Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease

Tsoporis, James N.; Mohammadzadeh, Forough; Parker, Thomas G.

doi:10.1155/2010/206073

Cited by 18 publications

(21 citation statements)

References 68 publications

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“…Importantly, endothelial cell-released STAT3 has a key role in inflammation that underlies cardiovascular disease, and conversely, cardiomyocyte STAT3 is important for maintaining endothelial cell functions and the capillary integrity (Zouein et al, 2019). Furthermore, PTX3 resulted the most correlated protein in the inflammatory/fibrotic pathway with higher correlation to Foxp3, ATG7, and S100β proteins that have been linked to endothelial cell functions (Kreisel et al, 2004;Krupnick et al, 2005;Pober and Sessa, 2007;Tsoporis et al, 2010;Singh et al, 2015;Vion et al, 2017). Overall, these results provide the first stringent correlation between PTX3 cardiac expression and inflammatory/fibrotic pathways in an animal model of DMD.…”

Section: Discussionmentioning

confidence: 99%

PTX3 Predicts Myocardial Damage and Fibrosis in Duchenne Muscular Dystrophy

et al. 2020

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Pentraxin 3 (PTX3) is a main component of the innate immune system by inducing complement pathway activation, acting as an inflammatory mediator, coordinating the functions of macrophages/dendritic cells and promoting apoptosis/necrosis. Additionally, it has been found in fibrotic regions co-localizing with collagen. In this work, we wanted to investigate the predictive role of PTX3 in myocardial damage and fibrosis of Duchenne muscular dystrophy (DMD). DMD is an X-linked recessive disease caused by mutations of the dystrophin gene that affects muscular functions and strength and accompanying dilated cardiomyopathy. Here, we expound the correlation of PTX3 cardiac expression with age and Toll-like receptors (TLRs)/interleukin-1 receptor (IL-1R)-MyD88 inflammatory markers and its modulation by the so-called alarmins IL-33, high-mobility group box 1 (HMGB1), and S100β. These findings suggest that cardiac levels of PTX3 might have prognostic value and potential in guiding therapy for DMD cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

PTX3 Predicts Myocardial Damage and Fibrosis in Duchenne Muscular Dystrophy

et al. 2020

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“…Thus, effects of the activity of the S100B/RAGE axis are likely to be strongly context-dependent. As mentioned earlier, S100B is induced by catecholamines in cardiomyocytes surviving an infarct, thereby modulating left ventricular remodeling [14,335]. However, S100B can be released by injured cardiomyocytes and at relatively high doses it causes RAGE-dependent cardiomyocyte apoptosis [336] (Fig.…”

Section: Extracellular Functions Of S100 Proteinsmentioning

confidence: 98%

Functions of S100 Proteins

Donato¹,

Cannon²,

Sorci³

et al. 2013

Current Molecular Medicine

1,123

709

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The S100 protein family consists of 24 members functionally distributed into three main subgroups: those that only exert intracellular regulatory effects, those with intracellular and extracellular functions and those which mainly exert extracellular regulatory effects. S100 proteins are only expressed in vertebrates and show cell-specific expression patterns. In some instances, a particular S100 protein can be induced in pathological circumstances in a cell type that does not express it in normal physiological conditions. Within cells, S100 proteins are involved in aspects of regulation of proliferation, differentiation, apoptosis, Ca2+ homeostasis, energy metabolism, inflammation and migration/invasion through interactions with a variety of target proteins including enzymes, cytoskeletal subunits, receptors, transcription factors and nucleic acids. Some S100 proteins are secreted or released and regulate cell functions in an autocrine and paracrine manner via activation of surface receptors (e.g. the receptor for advanced glycation end-products and toll-like receptor 4), G-protein-coupled receptors, scavenger receptors, or heparan sulfate proteoglycans and N-glycans. Extracellular S100A4 and S100B also interact with epidermal growth factor and basic fibroblast growth factor, respectively, thereby enhancing the activity of the corresponding receptors. Thus, extracellular S100 proteins exert regulatory activities on monocytes/macrophages/microglia, neutrophils, lymphocytes, mast cells, articular chondrocytes, endothelial and vascular smooth muscle cells, neurons, astrocytes, Schwann cells, epithelial cells, myoblasts and cardiomyocytes, thereby participating in innate and adaptive immune responses, cell migration and chemotaxis, tissue development and repair, and leukocyte and tumor cell invasion.

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“…Як доповнення до переліку важливих функцій кальційзв'язувального білка S-100b треба зазначити, що цей білок залучається також до регуляції формування серцево-судинної системи та вважається біохімічним маркером ушкодження цієї системи після шунтування та дилатаційної кардіоміопатії, після інфаркту міокарда (Faa et al, 2012), травм серця та головного мозку (Tsoporis et al, 2010). S-100b запропонований як маркер негативного прогнозу у пацієнтів із вадами серця для виявлення ризику розвитку гіпоксіє-ішемічної енцефалопатії (Faa et al, 2012).…”

Section: рис 3 концентрація рівня S-100b у гіпокампі мозочку та коunclassified

The role of astroglial proteins in the brains of rats under the influence of doxorubicin and Humilid

2016

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Doxorubicin causes toxic side effects which result in profound changes in various organs including the heart muscle, which leads to the development of cardiomyopathy, with further complications, as our earlier studies have shown. But there are complications in treatment by anthracycline chemotherapy. The reduction of toxicity of cytotoxic drugs without reduction of their antitumor action remains an important medical challenge. The S-100b and glial fibrillar acid protein (GFAP) are the key astroglial proteins which are widely used as biomarkers for neurotraumas and strokes. Thus the purpose of our work was to study the GFAP and S-100b levels under the experimental model of doxorubicin-induced cardiomyopathy and the effect of the cytostatic separately or combined with Humilid. The level of studied proteins was measured by ELISA using monospecific antibodies against GFAP and S-100b (Sigma, USA), secondary anti-IgG labeled with horseradish peroxidase (Sigma, USA) and GFAP and S-100b standards (Sigma, USA). The experiment was conducted on white Wistar male rats weighing 210 ±50 g, which were divided into 3 groups with 8 animals in each: 1 – control, rats received saline i/p, 2 – doxorubicin 1 mg/kg i/p once weekly during 4 weeks, 3 – doxorubicin by the same scheme plus 0.01% solution of Humilid during 4 weeks. Under impact of doxorubicin an increase of fibrillar GFAP content in the rats’ hippocampus was shown, which may have occurred as a result of the proliferation of astrocytes. An increase of concentration of S-100b to 20–26% compared with the control animals was also detected in the hippocampus, thalamus and the cerebral cortex of the studied animals. Concomitant administration of doxorubicin with Humilid partially prevented the increase in concentration of GFAP and S-100b in the rats’ hippocampus. The reciprocal change in the level of S-100b and GFAP in the peripheral nervous system of the heart tissue was defined with a high degree of correlation under impact of doxorubicin. Accordingly, we have proposed the hypothesis that the increase in of the filament GFAP in the hippocampus may occur due to the development of the ischemic state under the impact of doxorubicin-induced cardiomyopathy. Humilid with doxorubicin prevented changes in the researched astroglial proteins of the heart muscle and brain parts of rats.

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Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease

Cited by 18 publications

References 68 publications

PTX3 Predicts Myocardial Damage and Fibrosis in Duchenne Muscular Dystrophy

PTX3 Predicts Myocardial Damage and Fibrosis in Duchenne Muscular Dystrophy

Functions of S100 Proteins

The role of astroglial proteins in the brains of rats under the influence of doxorubicin and Humilid

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