Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice

Es, Thomas van; Puijvelde, Gijs H.M. van; Ramos, Ornélia H; Segers, Filip M.; Joosten, Leo A. B.; Berg, Wim B. van den; Michon, I.M.; Vos, Paul de; Berkel, Th.J.C. van; Kuiper, Johan

doi:10.1016/j.bbrc.2009.07.152

Cited by 143 publications

(110 citation statements)

References 35 publications

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“…The exact role of IL-17 in premature vascular damage in RA is believed to be unraveled; a recent research indicated that cytokines play a major role in atherosclerosis development in murine models of vascular diseases [32,33]. This study also reported elevated circulating level of IL-17 in cases with acute coronary syndrome [34].…”

Section: Pandya Et Alsupporting

confidence: 55%

“…Increased stiffness of arteries occurring in RA can be well correlated with CRP and IL-6 levels [26]. In patients with new onset of congestive heart failure, high sedimentation rate was found in 6 months preceding the detection of cardiac dysfunction which indicated that an enhanced inflammatory pathogenesis may lead to cardiac dysfunction due to inflammatory arthritis [31][32][33][34]. The extent and chronicity of inflammatory processes were measured with the circulating levels of inflammatory biomarkers and was linked to carotid atherosclerosis development in RA [27].…”

Section: Pandya Et Almentioning

confidence: 99%

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Co-Morbidity of Cardiovascular Diseases and Rheumatoid Arthritis

Pandya

et al. 2017

Asian J Pharm Clin Res

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Rheumatoid arthritis (RA) is a chronic disease related to swelling of joints which lead to restriction in movement due to pain and deformity mainly in feet, ankle, wrist, and fingers. It is an autoimmune disease, and the manifestations caused due to its occurrence are not clearly understood. In today's time, it has been observed that comorbid conditions account for most of the deaths as they influence the outcome of RA and limit therapeutic options. The most common comorbid conditions which are diagnosed in RA patients are generally cardiovascular (CV) abnormalities, several infections, certain mental disorders, and malignancies. Among which CV comorbid diseases are the most common kind relating to disorders of heart and blood vessel that eventually leads to severe conditions such as angina, myocardial infarction, stroke, rheumatic heart disease, and many more. RA affects the quality of life of patients directly or indirectly, but it mainly shows a significant increase in the prevalence of CV diseases. Hence, it is essential to diagnose and understand about the related manifestations when one is suffering from RA. These studies will aid to make better treatment and management strategies. Hence, an attempt has been made in this review article regarding the epidemiology, impact of both diseases and related risk factors. It also gives information in brief about the pathological causes of the comorbidity and summarizes measures that may be used in the prevention and treatment of these conditions.

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Section: Pandya Et Alsupporting

confidence: 55%

Section: Pandya Et Almentioning

confidence: 99%

Co-Morbidity of Cardiovascular Diseases and Rheumatoid Arthritis

Pandya

et al. 2017

Asian J Pharm Clin Res

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“…Moreover, its role in vascular dysfunction such as atherosclerosis is controversial 45, 46, 47. According to Madhur et al ., IL‐17A is necessary to induce superoxide vascular production in response to a high fat diet in ApoE −/− mice 48.…”

Section: Discussionmentioning

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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“…The role of Th17 in atherosclerosis is also debated as conflicting reports exist (30)(31)(32). In contrast to CD4 + T helper cells, CD8 + cytolytic T lymphocytes have not been extensively studied, even though CD8 + T cells are abundant in atherosclerotic plaques and they have been shown to be activated in hypercholesterolemic Apoe -/-mice (33).…”

Section: T Cells Modulate Inflammation In Atherosclerosismentioning

confidence: 99%