodies. However, OxLDL is not uniform, but rather contains complex structures, ranging from a small conformational change in surface lipids to the breakdown of the peptide chain. Therefore, the immune responses to the variety of OxLDL and their association to atherosclerosis progression are very different. For example, phosphorylcholine (PC) is a natural component of phospholipids and exists in LDL and plasma membranes. ?Natural' antibodies against PC can distinctively react to PC on bacteria, OxLDL and apoptotic cells, but not to those on unoxidized phospholipids, native LDL and viable cells, which suggests the broader role of such autoantibodies in maintaining the homeostasis of the host. While malondialdehyde-modified structures resemble more the exogenous changes and associate with advanced stage of lesion, they are more likely to associate with adaptive immunity.
5

Biomechanic shear stress in carotid arteries and atherosclerosis development

88%
Kazmierski R.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 6
713-725
EN
One of the major hemodynamic forces acting on blood vessels is shear stress, which is, the friction force between the endothelial cell surface and flowing blood. Arterial shear stress within physiologic range (15-70 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile. Low shear stress (< 4 dyne/cm2 ) stimulates atherogenic phenotype, whereas, high shear stress (>70 dyne/cm2 ) induce prothrombotic state.
6

The role of oxidatively modified low density lipoprotein in the pathogenesis of atherosclerosis

88%
Siennicka A., Zapolska-Downar D.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 2
219-237
EN
The precise mechanisms of LDL oxidation in vivo are not well-known but the presence of several enzymes and agents capable of modifying LDL particles was noted in arterial wall. These reactive agents modify lipid, protein as well as antioxidant component of the LDL particles. Postsecretory modification in LDL structure trigger its atherogenic potential. LDL particles retained in the artery wall interact with the various forms of proteoglycans in the extracellular matrix, that increases the resident time of LDL in endothelial space and allows extensive modification. The modified forms of LDL are able to activate intimal cells and to trigger various inflammatory signals. In turn, activated intimal cells can secrete enzymes and agents capable of modifying LDL. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression.
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