IL-6 Mobilizes Bone Marrow-Derived Cells to the Vascular Wall, Resulting in Neointima Formation via Inflammatory Effects

Miyake, Shoji; Furuyama, Fumiaki; Yokota, Yuya; Omori, Yasutoshi; Sato, Takatoshi; Tsunoda, Fumiyoshi; Iso, Yoshitaka; Koba, Shinji; Geshi, Eiichi; Kubo, Takashi; Suzuki, Hiroshi; Kobayashi, Youichi

doi:10.5551/jat.19414

Cited by 13 publications

(8 citation statements)

References 25 publications

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“…Immunostaining confirmed the presence of chronic inflammatory markers commonly seen in atherosclerotic plaque 8-10 . IL-6 was visualized throughout the vascular wall, within smooth muscle cells and within the interstitium of the plaque.…”

Section: Case Reportmentioning

confidence: 61%

Intracranial atherosclerosis: Correlation between in-vivo 3T high resolution MRI and pathology

et al. 2014

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Background High-resolution MRI (HRMRI) is a promising tool for studying intracranial atherosclerotic disease (ICAD) in-vivo, but its use to understand the pathophysiology of ICAD has been limited by a lack of correlation between MRI signal characteristics and pathology in intracranial arteries. Description of Case A patient with symptomatic left cavernous carotid stenosis underwent 3T HRMRI and died 4 days later. In-vivo HRMRI and postmortem histopathology images were compared. MRI signal characteristics consistent with atherosclerotic plaque composed of lipid and loose matrix, fibrous tissue, and calcium were correlated with pathology findings. Intraplaque hemorrhage was not present on HRMRI or pathology. Conclusions This report demonstrates correlation between atherosclerotic plaque components visualized on 3T HRMRI images obtained in-vivo and pathological specimens of a symptomatic ICAD plaque, providing an important step in developing HRMRI as an in-vivo research tool to understand ICAD pathology.

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Section: Case Reportmentioning

confidence: 61%

Intracranial atherosclerosis: Correlation between in-vivo 3T high resolution MRI and pathology

et al. 2014

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“…Sustained IL-6 production appears to drive chronic, low-level vascular inflammation that leads to neointimal thickening [39] , vascular dysfunction [40] , hypertension [41] , and increased risk of myocardial infarction [42] . An early step in the development of the vascular dysfunction that ultimately leads to the formation of atherosclerotic plaques is the conversion of VECs from an anticoagulant/anti-inflammatory to a prothrombotic/proinflammatory phenotype.…”

Section: Physiological Roles For Epac Isoforms: Vascular Functionmentioning

confidence: 99%

The future of EPAC-targeted therapies: agonism versus antagonism

Parnell

Palmer

Yarwood

2015

Trends in Pharmacological Sciences

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“…Macrophages play an important role in vascular inflammation and one of the cytokines macrophages produce during vascular inflammation is IL-6 [ 33 ]. Furthermore, it has been shown that IL-6 recruits bone marrow cells to the vessel wall and thereby contributes to intimal hyperplasia [ 34 ]. Niida et al .…”

Section: Discussionmentioning

confidence: 99%

The epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia development

et al. 2017

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ObjectiveGenetic P300/CBP-associated factor (PCAF) variation affects restenosis-risk in patients. PCAF has lysine acetyltransferase activity and promotes nuclear factor kappa-beta (NFκB)-mediated inflammation, which drives post-interventional intimal hyperplasia development. We studied the contributing role of PCAF in post-interventional intimal hyperplasia.Methods and resultsPCAF contribution to inflammation and intimal hyperplasia was assessed in leukocytes, macrophages and vascular smooth muscle cells (vSMCs) in vitro and in a mouse model for intimal hyperplasia, in which a cuff is placed around the femoral artery. PCAF deficiency downregulate CCL2, IL-6 and TNF-alpha expression, as demonstrated on cultured vSMCs, leukocytes and macrophages. PCAF KO mice showed a 71.8% reduction of vSMC-rich intimal hyperplasia, a 73.4% reduction of intima/media ratio and a 63.7% reduction of luminal stenosis after femoral artery cuff placement compared to wild type (WT) mice. The association of PCAF and vascular inflammation was further investigated using the potent natural PCAF inhibitor garcinol. Garcinol treatment reduced CCL2 and TNF-alpha expression, as demonstrated on cultured vSMCs and leukocytes.To assess the effect of garcinol treatment on vascular inflammation we used hypercholesterolemic ApoE*3-Leiden mice. After cuff placement, garcinol treatment resulted in reduced arterial leukocyte and macrophage adherence and infiltration after three days compared to untreated animals.ConclusionsThese results identify a vital role for the lysine acetyltransferase PCAF in the regulation of local inflammation after arterial injury and likely the subsequent vSMC proliferation, responsible for intimal hyperplasia.

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IL-6 Mobilizes Bone Marrow-Derived Cells to the Vascular Wall, Resulting in Neointima Formation via Inflammatory Effects

Cited by 13 publications

References 25 publications

Intracranial atherosclerosis: Correlation between in-vivo 3T high resolution MRI and pathology

Intracranial atherosclerosis: Correlation between in-vivo 3T high resolution MRI and pathology

The future of EPAC-targeted therapies: agonism versus antagonism

The epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia development

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