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Inflammatory biomarkers in atherosclerosis: pentraxin 3 can become a novel marker of plaque vulnerability.

Shindo A, Tanemura H, Yata K, Hamada K, Shibata M, Umeda Y, Asakura F, Toma N, Sakaida H, Fujisawa T, Taki W, Tomimoto H - PLoS ONE (2014)

Bottom Line: Serum levels of IL-6, IL-1β, IL-10, TNFα, E-selectin, VCAM-1, adiponectin, hs-CRP, and PTX3 were measured by multiplex bead array system and ELISA.The vulnerable group showed upregulation of the proinflammatory cytokines (IL-6 and TNFα), endothelial activation markers (E-selectin and VCAM-1), and inflammation markers (hs-CRP and PTX3) and downregulation of the anti-inflammatory markers (adiponectin and IL-10).PTX3 levels in both systemic and intracarotid samples before and after CAS were higher in the vulnerable group than in the stable group.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Mie University Graduate School of Medicine, 2-174 Edobasih, Tsu, Mie, Japan.

ABSTRACT
Inflammation is crucially involved in the development of carotid plaques. We examined the relationship between plaque vulnerability and inflammatory biomarkers using intraoperative blood and tissue specimens. We examined 58 patients with carotid stenosis. Following carotid plaque magnetic resonance imaging, 41 patients underwent carotid artery stenting (CAS) and 17 underwent carotid endarterectomy (CEA). Blood samples were obtained from the femoral artery (systemic) and common carotid artery immediately before and after CAS (local). Seventeen resected CEA tissue samples were embedded in paraffin, and histopathological and immunohistochemical analyses for IL-6, IL-10, E-selectin, adiponectin, and pentraxin 3 (PTX3) were performed. Serum levels of IL-6, IL-1β, IL-10, TNFα, E-selectin, VCAM-1, adiponectin, hs-CRP, and PTX3 were measured by multiplex bead array system and ELISA. CAS-treated patients were classified as stable plaques (n = 21) and vulnerable plaques (n = 20). The vulnerable group showed upregulation of the proinflammatory cytokines (IL-6 and TNFα), endothelial activation markers (E-selectin and VCAM-1), and inflammation markers (hs-CRP and PTX3) and downregulation of the anti-inflammatory markers (adiponectin and IL-10). PTX3 levels in both systemic and intracarotid samples before and after CAS were higher in the vulnerable group than in the stable group. Immunohistochemical analysis demonstrated that IL-6 was localized to inflammatory cells in the vulnerable plaques, and PTX3 was observed in the endothelial and perivascular cells. Our findings reveal that carotid plaque vulnerability is modulated by the upregulation and downregulation of proinflammatory and anti-inflammatory factors, respectively. PTX3 may thus be a potential predictive marker of plaque vulnerability.

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Proinflammatory and anti-inflammatory biomarkers in vulnerable plaques.Decreased adiponectin levels induce endothelial cell dysfunction with E-selectin release, with subsequent low IL-10 levels and high TNFα levels. Impaired endothelial cells release E-selectin, PTX3, and TNFα. Macrophages produce PTX3, TNFα, and IL-6.
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pone-0100045-g006: Proinflammatory and anti-inflammatory biomarkers in vulnerable plaques.Decreased adiponectin levels induce endothelial cell dysfunction with E-selectin release, with subsequent low IL-10 levels and high TNFα levels. Impaired endothelial cells release E-selectin, PTX3, and TNFα. Macrophages produce PTX3, TNFα, and IL-6.

Mentions: Inflammatory mechanisms are known to play a central role in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers, such as hs-CRP, IL-6, E-selectin, ICAM-1, and VCAM-1, have been previously identified [20]–[23]. IL-6 has been reported to be higher in local samples from patients with carotid artery plaques, increasing further after CAS with periprocedural new ischemic lesions [24]. In present study, serum IL-6, VCAM-1, E-selectin and PTX3 levels were significantly higher in the post-procedural local samples as compared to the systemic samples. This suggests an association between carotid atherosclerosis and the local production of not only IL-6 but also E-selectin, VCAM-1 and PTX3 (Figure 6).


Inflammatory biomarkers in atherosclerosis: pentraxin 3 can become a novel marker of plaque vulnerability.

Shindo A, Tanemura H, Yata K, Hamada K, Shibata M, Umeda Y, Asakura F, Toma N, Sakaida H, Fujisawa T, Taki W, Tomimoto H - PLoS ONE (2014)

Proinflammatory and anti-inflammatory biomarkers in vulnerable plaques.Decreased adiponectin levels induce endothelial cell dysfunction with E-selectin release, with subsequent low IL-10 levels and high TNFα levels. Impaired endothelial cells release E-selectin, PTX3, and TNFα. Macrophages produce PTX3, TNFα, and IL-6.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061039&req=5

pone-0100045-g006: Proinflammatory and anti-inflammatory biomarkers in vulnerable plaques.Decreased adiponectin levels induce endothelial cell dysfunction with E-selectin release, with subsequent low IL-10 levels and high TNFα levels. Impaired endothelial cells release E-selectin, PTX3, and TNFα. Macrophages produce PTX3, TNFα, and IL-6.
Mentions: Inflammatory mechanisms are known to play a central role in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers, such as hs-CRP, IL-6, E-selectin, ICAM-1, and VCAM-1, have been previously identified [20]–[23]. IL-6 has been reported to be higher in local samples from patients with carotid artery plaques, increasing further after CAS with periprocedural new ischemic lesions [24]. In present study, serum IL-6, VCAM-1, E-selectin and PTX3 levels were significantly higher in the post-procedural local samples as compared to the systemic samples. This suggests an association between carotid atherosclerosis and the local production of not only IL-6 but also E-selectin, VCAM-1 and PTX3 (Figure 6).

Bottom Line: Serum levels of IL-6, IL-1β, IL-10, TNFα, E-selectin, VCAM-1, adiponectin, hs-CRP, and PTX3 were measured by multiplex bead array system and ELISA.The vulnerable group showed upregulation of the proinflammatory cytokines (IL-6 and TNFα), endothelial activation markers (E-selectin and VCAM-1), and inflammation markers (hs-CRP and PTX3) and downregulation of the anti-inflammatory markers (adiponectin and IL-10).PTX3 levels in both systemic and intracarotid samples before and after CAS were higher in the vulnerable group than in the stable group.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Mie University Graduate School of Medicine, 2-174 Edobasih, Tsu, Mie, Japan.

ABSTRACT
Inflammation is crucially involved in the development of carotid plaques. We examined the relationship between plaque vulnerability and inflammatory biomarkers using intraoperative blood and tissue specimens. We examined 58 patients with carotid stenosis. Following carotid plaque magnetic resonance imaging, 41 patients underwent carotid artery stenting (CAS) and 17 underwent carotid endarterectomy (CEA). Blood samples were obtained from the femoral artery (systemic) and common carotid artery immediately before and after CAS (local). Seventeen resected CEA tissue samples were embedded in paraffin, and histopathological and immunohistochemical analyses for IL-6, IL-10, E-selectin, adiponectin, and pentraxin 3 (PTX3) were performed. Serum levels of IL-6, IL-1β, IL-10, TNFα, E-selectin, VCAM-1, adiponectin, hs-CRP, and PTX3 were measured by multiplex bead array system and ELISA. CAS-treated patients were classified as stable plaques (n = 21) and vulnerable plaques (n = 20). The vulnerable group showed upregulation of the proinflammatory cytokines (IL-6 and TNFα), endothelial activation markers (E-selectin and VCAM-1), and inflammation markers (hs-CRP and PTX3) and downregulation of the anti-inflammatory markers (adiponectin and IL-10). PTX3 levels in both systemic and intracarotid samples before and after CAS were higher in the vulnerable group than in the stable group. Immunohistochemical analysis demonstrated that IL-6 was localized to inflammatory cells in the vulnerable plaques, and PTX3 was observed in the endothelial and perivascular cells. Our findings reveal that carotid plaque vulnerability is modulated by the upregulation and downregulation of proinflammatory and anti-inflammatory factors, respectively. PTX3 may thus be a potential predictive marker of plaque vulnerability.

Show MeSH
Related in: MedlinePlus