Galectin-3, Carotid Plaque Vulnerability, and Potential Effects of Statin Therapy
Objectives Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vul...
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Published in | European journal of vascular and endovascular surgery Vol. 49; no. 1; pp. 4 - 9 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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England
Elsevier Ltd
01.01.2015
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Abstract | Objectives Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. Methods This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. Results There were no significant differences in clinical and demographic parameters between SG and AG ( p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG ( p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR = 0.634, p < .001), and GSM score (OR = 0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment ( p < .05). Conclusions A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization. |
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AbstractList | OBJECTIVESGalectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis.METHODSThis was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined.RESULTSThere were no significant differences in clinical and demographic parameters between SG and AG(p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG (p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR=0.634, p < .001), and GSM score (OR=0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment (p < .05).CONCLUSIONSA low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization. Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. There were no significant differences in clinical and demographic parameters between SG and AG (p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG (p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR = 0.634, p < .001), and GSM score (OR = 0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment (p < .05). A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization. Galectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. There were no significant differences in clinical and demographic parameters between SG and AG(p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG (p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR=0.634, p < .001), and GSM score (OR=0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment (p < .05). A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization. Objectives Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. Methods This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. Results There were no significant differences in clinical and demographic parameters between SG and AG ( p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG ( p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR = 0.634, p < .001), and GSM score (OR = 0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment ( p < .05). Conclusions A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization. |
Author | Spathis, A Liapis, C.D Gkekas, C Karakitsos, P Mantas, G Gastounioti, A Sfyroeras, G.S Kadoglou, N.P.E Nikita, K.S |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25457298$$D View this record in MEDLINE/PubMed |
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Keywords | Stroke/transient ischemic attack Plaque vulnerability Galectin-3 Carotid atherosclerosis Statins |
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Snippet | Objectives Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of... Galectin-3, a member of galectines, a family of β-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in... Galectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in... OBJECTIVESGalectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of... |
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SubjectTerms | Aged Antigens, CD - analysis Antigens, Differentiation, Myelomonocytic - analysis C-Reactive Protein - analysis Carotid Artery Diseases - complications Carotid Artery Diseases - diagnostic imaging Carotid Artery Diseases - pathology Carotid Artery Diseases - therapy Carotid atherosclerosis Carotid Stenosis - etiology Cross-Sectional Studies Endarterectomy, Carotid Female Galectin 3 - analysis Galectin 3 - blood Galectin-3 Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Immunohistochemistry Laminin - analysis Macrophages - immunology Macrophages - pathology Male Plaque vulnerability Plaque, Atherosclerotic - chemistry Plaque, Atherosclerotic - diagnostic imaging Regression Analysis Statins Stroke/transient ischemic attack Surgery Ultrasonography |
Title | Galectin-3, Carotid Plaque Vulnerability, and Potential Effects of Statin Therapy |
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