Danger Signals in the Initiation of the Inflammatory Response after Myocardial Infarction

Haan, Judith J. de; Smeets, Mirjam B.; Pasterkamp, Gérard; Arslan, Fatih

doi:10.1155/2013/206039

Cited by 102 publications

(80 citation statements)

References 159 publications

(143 reference statements)

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“…The impact of CLPs may thus be indirect via interaction or competition for ligands with their carbohydrate partners. In this regard, CLPs may be like other nonstructural proteins expressed in the ECM, such as Osteopontins and various galectins, which are upregulated upon injury and have been described as danger signals [74]. In addition, the propensity of Ym1 to form crystals [75] may be particularly relevant, as crystals are known inflammasome activators [76].…”

Section: Chitinase-like Proteins -A Bridge Between Il-17 and Type 2 Rmentioning

confidence: 99%

IL-17 and neutrophils: unexpected players in the type 2 immune response

Allen¹,

Sutherland²,

Rückerl³

2015

Current Opinion in Immunology

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The study of immunity to helminth infection has been central to understanding the function of type 2 cytokines and their targets. Although type 2 cytokines are considered anti-inflammatory and promote tissue repair, they also contribute to allergy and fibrosis. Here, we utilise data from helminth infection models, to illustrate that IL-17 and neutrophils, typically associated with pro-inflammatory responses, are intimately linked with type 2 immunity. Neutrophils work with IL-4Rα-activated macrophages to control incoming larvae but this comes at a cost of enhanced tissue damage. Chitinase like proteins (CLPs) bridge these diverse outcomes, inducing both protective IL-17 and reparative Th2 responses. Dysregulation of CLPs, IL-17 and neutrophils likely contribute to disease severity and pathology associated with type 2 immunity.

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Section: Chitinase-like Proteins -A Bridge Between Il-17 and Type 2 Rmentioning

confidence: 99%

IL-17 and neutrophils: unexpected players in the type 2 immune response

Allen¹,

Sutherland²,

Rückerl³

2015

Current Opinion in Immunology

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“…Inflammatory cells such as monocytes, macrophages, and dendritic cells secrete HMGB1 and, hence, further enhance the inflammatory reaction [19]. As a damage-associated molecular pattern (DAMP) molecule, HMGB1 signals through the receptor for advanced glycation end-products (RAGE), Toll-like receptor 2 (TLR2), and Toll-like receptor 4 (TLR4), subsequently stimulating inflammatory cells to release pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and IL-6 [20, 21]. Additionally, HMGB1 initiates inflammatory cascades which contribute to cardiac dysfunction and remodeling [9].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-converting enzyme 2 inhibits high-mobility group box 1 and attenuates cardiac dysfunction post-myocardial ischemia

Zhang

Wang

et al. 2015

J Mol Med

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High-mobility group box 1 (HMGB1) triggers and amplifies inflammation cascade following ischemic injury, and its elevated levels are associated with adverse clinical outcomes in patients with myocardial infarction (MI). Angiotensin-converting enzyme 2 (ACE2), a key member of vasoprotective axis of the renin-angiotensin system (RAS), regulates cardiovascular functions and exerts beneficial effects in cardiovascular disease. However, the association between HMGB1 and ACE2 has not been studied. We hypothesized that overexpression of ACE2 provides cardioprotective effects against MI via inhibiting HMGB1 and inflammation. ACE2 knock-in (KI) mice and littermate wild-type (WT) controls were subjected to either sham or coronary artery ligation surgery to induce MI. Heart function was assessed 4 weeks after surgery using echocardiography and Millar catheterization. Tissues were collected for histology and analysis of the expression of HMGB1, RAS components, and inflammatory cytokines. ACE2 in the heart of the ACE2 KI mice was 58-fold higher than WT controls. ACE2-MI mice exhibited a remarkable preservation of cardiac function and reduction of infarct size in comparison to WT-MI mice. Notably, ACE2 overexpression significantly reduced the MI-induced increase in apoptosis, macrophage infiltration, and HMGB1 and pro-inflammatory cytokine expression (TNF-α and IL-6). Moreover, in an in vitro study, ACE2 activation prevented the hypoxia-induced cell death and upregulation of HMGB1 in adult cardiomyocytes. This protective effect is correlated with downregulation of HMGB1 and downstream pro-inflammatory cascades, which could be useful for the development of novel treatment for ischemic heart disease.

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“…15 More recent reports have also described its role in immune cell migration, inflammation and ischemic injury. 9,[16][17][18][19][20] However, the expression and role of CCN1 in the intestinal tract has been poorly investigated. 21 Our current studies investigated the regulation of CCN1 in intestinal tissue subjected to I/R in pigs.…”

Section: Introductionmentioning

confidence: 99%

Regulation of CCN1 (Cyr61) in a porcine model of intestinal ischemia/reperfusion

et al. 2015

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Intestinal ischemia is a serious condition that may lead to both local and systemic inflammatory responses. Restoration of blood supply (reperfusion) to ischemic tissues often increases the extent of the tissue injury. Cysteine-rich angiogenic inducer 61 (Cyr61)/CCN1 is an extracellular matrix-associated signaling protein that has diverse functions. CCN1 is highly expressed at sites of inﬂammation and wound repair, and may modify cell responses. This study aimed to investigate regulation and cellular distribution of CCN1 in intestinal ischemia/reperfusion (I/R) injury in pigs. After intestinal I/R, increased expression of CCN1 was detected by quantitative RT-PCR, Western blot analysis and immunohistochemistry compared with non-ischemic intestine. Immunoflorescence staining revealed that CCN1 was mainly up-regulated in intestinal mucosa after intestinal I/R. Microvillus epithelial cells and vascular endothelial cells were strongly positive for CCN1 in intestinal I/R, while natural killer cells and/or subsets of neutrophils were only modestly positive for CCN1. Furthermore, blood samples taken from the portal and caval veins during ischemia and after reperfusion showed no change of the CCN1 levels, indicating that CCN1 was locally regulated. In conclusion, these observations show, for the first time, that the CCN1 molecule is up-regulated in response to intestinal I/R in a local manner.

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Danger Signals in the Initiation of the Inflammatory Response after Myocardial Infarction

Cited by 102 publications

References 159 publications

IL-17 and neutrophils: unexpected players in the type 2 immune response

IL-17 and neutrophils: unexpected players in the type 2 immune response

Angiotensin-converting enzyme 2 inhibits high-mobility group box 1 and attenuates cardiac dysfunction post-myocardial ischemia

Regulation of CCN1 (Cyr61) in a porcine model of intestinal ischemia/reperfusion

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