Identification of Serum Soluble ST2 Receptor as a Novel Heart Failure Biomarker

Weinberg, Ellen O.; Shimpo, Masahisa; Hurwitz, Shelley; Tominaga, Shin‐ichi; Rouleau, Jean‐Lucien; Lee, Richard T.

doi:10.1161/01.cir.0000047274.66749.fe

Cited by 464 publications

(372 citation statements)

References 30 publications

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“…Increased serum levels of sST2 have been detected in a number of human diseases, including asthma and allergic airway inflammation, acute myocardial infarctions, and sepsis [10][11][12][13][14]. Although the biological significance for the increase in sST2 is not understood, several studies have demonstrated beneficial effects of sST2 treatment in animal models of diseases [2,4,6,15], suggesting that it may reduce inflammation.…”

Section: Discussionmentioning

confidence: 99%

IL‐33 is a chemoattractant for human Th2 cells

et al. 2007

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IL‐33 is a novel cytokine of the IL‐1 family and mediates its biological effect via the receptor ST2, which is selectively expressed on Th2 cells but not Th1 cells. IL‐33 drives production of Th2‐associated cytokines including IL‐5 and IL‐13 and thereby promotes defense and pathology in mucosal organs. Cell locomotion is crucial to the induction of an effective immune response. We report here the chemoattraction of Th2 cells by IL‐33. Recombinant IL‐33 increased the proportion of human Th2 cells, but not Th1 cells, in polarized morphology in vitro and stimulated their subsequent invasion into collagen gels in an IL‐33 concentration‐dependent manner. Injection of recombinant IL‐33 into the footpad of ST2–/– mice which had been adoptively transferred with polarized Th2 cells, led to local accumulation of the transferred Th2 cells. These data therefore demonstrate that IL‐33 is a selective Th2 chemoattractant associated with the pro‐inflammatory property of this novel cytokine.

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Section: Discussionmentioning

confidence: 99%

IL‐33 is a chemoattractant for human Th2 cells

et al. 2007

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“…The secreted ST2 can be detected in serum from both mice and humans with mechanically overloaded hearts. Clinical and laboratory studies have confirmed that the soluble receptor is increased in the blood of patients with heart failure, and an increase in blood level over time reflects a worsening patient prognosis (91). The pathophysiology of ST2 in heart failure is undefined in part because the ligand for the receptor remains unidentified, but this genomic discovery approach shows how mechanically overloaded cultured cells can identify a new pathway and biomarker relevant to mechanically overloaded myocardium.…”

Section: Molecular Responses Of Cells and Tissues To Mechanical Stimulimentioning

confidence: 97%

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Huang

Kamm²,

Lee³

2004

American Journal of Physiology-Cell Physiology

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487

367

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not only a complex biochemical environment but also a diverse biomechanical environment. How cells respond to variations in mechanical forces is critical in homeostasis and many diseases. The mechanisms by which mechanical forces lead to eventual biochemical and molecular responses remain undefined, and unraveling this mystery will undoubtedly provide new insight into strengthening bone, growing cartilage, improving cardiac contractility, and constructing tissues for artificial organs. In this article we review the physical bases underlying the mechanotransduction process, techniques used to apply controlled mechanical stresses on living cells and tissues to probe mechanotransduction, and some of the important lessons that we are learning from mechanical stimulation of cells with precisely controlled forces.cytoskeleton; micromanipulation; cell signaling ALL LIVING ORGANISMS face mechanical forces, from the fluid forces around a bacterium to the high forces in a human knee during stair climbing. The process of converting physical forces into biochemical signals and integrating these signals into the cellular responses is referred to as mechanotransduction. Although this review cannot cover all that has been discovered about mechanotransduction, we discuss the molecule-and cell-level structures that may participate in mechanotransduction, provide an overview of prominent techniques currently used for exerting mechanical stresses on cells, and conclude with an overview of the tissue-level response to mechanical signaling. FORCE TRANSDUCTION PATHWAYS AND SIGNALINGForce transmission pathways at the cellular and subcellular scales. Understanding the molecular basis for mechanotransduction requires knowledge of the magnitude and distribution of forces throughout the cell at the molecular scale. At present, we have sufficient information to measure molecular scale forces in only a very few cases. We can, however, analyze the mechanisms by which force is transmitted throughout the cell and use that as a basis for speculation about the molecular mechanisms of mechanotransduction. A variety of different methods have been used to mechanically stimulate a cell, and the cellular response is multifaceted and diverse. Similarly, there are likely to be a variety of sensing mechanisms and locations within the cell where forces can be transduced from a mechanical to a biochemical signal. Despite this apparent complexity, it is probable that cells stimulated in different ways are activated by similar mechanisms at the molecular level. To identify these commonalities, it is useful to consider how externally applied forces are transmitted into and throughout the cell, as well as the magnitudes and distribution of force corresponding to these different methods of stimulation.Both continuum and microstructural approaches have been used to determine force distributions. In the case of a continuum model, the details of the microstructure are ignored, and the forces transmitted via the individual microstructural elements are described in...

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“…Elevated levels of sST2 have been found in patients with inflammatory disorders associated with abnormal Th2 mediated responses, including autoimmune diseases [31], asthma [32,33], idiopathic pulmonary fibrosis [29], and sepsis [34]; sST2 levels are also found elevated in patients with other inflammatory conditions, like LPS induced inflammation [35] and myocardial infarction [36]. Additionally, sST2 has been proposed as a biomarker for heart failure [37].…”

Section: Introductionmentioning

confidence: 99%

Elevated levels of soluble ST2 protein in dengue virus infected patients

et al. 2008

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Levels of the soluble form of the interleukin-1 receptor like 1 protein (IL-1RL-1 / ST2) are elevated in the serum of patients with diseases characterized by an inflammatory response. The objective of this study was to determine the concentration of soluble ST2 (sST2) in dengue infected patients during the course of the disease. Twenty four patients with confirmed dengue infection, classified as dengue fever, and eleven patients with other febrile illness (OFI) were evaluated. Levels of sST2 in serum and laboratory variables usually altered during dengue infections were measured. Dengue infected patients had higher serum sST2 levels than OFI at the end of the febrile stage and at defervescence (p=0.0088 and p=0.0004 respectively). Patients with secondary dengue infections had higher serum sST2 levels compared with patients with primary dengue infections (p=0.047 at last day of fever and p=0.030 at defervescence). Furthermore, in dengue infected patients, we found a significant negative correlation of sST2 with platelet and WBC counts, and positive correlation with thrombin time and transaminases activity. We suggest that sST2 could be a potential marker of dengue infection, could be associated with severity or could play a role in the immune response in secondary dengue virus infection.

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Identification of Serum Soluble ST2 Receptor as a Novel Heart Failure Biomarker

Cited by 464 publications

References 30 publications

IL‐33 is a chemoattractant for human Th2 cells

IL‐33 is a chemoattractant for human Th2 cells

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Elevated levels of soluble ST2 protein in dengue virus infected patients

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