Endothelial-monocyte-activating polypeptide II

Tas, Maarten; Murray, James F.

doi:10.1016/1357-2725(96)00038-6

Cited by 57 publications

(25 citation statements)

References 9 publications

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“…Although the mechanisms underlying the neutrophil migration into the meconiumcontaminated lungs remain unclear, direct chemotactic effect or activation of alveolar macrophages by the intrapulmonary meconium have been proposed (27,28). Correspondingly, we bring here evidence showing that meconium instillation is associated with stimulated pulmonary production of a novel chemotactic cytokine EMAP II, which is found to augment leukocyte migration and increase peroxidase activity in neutrophils (29). Administration of the ANG II receptor antagonist saralasin prevented the up-regulation of EMAP II and the rise 331 in lung tissue MPO activity after the meconium insult, indicating that ANG II receptor action may, probably through stimulated EMAP II production, affect processes that lead to the activation of infiltrating neutrophils in this model (13).…”

Section: Discussionmentioning

confidence: 57%

“…Because administration of ANG II receptor antagonist saralasin prevented epithelial apoptosis and simultaneously down-regulated EMAP II expression in our model, it is possible that apoptosis-induced release of the mature EMAP II contributes to the inflammatory response in the meconium-contaminated lungs. Nevertheless, the role of EMAP II in the development of apoptosis-induced inflammation after the meconium insult still remains uncertain, especially because this polypeptide itself has been proposed to induce apoptosis (29). Similarly, although an antiapoptotic effect of saralasin through direct inhibition of neutrophil function cannot be excluded in the present study, there is evidence to suggest that saralasin does not directly influence the neutrophil activation (13,14).…”

Section: Discussionmentioning

confidence: 63%

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Angiotensin II Receptor Blockade Inhibits Pneumocyte Apoptosis in Experimental Meconium Aspiration

et al. 2004

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Lung tissue inflammation and apoptosis are implicated in the pathogenesis of meconium aspiration-induced lung injury in the newborn, but the mechanisms of these reactions are still poorly known. We investigated the time-dependent leukocyte influx and appearance of apoptosis, as well as the contribution of angiotensin (ANG) II receptor action on these processes in the meconium-induced lung injury. Experimental meconium aspiration was induced by intratracheal instillation of human meconium in 18 rats, and eight rats were further pretreated with an unspecific ANG II receptor inhibitor saralasin. Rats were ventilated with 60% oxygen for 1, 3, or 5 h, and the lungs were then studied histologically for tissue injury and with DNA nick-end labeling and electron microscopy for apoptotic cell death. Lung tissue myeloperoxidase activity and expression of angiotensinogen mRNA and endothelial monocyte-activating polypeptide (EMAP) II protein were also analyzed. The meconium-instilled lungs showed increasing neutrophil migration and histologic injury after the first hour, whereas the number of epithelial apoptotic cells was elevated from the control level throughout the study. Myeloperoxidase activity was high, and the angiotensinogen mRNA and EMAP II protein was up-regulated at 5 h after the meconium insult. Pretreatment with saralasin significantly prevented the increase in lung tissue myeloperoxidase activity, EMAP II, and lung epithelial apoptosis. The results suggest that pulmonary meconium insult rapidly results in epithelial apoptosis, before significant neutrophil sequestration into the lungs. Perinatal aspiration of meconium frequently results in severe pulmonary failure with ventilation-perfusion mismatching in the lungs, hypoxemia, and increase in pulmonary vascular resistance, associated with high morbidity and mortality in fullor postterm newborn infants. The pathophysiology of the neonatal meconium aspiration syndrome (MAS) is complex, but inflammation with accumulation of polymorphonuclear leukocytes in the pulmonary tissue is believed to be a central event in the development of acute tissue damage (1, 2). This inflammatory reaction is associated with increased pulmonary vascular permeability leading to proteinaceous exudation into the alveolar spaces and inactivation of the pulmonary surfactant and may together with direct toxic effects of meconium significantly contribute to the lung injury process (1, 2). Still, the clinical effects of anti-inflammatory therapeutic approaches and surfactant replacement treatment have often been unsatisfactory and have not consistently improved the outcome of severe complications of this disease (1-3). New advances in the pathophysiology of MAS therefore are needed.Apoptosis, programmed cell death, is usually regarded as a physiologic mechanism in organ remodeling (4) but has been

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 63%

Angiotensin II Receptor Blockade Inhibits Pneumocyte Apoptosis in Experimental Meconium Aspiration

et al. 2004

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“…The C-terminal fragment of AIMP1 has been well studied in the context of proinflammatory cytokines involved in angiogenesis; however, full-length AIMP1 demonstrates higher potency in inflammation as well as angiogenesis [87]. The C-terminal peptide of AIMP1 has been detected in the culture medium of stimulated murine fibrosarcoma cells and prostate adenocarcinoma cells [86,88].…”

Section: Cleavagementioning

confidence: 99%

Association of Aminoacyl-tRNA Synthetases with Cancer

Kim

Kwon

Kim

2013

Topics in Current Chemistry

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Although aminoacyl-tRNA synthetases (ARSs) and ARS-interacting multi-functional proteins (AIMPs) have long been recognized as housekeeping proteins, evidence indicating that they play a key role in regulating cancer is now accumulating. In this chapter we will review the conventional and non-conventional functions of ARSs and AIMPs with respect to carcinogenesis. First, we will address how ARSs and AIMPs are altered in terms of expression, mutation, splicing, and post-translational modifications. Second, the molecular mechanisms for ARSs' and AIMPs' involvement in the initiation, maintenance, and progress of carcinogenesis will be covered. Finally, we will introduce the development of therapeutic approaches that target ARSs and AIMPs with the goal of treating cancer.

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“…Although p43 is universally expressed (10), its expression level is varied temporally and spatially in developing mouse (11). For instance, there is a significant surge in the expression of p43 within the lungs on postnatal days 8 -16 of mouse.…”

mentioning

confidence: 99%

A Cofactor of tRNA Synthetase, p43, Is Secreted to Up-regulate Proinflammatory Genes

Park²,

Kim

et al. 2001

Journal of Biological Chemistry

131

125

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An auxiliary factor of mammalian multi-aminoacyltRNA synthetases, p43, is thought to be a precursor of endothelial monocyte-activating polypeptide II (EMAP II) that triggers proinflammation in leukocytes and macrophages. In the present work, however, we have shown that p43 itself is specifically secreted from intact mammalian cells, while EMAP II is released only when the cells are disrupted. Secretion of p43 was also observed when its expression was increased. These results suggest that p43 itself should be a real cytokine secreted by an active mechanism. To determine the cytokine activity and active domain of p43, we investigated tumor necrosis factor (TNF) and interleukin-8 (IL-8) production from human monocytic THP-1 cells treated with various p43 deletion mutants. The full length of p43 showed higher cytokine activity than EMAP II, further supporting p43 as the active cytokine. p43 was also shown to activate MAPKs and NFB, and to induce cytokines and chemokines such as TNF, IL-8, MCP-1, MIP-1␣, MIP-1␤, MIP-2␣, IL-1␤, and RANTES. Interestingly, the high level of p43 was observed in the foam cells of atherosclerotic lesions. Therefore, p43 could be a novel mediator of atherosclerosis development as well as other inflammation-related diseases.

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Endothelial-monocyte-activating polypeptide II

Cited by 57 publications

References 9 publications

Angiotensin II Receptor Blockade Inhibits Pneumocyte Apoptosis in Experimental Meconium Aspiration

Angiotensin II Receptor Blockade Inhibits Pneumocyte Apoptosis in Experimental Meconium Aspiration

Association of Aminoacyl-tRNA Synthetases with Cancer

A Cofactor of tRNA Synthetase, p43, Is Secreted to Up-regulate Proinflammatory Genes

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