BACKGROUND: Most atherosclerotic lesions are vascularized, so neovessels may also contribute to plaque progression and vulnerability, but their precise role of neovessels in atherosclerosis is still unknown. The aim of this study was to analyze the possible relationships among neovascularization, relevant angiogenic factors, and plaque vulnerability in patients with advanced carotid artery stenosis. METHODS AND RESULTS: The study group comprised 56 patients (stable: n=28, unstable: n=28) with advanced carotid artery stenosis (>70%). Immunohistochemistry was performed for smooth muscle, endothelial, and inflammatory cells, macrophages, vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR-2), platelet-derived growth factor (PDGF), and angiopoietin-1,-2 (Ang-1,-2). Furthermore, the concentrations of angiogenic factors were measured in serum. Quantitative expression analysis was performed by SYBR-Green-based real-time polymerase chain reaction. Compared with stable carotid lesions, unstable carotid lesions showed 1.8-fold increase in neovascularization (P=0.013), which significantly correlated with accumulation of inflammatory cells (factor 1.9, P<0.001). In unstable lesions, compared with stable lesions, VEGF was 1.7-fold increased (P=0.032) and Ang-1 was 1.9-fold reduced (P=0.029). Furthermore, VEGF was higher in the blood of patients with unstable plaques than in stable plaques (0.32 ± 0.22 vs. 0.22 ± 0.16 ng/ml; P=0.002). Significant correlations were observed between plaque vulnerability, VEGF, neovascularization and inflammatory cells. CONCLUSIONS: Our results show a close association between neovascularization, expression of angiogenic factors, inflammation, and plaque vulnerability in patients with advanced carotid stenosis.
BACKGROUND: Most atherosclerotic lesions are vascularized, so neovessels may also contribute to plaque progression and vulnerability, but their precise role of neovessels in atherosclerosis is still unknown. The aim of this study was to analyze the possible relationships among neovascularization, relevant angiogenic factors, and plaque vulnerability in patients with advanced carotid artery stenosis. METHODS AND RESULTS: The study group comprised 56 patients (stable: n=28, unstable: n=28) with advanced carotid artery stenosis (>70%). Immunohistochemistry was performed for smooth muscle, endothelial, and inflammatory cells, macrophages, vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR-2), platelet-derived growth factor (PDGF), and angiopoietin-1,-2 (Ang-1,-2). Furthermore, the concentrations of angiogenic factors were measured in serum. Quantitative expression analysis was performed by SYBR-Green-based real-time polymerase chain reaction. Compared with stable carotid lesions, unstable carotid lesions showed 1.8-fold increase in neovascularization (P=0.013), which significantly correlated with accumulation of inflammatory cells (factor 1.9, P<0.001). In unstable lesions, compared with stable lesions, VEGF was 1.7-fold increased (P=0.032) and Ang-1 was 1.9-fold reduced (P=0.029). Furthermore, VEGF was higher in the blood of patients with unstable plaques than in stable plaques (0.32 ± 0.22 vs. 0.22 ± 0.16 ng/ml; P=0.002). Significant correlations were observed between plaque vulnerability, VEGF, neovascularization and inflammatory cells. CONCLUSIONS: Our results show a close association between neovascularization, expression of angiogenic factors, inflammation, and plaque vulnerability in patients with advanced carotid stenosis.
Authors: Andrea Caporali; Magnus Bäck; Mat J Daemen; Imo E Hoefer; Elizabeth A Jones; Esther Lutgens; Christian M Matter; Marie-Luce Bochaton-Piallat; Arndt F Siekmann; Judith C Sluimer; Sabine Steffens; José Tuñón; Cecile Vindis; Jolanda J Wentzel; Seppo Ylä-Herttuala; Paul C Evans Journal: Cardiovasc Res Date: 2018-09-01 Impact factor: 10.787
Authors: L Saba; S Zucca; A Gupta; G Micheletti; J S Suri; A Balestrieri; M Porcu; P Crivelli; G Lanzino; Y Qi; V Nardi; G Faa; R Montisci Journal: AJNR Am J Neuroradiol Date: 2020-07-30 Impact factor: 3.825
Authors: Enrico Ammirati; Francesco Moroni; Giuseppe Danilo Norata; Marco Magnoni; Paolo G Camici Journal: Mediators Inflamm Date: 2015-04-16 Impact factor: 4.711
Authors: Thomas L Theelen; Jari P Lappalainen; Judith C Sluimer; Erika Gurzeler; Jack P Cleutjens; Marion J Gijbels; Erik A L Biessen; Mat J A P Daemen; Kari Alitalo; Seppo Ylä-Herttuala Journal: Atherosclerosis Date: 2015-06-03 Impact factor: 5.162