Immunohistochemical detection of S100A1 in the postmortem diagnosis of acute myocardial infarction

Bi, Haitao; Yang, Ying; J, Huang; Li, Yingmin; Ma, Chunling; Cong, Bin

doi:10.1186/1746-1596-8-84

Cited by 33 publications

(22 citation statements)

References 25 publications

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“…The contrast results showed that hypoxia could cause the release of S100A1 in damaged cardiomyocytes. This is consistent with the results of Wang et al ‘s, namely, the depleted areas of S100A1 further expanded and S100A1 plasma concentrations further increased with continuation of the hypoxia time [26]. Activated cardiomyocytes can secrete various pro‐inflammatory cytokines and mediators, which may contribute to hypoxic injury in the developing cardiomyocytes dysfunction.…”

Section: Discussionsupporting

confidence: 91%

Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

et al. 2015

Journal of Pharmacy and Pharmacology

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Section: Discussionsupporting

confidence: 91%

Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

et al. 2015

Journal of Pharmacy and Pharmacology

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“…274, 275 Once released, S100A1 activates the surrounding cardiac fibroblasts through TLR4 and triggers the MAPK and NF-κB proinflammatory pathways. 274 However, S100A1 not only promotes proinflammatory signals but also regulates a complex balance between pro- and anti-inflammatory pathways associated with the antifibrotic upregulation of matrix metalloproteinase 9 (MMP9) and the downregulation of type I collagen and connective tissue growth factor.…”

Section: S100mentioning

confidence: 99%

HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins

2016

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Our immune system is based on the close collaboration of the innate and adaptive immune systems for the rapid detection of any threats to the host. Recognition of pathogen-derived molecules is entrusted to specific germline-encoded signaling receptors. The same receptors have now also emerged as efficient detectors of misplaced or altered self-molecules that signal tissue damage and cell death following, for example, disruption of the blood supply and subsequent hypoxia. Many types of endogenous molecules have been shown to provoke such sterile inflammatory states when released from dying cells. However, a group of proteins referred to as alarmins have both intracellular and extracellular functions which have been the subject of intense research. Indeed, alarmins can either exert beneficial cell housekeeping functions, leading to tissue repair, or provoke deleterious uncontrolled inflammation. This group of proteins includes the high-mobility group box 1 protein (HMGB1), interleukin (IL)-1α, IL-33 and the Ca2+-binding S100 proteins. These dual-function proteins share conserved regulatory mechanisms, such as secretory routes, post-translational modifications and enzymatic processing, that govern their extracellular functions in time and space. Release of alarmins from mesenchymal cells is a highly relevant mechanism by which immune cells can be alerted of tissue damage, and alarmins play a key role in the development of acute or chronic inflammatory diseases and in cancer development.

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“…Reproduced with permission from [12]. damaged cardiomyocytes in ischemic myocardial tissue [11,28]. A most recent study indicated that extracellular S100A1 is specifically internalized by cardiac fibroblasts transforming them into an immune-modulatory and antifibrotic phenotype via an endosomal TLR4 signaling pathway that beneficially shapes the myocardial healing process [11].…”

Section: S100a1 Expression Regulation and Pathophysiologiesmentioning

confidence: 99%

“…Elevated S100A1 serum levels were reported in patients after open heart surgery and myocardial infarction [55,56] and rapid depletion of S100A1 was subsequently demonstrated in ischemic rat and human myocardium [28]. Among the proteins passively released from damaged cells, distinct molecules may play an active role in the restoration of tissue homeostasis [57].…”

Section: Extracellular S100a1 Targeting Cardiac Fibroblastsmentioning

confidence: 99%

Cardiomyocytes, Endothelial Cells and Cardiac Fibroblasts: S100A1’s Triple Action in Cardiovascular Pathophysiology

et al. 2015

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Over the past decade, basic and translational research delivered comprehensive evidence for the relevance of the Ca(2+)-binding protein S100A1 in cardiovascular diseases. Aberrant expression levels of S100A1 surfaced as molecular key defects, driving the pathogenesis of chronic heart failure, arterial and pulmonary hypertension, peripheral artery disease and disturbed myocardial infarction healing. Loss of intracellular S100A1 renders entire Ca(2+)-controlled networks dysfunctional, thereby leading to cardiomyocyte failure and endothelial dysfunction. Lack of S100A1 release in ischemic myocardium compromises cardiac fibroblast function, entailing impaired damage healing. This review focuses on molecular pathways and signaling cascades regulated by S100A1 in cardiomyocytes, endothelial cells and cardiac fibroblasts in order to provide an overview of our current mechanistic understanding of S100A1's action in cardiovascular pathophysiology.

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Immunohistochemical detection of S100A1 in the postmortem diagnosis of acute myocardial infarction

Cited by 33 publications

References 25 publications

Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins

Cardiomyocytes, Endothelial Cells and Cardiac Fibroblasts: S100A1’s Triple Action in Cardiovascular Pathophysiology

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