Cytokines and atherosclerosis: a comprehensive review of studies in mice

Kleemann, Robert; Zadelaar, Susanne; Kooistra, Teake

doi:10.1093/cvr/cvn120

Cited by 541 publications

(477 citation statements)

References 93 publications

(130 reference statements)

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“…The surgical procedure caused a marked acute systemic inflammatory response as demonstrated by a rapid increase in SAA, a relatively stable inflammation marker that integrates the signals of proatherogenic cytokines (IL1, TNFα, IL6), many of which may have contributed to the effect on the atherosclerotic leasion 16,17 . Several studies suggest that SAA itself participates in the pathogenesis of atherosclerosis and a recent study shows that it may contribute to plaque vulnerability 18 .…”

Section: Discussionmentioning

confidence: 99%

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

et al. 2016

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“…In addition, VCAM‐1 level is increased in fibroblast‐like synoviocytes and endothelial cells (ECs) from RA synovium 10, 11. Vascular cell adhesion molecule‐1 is mainly involved in leucocyte transendothelial migration and leucocyte retention in the inflamed joint.…”

Section: Introductionmentioning

confidence: 99%

Aortic VCAM‐1: an early marker of vascular inflammation in collagen‐induced arthritis

Denys

Clavel

Lemeiter

et al. 2016

J Cellular Molecular Medi

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Cardiovascular disease (CVD) is a major cause of morbidity and mortality in rheumatoid arthritis (RA). There are limited experimental data on vascular involvement in arthritis models. To study the link between CVD and inflammation in RA, we developed a model of vascular dysfunction and articular inflammation by collagen‐induced arthritis (CIA) in C57Bl/6 (B6) mice. We studied the expression of vascular inflammatory markers in CIA with and without concomitant hyperlipidic diet (HD). Collagen‐induced arthritis was induced with intradermal injection of chicken type‐II collagen followed by a boost 21 days later. Mice with and without CIA were fed a standard diet or an HD for 12 weeks starting from the day of the boost. Arthritis severity was evaluated with a validated clinical score. Aortic mRNA levels of vascular cell adhesion molecule‐1 (VCAM‐1), inducible nitric oxide synthase (iNOS) and interleukin‐17 were analysed by quantitative RT‐PCR. Vascular cell adhesion molecule‐1 localization in the aortic sinus was determined by immunohistochemistry. Atherosclerotic plaque presence was assessed in aortas. Collagen‐induced arthritis was associated with increased expression of VCAM‐1, independent of diet. VCAM‐1 overexpression was detectable as early as 4 weeks after collagen immunization and persisted after 15 weeks. The HD induced atheroma plaque formation and aortic iNOS expression regardless of CIA. Concomitant CIA and HD had no additive effect on atheroma or VCAM‐1 or iNOS expression. CIA and an HD diet induced a distinct and independent expression of large‐vessel inflammation markers in B6 mice. This model may be relevant for the study of CVD in RA.

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“…HIF-1 induces transcription of more than 60 genes, involved in angiogenesis, erythropoiesis, cell proliferation, iron metabolism, and inflammation. Indeed, antiinflammatory mechanisms have been described in apoE -/-mice involving decreased interferon-gamma (INF-γ) expression [9,10] and resultant increase in the anti-inflammatory cytokine, interleukin-10 (IL-10).…”

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confidence: 99%

“…Mice in the IHH group were exposed to a hypobaric chamber that replicated the hypobaric hypoxia conditions found at 4000 m altitude for Fig. 1 Others have categorized cytokines into pro-atherogenic, antiatherogenic, and variable, that is, Bnot so sure^ [10]. Kang et al [11] suggest that chronic hypoxemia via INF-γ influences the antiinflammatory IL-10 to protect against atherosclerosis in apoE -/-mice 8 h a day.…”

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confidence: 99%

Hypoxemia as a model for high altitude and cardiovascular risk reduction

Luft

2016

J Mol Med

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Is high-altitude living healthy? Perhaps in wealthy Aspen, Colorado. Data from China suggest that the least healthy place to live there is in Tibet [1]. Of course epidemiological surveys have to be taken with (do I dare say it?) a grain of salt. High altitude could benefit cardiovascular function. Residents of the Himalayan valleys are uniquely adapted to their hypoxic environment in terms of pulmonary vasculature. Bruno et al.[2] inspected their systemic cardiovascular function. They studied 95 high-altitude dwellers and 64 controls. Bruno et al. [2] conducted cardiac ultrasound, flow-mediated dilation (FMD) of the brachial artery, carotid geometry and stiffness, and aortic pulse wave velocity (PWV) in their subjects. Eleven high-altitude dwellers that had reduced FMD were studied after 1 h 100 % O 2 administration. High-altitude dwellers presented lower FMD and hyperemic velocity than controls, while systolic pulmonary artery pressure was higher, despite their adaptation. In multiple regression analysis performed in high-altitude dwellers, hyperemic velocity remained an independent predictor of FMD, after adjustment for baseline brachial artery diameter, room temperature and pulse pressure, explaining almost 10 % of its variance. On the contrary, in controls, brachial artery diameter remained the only independent predictor of FMD, after adjustment for confounders. The 100 % O 2 administration did not modify vascular variables.The risk factors for ischemic heart disease in Tibetan highlanders have been investigated. Fujimoto et al. [3] found that although Tibetans had remarkably high hematocrit values and a decrease of eicosapentaenoic acid in both serum total lipids and serum phospholipid possibly due to their diet, they were considered to have a low incidence of ischemic heart disease. These positive risk factors are likely counteracted by other negative risk factors that were identified. Tibetan highlanders showed a decreased level of palmitic acid and an increased level of linoleic acid in serum phospholipids, which could protect against atherosclerosis. In a study of cardiovascular risk in indigenous Argentinean children living at high altitude, there was a substantially higher prevalence of high triglycerides and low high-density lipoprotein cholesterol, compared to similar children from Buenos Aires [4]. These results are not encouraging. For hypertension, the main cardiovascular risk factor, the epidemiological data at altitude also do not inspire confidence. For instance, Mingji et al. [5] studied the relationship between altitude and the prevalence of hypertension in Tibet. In their investigation, a scatter plot of altitude against overall prevalence revealed a direct correlation. Metaregression analysis revealed a 2 % increase in the prevalence of hypertension with every 100 m increase in altitude. The locations and socioeconomic status of subjects affected the awareness and subsequent treatment and control of hypertension. Thus, an immediate argument that living at high altitude leads to cardiovascu...

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Cytokines and atherosclerosis: a comprehensive review of studies in mice

Cited by 541 publications

References 93 publications

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

Aortic VCAM‐1: an early marker of vascular inflammation in collagen‐induced arthritis

Hypoxemia as a model for high altitude and cardiovascular risk reduction

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