Modulation of interleukin signalling and gene expression in cardiac myocytes by endothelin-1

Yndestad, Arne; Marshall, Andrew K.; Hodgkinson, J. D.; Tham, El Li; Sugden, Peter H.; Clerk, Angela

doi:10.1016/j.biocel.2009.10.021

Cited by 26 publications

(18 citation statements)

References 48 publications

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“…In neonatal rat cardiac myocytes and fibroblasts, sST2 expression is increased by IL-1β, phorbol ester, uridine triphosphate and endothelin-1, but not by TNF-α, angiotensin II, hydrogen peroxide, IL-4 or lipopolysaccharide (LPS) [6], [28], [29]. However, in human endothelial cells, sST2 was shown to be upregulated by the inflammatory cytokines IL-1β, TNF-α and by phorbol ester [27].…”

Section: Discussionmentioning

confidence: 98%

Soluble ST2 and Interleukin-33 Levels in Coronary Artery Disease: Relation to Disease Activity and Adverse Outcome

et al. 2014

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ObjectivesST2 is a receptor for interleukin (IL)-33. We investigated an association of soluble ST2 (sST2) and IL-33 serum levels with different clinical stages of coronary artery disease. We assessed the predictive value of sST2 and IL-33 in patients with stable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).MethodsWe included 373 patients of whom 178 had stable angina, 97 had NSTEMI, and 98 had STEMI. Patients were followed for a mean of 43 months. The control group consisted of 65 individuals without significant stenosis on coronary angiography. Serum levels of sST2 and IL-33 were measured by ELISAs.ResultssST2 levels were significantly increased in patients with STEMI as compared to patients with NSTEMI and stable angina as well as with controls. IL-33 levels did not differ between the four groups. During follow-up, 37 (10%) patients died and the combined endpoint (all cause death, MI and rehospitalisation for cardiac causes) occurred in 66 (17.6%) patients. sST2 serum levels significantly predicted mortality in the total cohort. When patients were stratified according to their clinical presentation, the highest quintile of sST2 significantly predicted mortality in patients with STEMI, but not with NSTEMI or stable coronary artery disease. sST2 was a significant predictor for the combined endpoint in STEMI patients and in patients with stable angina. Serum levels of IL-33 were not associated with clinical outcome in the total cohort, but the highest quintile of IL-33 predicted mortality in patients with STEMI.ConclusionsSerum levels of sST2 are increased in patients with acute coronary syndromes as compared to levels in patients with stable coronary artery disease and in individuals without coronary artery disease. sST2 and IL-33 were associated with mortality in patients with STEMI but not in patients with NSTEMI or stable angina.

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Section: Discussionmentioning

confidence: 98%

Soluble ST2 and Interleukin-33 Levels in Coronary Artery Disease: Relation to Disease Activity and Adverse Outcome

et al. 2014

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“…IL‐33 induces phosphorylation of MAPKs in human mast cells (Iikura et al, ), murine embryonic fibroblasts (Funakoshi‐Tago et al, ) and rat cardiac myocytes (Yndestad et al, ). We demonstrated that IL‐33 similarly induced phosphorylation of all three MAPKs (ERK, JNK and p38) in MC3T3‐E1 cells.…”

Section: Discussionmentioning

confidence: 99%

Involvement of ERK and p38 MAPK pathways on Interleukin‐33‐induced RANKL expression in osteoblastic cells

Mine

Makihira

Yamaguchi

et al. 2014

Cell Biology International

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The receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG) system is a well-known key factor in osteoclast differentiation, and osteoblastic lineage cells are the major sources of RANKL and OPG in local bone tissue. Recently, a new molecule from the interleukin (IL)-1 family, IL-33, was identified. Here, we report the possible involvement of IL-33 in RANKL and OPG expression, and the signaling pathways that are required for maximal IL-33-induced RANKL expression in MC3T3-E1 osteoblastic cells. Stimulation with IL-33 increased the mRNA expression and secretion of RANKL in MC3T3-E1 cells. The IL-33-induced RANKL mRNA expression was inhibited by an anti-IL-33 monoclonal antibody. Furthermore, ERK and p38 MAPK inhibitors, but not a JNK inhibitor, suppressed IL-33-induced RANKL mRNA expression. On the other hand, IL-33 had no effect on OPG mRNA expression and protein secretion. These results taken together suggest that IL-33 stimulates RANKL expression through mechanisms dependent on the ERK and p38 MAPK pathways in MC3T3-E1 cells.

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“…Today studies from animal models suggest that sST2 is more than just a marker in cardiovascular disease and implicate IL33/ST2 signaling as an important protective pathway in which the role of sST2 remains obscure [13]. In states of oxidative stress as in diabetes increased expression of endothelin 1 has been found paradoxically to restore diastolic dysfunction [27] and endothelin 1 is a known inducer of sST2 expression and inhibitor of IL-33 signaling through p38 MAPK [28]. From this point of view, increased levels of sST2 in patients with diabetes and LVDD might be an epiphenomenon of other counteregulatory mechanisms such as endothelin 1 or to signify patients with failure of IL-33-induced cardioprotection, through sST2 acting as a decoy receptor.…”

Section: Discussionmentioning

confidence: 99%

Toll/Interleukin-1 receptor member ST2 exhibits higher soluble levels in type 2 diabetes, especially when accompanied with left ventricular diastolic dysfunction

Fousteris

Μelidonis

Panoutsopoulos

et al. 2011

Cardiovasc Diabetol

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BackgroundSoluble ST2, a member of the of the Toll/IL-1 superfamily, is a novel biomarker with exceptional predictive value in heart failure and myocardial infarction- related mortality as well as in acute dyspneic states. Soluble ST2 is considered a decoy receptor of IL 33 that blocks the protective effects of the cytokine in atherosclerosis and cardiac remodeling. In the present study we investigated the differences in the levels of soluble ST2, BNP and hs-CRP between healthy controls and patients with type 2 diabetes with and without left ventricular diastolic dysfunction. A secondary aim was to investigate correlations between sST2 and other biomarkers of type 2 diabetes, such as HbA1c.Methods158 volunteers were recruited and underwent a complete Doppler-echocardiographic evaluation of both systolic & diastolic cardiac function. All subjects with ejection fraction < 50% were excluded. The study population was divided in 4 groups as follows: A: 42 healthy controls, B: 18 subjects without diabetes with LVDD, C: 48 patients with type 2 diabetes without LVDD & D: 50 patients with type 2 diabetes & LVDD. ELISA technique was performed to measure sST2 levels. Statistical analysis was performed with Kruskal-Wallis & Mann-Whitney test (continuous variables), chi squared & Fischer exact test (discrete variables), Spearman coefficient (univariate analysis) and step-wise backward method (multivariate analysis).ResultsPatients with type 2 diabetes with (p < 0.001) or without LVDD (p = 0.007) had higher serum ST2 levels compared to healthy controls, state found also for hs-CRP levels but not for the corresponding BNP levels (p = 0.213 & p = 0.207 respectively). Patients with type 2 diabetes & LVDD had higher serum ST2 in relation to diabetic patients without LVDD (p = 0.001). In multivariate analysis HbA1c positively and independently correlated with sST2 levels in both groups of patients with type 2 diabetes.ConclusionsPatients with type 2 diabetes exhibit higher sST2 levels compared to healthy controls. The presence of LVDD in patients with type 2 diabetes is associated with even higher sST2 levels. A significant correlation between glycemic control and sST2 levels was also revealed.

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Modulation of interleukin signalling and gene expression in cardiac myocytes by endothelin-1

Cited by 26 publications

References 48 publications

Soluble ST2 and Interleukin-33 Levels in Coronary Artery Disease: Relation to Disease Activity and Adverse Outcome

Soluble ST2 and Interleukin-33 Levels in Coronary Artery Disease: Relation to Disease Activity and Adverse Outcome

Involvement of ERK and p38 MAPK pathways on Interleukin‐33‐induced RANKL expression in osteoblastic cells

Toll/Interleukin-1 receptor member ST2 exhibits higher soluble levels in type 2 diabetes, especially when accompanied with left ventricular diastolic dysfunction

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