VOJNOSANIT PREGL

2010

DOI: 10.2298/vsp1012007v

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Recent views on cytohistological characteristics and pathogenic mechanisms of atherosclerotic lesions types I, II and III

Irena Vukovic¹,

Vesna Lačković²,

et al.

Abstract: nem

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Discussion2

Connective Tissue Fibers In the Wall Of The Blood Vessels2

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Cited by 6 publications

(4 citation statements)

References 13 publications

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“…In this cell population, cells that demonstrate an immunohistochemical response to α-SMA, vimentin, and S100 protein are present. According to the literature data, as well as to the results of our previous research, immunoreactivity to α-SMA is a common characteristic of vascular smooth muscle cells, while immunoreactivity to vimentin, in the absence of immunoreactivity to desmin as a marker of highly differentiated contractile phenotype, suggests that smooth muscle cells of the synthetic phenotype are in question (Vukovic et al, 2010). It is also observed that these synthetically active smooth muscle cells demonstrate immunoreactivity to S100 protein, which we will consider separately.…”

Section: Discussionmentioning

confidence: 62%

“…We have already mentioned that the target molecule of S100100 / S100A9 protein complex is the intermediate filament vimentin, which would suggest that its expression, occurred due to the loss of contractile characteristics of smooth muscle cells derived from mesenchyme, presents a predisposing factor for protein binding and further promoting cell migration, proliferation and differentiation. This complex also demonstrates marked susceptibility to oxidation, probably having a bifunctional, proinflammatory or antiinflammatory role, depending on its own redox status - (Gould et al, 1986;Libby, 1996;Donato et al;Vukovic et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Function of s100 Protein in Coronary Atherosclerosis

¹

,

²

,

³

et al. 2022

Int. J. Morphol.

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Atherosclerosis is a complex disease whose pathogenesis includes endothelial activation, accumulation of lipids in the subendothelium, formation of foam cells, fat bands and formation of atherosclerotic plaque. These complex mechanisms involve different cell populations in the intimate sub-endothelium, and the S-100 protein family plays a role in a number of extracellular and intracellular processes during the development of atherosclerotic lesions. The aim of this study was to determine the phenotypic characteristics of smooth muscle cells and the consequent expression of S100 protein in atherosclerotic altered coronary arteries in advanced stages of atherosclerosis. 19 samples of right atherosclerotic coronary arteries in stages of fibro atheroma (type V lesion) and complicated lesions (type VI lesion) have been analyzed. According to the standard protocol, the following primary antibodies have been used in the immunohistochemical analysis: a-smooth muscle actin (α-SMA), vimentin and S-100 protein. All analyzed samples have been in advanced stages of atherosclerosis, fibro atheroma (stage V lesions) and complicated lesions (type VI lesions). Most of them have had the structure of a complicated lesion with atheroma or fibro atheroma as a basis, subsequently complicated by disruption (subtype VI a), hemorrhage (subtype VI b) or thrombosis (subtype VI c), as well as by the presence of several complications on the same sample. Marked hypocellularity is present in the subendothelium of plaques. Cell population at plaque margins is characterized by immunoreactivity to α-SMA, vimentin, and S100 protein. Some of these cells accumulate lipids and look like foam cells. In the cell population at the margins of the plaques, smooth muscle cells of the synthetic phenotype are present, some of which accumulate lipids and demonstrate S100 immunoreactivity. Summarizing numerous literature data and our results, we could assume that smooth muscle cells, due to their synthetic and proliferative activity in the earlier stages of pathogenesis, as well as the consequent expression of S100 protein, could accumulate lipids in the earlier stages of atherosclerosis which, in advanced stages analyzed in this study, result in immunoreactivity of foam cells of smooth muscle origin to S100 protein.

“…In this cell population, cells that demonstrate an immunohistochemical response to α-SMA, vimentin, and S100 protein are present. According to the literature data, as well as to the results of our previous research, immunoreactivity to α-SMA is a common characteristic of vascular smooth muscle cells, while immunoreactivity to vimentin, in the absence of immunoreactivity to desmin as a marker of highly differentiated contractile phenotype, suggests that smooth muscle cells of the synthetic phenotype are in question (Vukovic et al, 2010). It is also observed that these synthetically active smooth muscle cells demonstrate immunoreactivity to S100 protein, which we will consider separately.…”

Section: Discussionmentioning

confidence: 62%

“…We have already mentioned that the target molecule of S100100 / S100A9 protein complex is the intermediate filament vimentin, which would suggest that its expression, occurred due to the loss of contractile characteristics of smooth muscle cells derived from mesenchyme, presents a predisposing factor for protein binding and further promoting cell migration, proliferation and differentiation. This complex also demonstrates marked susceptibility to oxidation, probably having a bifunctional, proinflammatory or antiinflammatory role, depending on its own redox status - (Gould et al, 1986;Libby, 1996;Donato et al;Vukovic et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Function of s100 Protein in Coronary Atherosclerosis

¹

,

²

,

³

et al. 2022

Int. J. Morphol.

Self Cite

View full text Add to dashboard Cite

Atherosclerosis is a complex disease whose pathogenesis includes endothelial activation, accumulation of lipids in the subendothelium, formation of foam cells, fat bands and formation of atherosclerotic plaque. These complex mechanisms involve different cell populations in the intimate sub-endothelium, and the S-100 protein family plays a role in a number of extracellular and intracellular processes during the development of atherosclerotic lesions. The aim of this study was to determine the phenotypic characteristics of smooth muscle cells and the consequent expression of S100 protein in atherosclerotic altered coronary arteries in advanced stages of atherosclerosis. 19 samples of right atherosclerotic coronary arteries in stages of fibro atheroma (type V lesion) and complicated lesions (type VI lesion) have been analyzed. According to the standard protocol, the following primary antibodies have been used in the immunohistochemical analysis: a-smooth muscle actin (α-SMA), vimentin and S-100 protein. All analyzed samples have been in advanced stages of atherosclerosis, fibro atheroma (stage V lesions) and complicated lesions (type VI lesions). Most of them have had the structure of a complicated lesion with atheroma or fibro atheroma as a basis, subsequently complicated by disruption (subtype VI a), hemorrhage (subtype VI b) or thrombosis (subtype VI c), as well as by the presence of several complications on the same sample. Marked hypocellularity is present in the subendothelium of plaques. Cell population at plaque margins is characterized by immunoreactivity to α-SMA, vimentin, and S100 protein. Some of these cells accumulate lipids and look like foam cells. In the cell population at the margins of the plaques, smooth muscle cells of the synthetic phenotype are present, some of which accumulate lipids and demonstrate S100 immunoreactivity. Summarizing numerous literature data and our results, we could assume that smooth muscle cells, due to their synthetic and proliferative activity in the earlier stages of pathogenesis, as well as the consequent expression of S100 protein, could accumulate lipids in the earlier stages of atherosclerosis which, in advanced stages analyzed in this study, result in immunoreactivity of foam cells of smooth muscle origin to S100 protein.

“…Cellular population (10)(11)(12). The principal cell of the connective tissue is fibroblast because it produces elements of the extracellular matrix and the reticular lamina of the basement membrane as well (9).…”

Section: Organization Of the Connective Tissue In The Vascular Wallmentioning

confidence: 99%

“…This causes loss of elasticity. Elastic fibers are produced by fibroblasts and smooth muscle cell with synthetic phenotype (11,12). According to the degree of maturity, there are three types of elastic fibers: oxytalan, elaunin and mature fibers (49,50).…”

Section: Connective Tissue Fibers In the Wall Of The Blood Vesselsmentioning

confidence: 99%

Modern view on the structure of the vascular extracellular matrix

Tanasković-Stanković¹,

et al. 2015

Medicinski casopis

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No abstract

The influence of extracellular matrix composition on the pathogenesis of coronary atherosclerosis

¹

,

³

et al. 2011

ARCH BIOL SCI BELGRA

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The modern concept of the development of atherosclerosis implies that the underlying pathogenesis of this disease is vascular remodeling as a response of the vessel wall to hypertension associated with hyperlipidemia and subsequent inflammation. However, even though this disease has been investigated for decades, both from a basic and clinical research aspect, there are still many doubts as to what the initial phase of the disease is. In contemporary literature there are an increasing number of papers that stress the importance of the extracellular matrix (ECM) of the blood vessels connective tissue, particularly proteoglycans, in the formation of early atherosclerotic lesions of human coronary arteries

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