Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis
Background: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaq...
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MDPI AG
2023-12-01
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| Online Access: | https://www.mdpi.com/2227-9059/11/12/3275 |
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| author | Ioan Alexandru Balmos Mark Slevin Klara Brinzaniuc Adrian Vasile Muresan Horatiu Suciu Gyopár Beáta Molnár Adriana Mocian Béla Szabó Előd Ernő Nagy Emőke Horváth |
| author_facet | Ioan Alexandru Balmos Mark Slevin Klara Brinzaniuc Adrian Vasile Muresan Horatiu Suciu Gyopár Beáta Molnár Adriana Mocian Béla Szabó Előd Ernő Nagy Emőke Horváth |
| author_sort | Ioan Alexandru Balmos |
| collection | DOAJ |
| description | Background: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. Methods: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation. Results: Patients with intraplaque hemorrhage had greater CD68+ macrophage infiltration (<i>p</i> = 0.003). In 12 cases where iNOS2 predominated over Arg1 positivity, the occurrence of atherothrombotic events was significantly more frequent (<i>p</i> = 0.046). CD31 expression, representing neovessel formation, correlated positively with atherothrombosis (<i>p</i> = 0.020). Conclusions: Intraplaque hemorrhage is often described against the background of an intense inflammatory cell infiltrate. Atherothrombosis is associated with the presence of neovessels and pro-inflammatory macrophages expressing iNOS2. Modulating macrophage polarization may be a successful therapeutic approach to prevent plaque destabilization. |
| first_indexed | 2024-03-08T20:58:47Z |
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| language | English |
| last_indexed | 2024-03-08T20:58:47Z |
| publishDate | 2023-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomedicines |
| spelling | doaj.art-920d7f478a7f46f69e82a25ac5b7268d2023-12-22T13:55:09ZengMDPI AGBiomedicines2227-90592023-12-011112327510.3390/biomedicines11123275Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid AtherosclerosisIoan Alexandru Balmos0Mark Slevin1Klara Brinzaniuc2Adrian Vasile Muresan3Horatiu Suciu4Gyopár Beáta Molnár5Adriana Mocian6Béla Szabó7Előd Ernő Nagy8Emőke Horváth9Doctoral School of Medicine and Pharmacy, I.O.S.U.D., George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaCenter for Advanced Medical and Pharmaceutical Research (CCAMF), George Emil Palade University of Medicine, Pharmacy, Science and Technology, 540142 Targu Mures, RomaniaDepartment of Anatomy, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaVascular Surgery Clinic, County Emergency Clinical Hospital of Targu Mures, 540136 Targu Mures, RomaniaM3 Department of Surgery, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaDoctoral School of Medicine and Pharmacy, I.O.S.U.D., George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaDoctoral School of Medicine and Pharmacy, I.O.S.U.D., George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaM3 Department of Surgery, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Targu Mures, RomaniaDepartment of Biochemistry and Environmental Chemistry, George Emil Palade University of Medicine, Pharmacy, Sciences, and Technology of Targu Mures, 540142 Targu Mures, RomaniaPathology Service, County Emergency Clinical Hospital of Targu Mures, 50 Gheorghe Marinescu Street, 540136 Targu Mures, RomaniaBackground: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. Methods: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation. Results: Patients with intraplaque hemorrhage had greater CD68+ macrophage infiltration (<i>p</i> = 0.003). In 12 cases where iNOS2 predominated over Arg1 positivity, the occurrence of atherothrombotic events was significantly more frequent (<i>p</i> = 0.046). CD31 expression, representing neovessel formation, correlated positively with atherothrombosis (<i>p</i> = 0.020). Conclusions: Intraplaque hemorrhage is often described against the background of an intense inflammatory cell infiltrate. Atherothrombosis is associated with the presence of neovessels and pro-inflammatory macrophages expressing iNOS2. Modulating macrophage polarization may be a successful therapeutic approach to prevent plaque destabilization.https://www.mdpi.com/2227-9059/11/12/3275carotid atherosclerosismacrophageintraplaque neovascularizationatherothrombosisintraplaque hemorrhage |
| spellingShingle | Ioan Alexandru Balmos Mark Slevin Klara Brinzaniuc Adrian Vasile Muresan Horatiu Suciu Gyopár Beáta Molnár Adriana Mocian Béla Szabó Előd Ernő Nagy Emőke Horváth Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis Biomedicines carotid atherosclerosis macrophage intraplaque neovascularization atherothrombosis intraplaque hemorrhage |
| title | Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis |
| title_full | Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis |
| title_fullStr | Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis |
| title_full_unstemmed | Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis |
| title_short | Intraplaque Neovascularization, CD68+ and iNOS2+ Macrophage Infiltrate Intensity Are Associated with Atherothrombosis and Intraplaque Hemorrhage in Severe Carotid Atherosclerosis |
| title_sort | intraplaque neovascularization cd68 and inos2 macrophage infiltrate intensity are associated with atherothrombosis and intraplaque hemorrhage in severe carotid atherosclerosis |
| topic | carotid atherosclerosis macrophage intraplaque neovascularization atherothrombosis intraplaque hemorrhage |
| url | https://www.mdpi.com/2227-9059/11/12/3275 |
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