Ficolin-2 serum levels predict the occurrence of acute coronary syndrome in patients with severe carotid artery stenosis

Carbone, Federico; Valente, Alessia; Perego, Carlo; Bertolotto, Maria; Pane, Bianca; Spinella, Giovanni; Palombo, Domenico; Simoni, Maria Grazia De; Montecucco, Fabrizio; Fumagalli, Stefano

doi:10.1016/j.phrs.2021.105462

Cited by 11 publications

(9 citation statements)

References 47 publications

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“…Previous studies have shown that high ficolin‐2 levels are associated with risk of myocardial infarction in population based studies 40 . Recently it has also been shown that increased serum levels of ficolin‐2 predict the occurrence of acute coronary syndrome in patients with severe carotid artery stenosis 41 . Thus, we anticipate that it is not the dialysis per se that might be associated, but the underlying molecular regulation of ficolin‐2 or ficolin‐2 directly that might be associated with increased overall mortality.…”

Section: Discussionmentioning

confidence: 99%

“…40 Recently it has also been shown that increased serum levels of ficolin-2 predict the occurrence of acute coronary syndrome in patients with severe carotid artery stenosis. 41 Thus, we anticipate that it is not the dialysis per se that might be associated, but the underlying molecular regulation of ficolin-2 or ficolin-2 directly that might be associated with increased overall mortality. We suggest that the reason why we observe a significant association only after dialysis is that this might reflect the true inter-individual serum variation between each individual, while the underlying disease might blur pre-dialysis variation.…”

Section: Complement Activationmentioning

confidence: 99%

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Hemodialysis leads to plasma depletion of lectin complement pathway initiator molecule ficolin‐2

Nielsen

Pilely

Lund

et al. 2021

Hemodialysis International

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Introduction: This study aimed to investigate changes in complement system-related molecules in patients undergoing hemodialysis. Methods: Patients >18 years of age on maintenance hemodialysis were included. Using enzyme-linked immunosorbent assays (ELISA) methods complement related molecules ficolin-1, ficolin-2, ficolin-3 mannose-binding lectin, long pentraxin 3, complement activation products C3c, and complement activation potentials were measured before and after a single hemodialysis treatment. All patients were dialyzed with synthetic high flux filters >1.6 m 2 , respectively, Polyamix and Polysulfone, and the Kt/V was maintained >1.3. Findings: Three hundred and four patients were included. There was a modest decrease in plasma level of ficolin-1 (p < 0.001). Ficolin-2 was virtually depleted with median 3.9 (interquartile range [IQR]: 2.6-6.1, range 0.3-13.5) μg/ml before dialysis to median 0.0 (IQR: 0.0-0.5, range 0.0-5.5) μg/ml after dialysis (p < 0.001). No significant difference before and after hemodialysis was seen for mannose-binding lectin and long pentraxin 3 (p > 0.05). In a random subgroup of 160 patients ficolin-2-binding, ficolin-3-mediated lectin pathway capacity and classical pathway capacity were significantly decreased due to hemodialysis. The complement capacity of the alternative pathway was increased after hemodialysis (p = 0.0101), while mannose-binding lectinmediated lectin pathway capacity was unaltered (p = 0.79). There was an increase in the complement activation product C3c (p < 0.0001), while the concentration of total C4 and C3 did not change (p > 0.158). Multivariate Cox proportional hazard analyses showed an increased risk for all-cause mortality with increasing ficolin-2 (p = 0.002) after hemodialysis.Discussion: Plasma ficolin-2 was virtually depleted from the circulation after hemodialysis. However, elevated plasma ficolin-2 levels after hemodialysis was independently associated with increased mortality.

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Section: Discussionmentioning

confidence: 99%

Section: Complement Activationmentioning

confidence: 99%

Hemodialysis leads to plasma depletion of lectin complement pathway initiator molecule ficolin‐2

Nielsen

Pilely

Lund

et al. 2021

Hemodialysis International

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“…Constitutively produced by M1 macrophages and up-regulated through IL-6 trans-signaling [ 17 ], OPN generates a positive feedback loop that sustains macrophage proliferation, polarization, activation, and chemotaxis in autocrine/paracrine manner [ 18 , 19 , 20 ]. We have previously demonstrated that high circulating levels of OPN are associated with features of plaque instability: increased lipid content, reduced smooth muscle cells, complement activation and pro-inflammatory infiltrate including M1-polarized macrophages, neutrophils, and related products (namely matrix metalloproteinase-9) [ 11 , 21 ]. These features add to the classic involvement of OPN in vascular calcification [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Osteopontin as Candidate Biomarker of Coronary Disease despite Low Cardiovascular Risk: Insights from CAPIRE Study

Carbone

Meessen

Magnoni

et al. 2022

Cells

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Stratification according high cardiovascular (CV) risk categories, still represents a clinical challenge. In this analysis of the CAPIRE study (NCT02157662), we investigate whether inflammation could fit between CV risk factors (RFs) and the presence of coronary artery disease (CAD). In total, 544 patients were included and categorized according with the presence of CAD and CV risk factor burden (low/multiple). The primary endpoint was to verify any independent association of neutrophil-related biomarkers with CAD across CV risk categories. The highest values of osteopontin (OPN) were detected in the low RF group and associated with CAD (23.2 vs. 19.4 ng/mL; p = 0.001), although no correlation with plaque extent and/or composition were observed. Conversely, myeloperoxidase (MPO) and resistin did not differ by CAD presence. Again, OPN was identified as independent variable associated with CAD but only in the low RF group (adjOR 8.42 [95% CI 8.42–46.83]; p-value = 0.015). As an ancillary finding, a correlation linked OPN with the neutrophil degranulation biomarker MPO (r = 0.085; p = 0.048) and resistin (r = 0.177; p = 3.4 × 10−5). In the present study, OPN further strengthens its role as biomarker of CAD, potentially bridging subclinical CV risk with development of atherosclerosis.

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“…It has been shown that ficolin in calcified plaques and ficolin-2 in cholesterol-enriched plaque regions are associated with macrophages. Ficolin promotes intraplaque immune cell recruitment and inflammatory processes, leading to plaque vulnerability (Carbone et al 2021). A nested case-control design of 50 participants suggested an association between complement factor B expression and incident CVD after adjustment for diabetes (Ngo et al 2021).…”

Section: Discussionmentioning

confidence: 99%

Identification of Hub Genes Associated with Abnormal Endothelial Function in Early Coronary Atherosclerosis

et al. 2021

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Abnormal coronary endothelial function is an important step in the development of atherosclerosis. Coronary atherosclerosis is one of the main causes of death worldwide. We constructed a co-expression network to identify hub genes associated with abnormal coronary endothelial function in early coronary atherosclerosis. In brief, we used the GSE132651 dataset from the gene expression omnibus database. The top 5000 genes with greatest variances were used for weighted gene co-expression network analysis, and the module most strongly correlated with abnormal coronary endothelial function was chosen as key module. Functional enrichment analysis was performed for genes in the key module, a protein-protein interaction network was constructed to find hub genes, and gene set enrichment analysis (GSEA) was also performed. Genes were classified into 7 modules, with the midnightblue module being the one that was most related to abnormal coronary endothelial function and containing genes enriched in DNA replication, cell cycle, nucleotide excision repair, and Human T-cell leukemia virus 1 infection. We identified nine hub genes (HOXC5, PRND, PADI3, RC3H1, DAPP1, SIT1, DRICH1, GPRIN2, and RHO), which differently expressed in abnormal and normal coronary endothelial function samples. GSEA suggested that samples associated with abnormal coronary endothelial function and highly expressed hub genes were linked with immune, coagulation, hypoxia, and angiogenesis processes. These hub genes, their expression pattern, and pathways may be involved in the development of abnormal coronary endothelial function and promotion of early coronary atherosclerosis.

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Ficolin-2 serum levels predict the occurrence of acute coronary syndrome in patients with severe carotid artery stenosis

Cited by 11 publications

References 47 publications

Hemodialysis leads to plasma depletion of lectin complement pathway initiator molecule ficolin‐2

Hemodialysis leads to plasma depletion of lectin complement pathway initiator molecule ficolin‐2

Osteopontin as Candidate Biomarker of Coronary Disease despite Low Cardiovascular Risk: Insights from CAPIRE Study

Identification of Hub Genes Associated with Abnormal Endothelial Function in Early Coronary Atherosclerosis

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