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regulating role in neutrophil migration ( Ren et al . 2015 ), and this finding motivated us to further explore the potential effect of exogenous melatonin on neutrophil function. Thus, this study aimed to investigate, in vivo , the effect of exogenous
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regulates macrophage locomotion in response to metabolic stresses remains unclear. Cell migration is a complicated process regulated by the activation of various signaling molecules. Results from several studies have indicated that nuclear factor kappa B
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, Ouedraogo et al . 2006 ). In in vitro studies, adiponectin has been reported to inhibit platelet-derived growth factor (PDGF)- or heparin-binding epidermal growth factor-like growth factor-induced vascular smooth muscle cell (VSMC) migration ( Arita et
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suppresses neuronal migration ( Fukumoto et al. 2009 ), which is a key step in establishing correct cortical lamination. Cortical neurons originating from the ventricular zone (VZ) and subventricular zone (SVZ) follow an inside–out pattern to reach their
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hypertensive hormone, AngII has various biological effects on cell proliferation, migration, and invasion. Locally or systematically generated AngII influences vascular function in both physiological and pathological states via several mechanisms, such as
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) ( Ruderman & Prentki 2004 ). Based on the requirement for AMPK to alleviate hepatic steatosis, there is growing demand to identify mediators of AMPK activation in response to dynamic physiological activity. Although macrophage migration inhibitory factor (MIF
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Surgical Research Unit, Department of Surgery, Laboratory of Metabolism, Infectious Diseases Service, Clinical Diabetes Unit, Radiology, Cell Physiology and Metabolism, Internal Medicine, Department of Surgery
Surgical Research Unit, Department of Surgery, Laboratory of Metabolism, Infectious Diseases Service, Clinical Diabetes Unit, Radiology, Cell Physiology and Metabolism, Internal Medicine, Department of Surgery
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Introduction Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in both innate and adaptive immunity. Originally described as a T-cell-derived product, MIF has now been shown to be released by numerous cell types and
Departamento de Fisiología, Departamento de Ginecología, Clinical Sciences Research Laboratories, Departments of Medicine and Pharmacology, Centro de Estudios Moleculares de la Célula (CEMC), Biomedical Research Consortium (BMRC) Chile, Facultad de Ciencias Biológicas and
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Departamento de Fisiología, Departamento de Ginecología, Clinical Sciences Research Laboratories, Departments of Medicine and Pharmacology, Centro de Estudios Moleculares de la Célula (CEMC), Biomedical Research Consortium (BMRC) Chile, Facultad de Ciencias Biológicas and
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Departamento de Fisiología, Departamento de Ginecología, Clinical Sciences Research Laboratories, Departments of Medicine and Pharmacology, Centro de Estudios Moleculares de la Célula (CEMC), Biomedical Research Consortium (BMRC) Chile, Facultad de Ciencias Biológicas and
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has been speculated that progestins hijack these signaling pathways in breast cancer cells. Progesterone and progestins have been previously reported to stimulate breast cancer cell migration and invasion ( Carvajal et al . 2005 , Kato et al . 2005
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The diverse actions of macrophage migration inhibitory factor (MIF) within the immuno-neuroendocrine system are yet to be fully understood, but it is clear that MIF plays a pivotal role in the regulation of both the innate and adaptive immune response. An emerging body of data presently indicates that MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control the 'set point' and magnitude of the immune and inflammatory response. In this article we will review the actions of MIF within the immune system and discuss the overlapping and contrasting aspects of MIF and glucocorticoid biology. In particular we will focus on the role of MIF within the immuno-neuroendocrine interface and suggest molecular mechanisms by which MIF may counter-regulate glucocorticoid function. Finally we will discuss emerging evidence that functional MIF gene-promoter polymorphisms render one susceptible to elevated MIF expression, and the development of an exaggerated immune/inflammatory response that potentiates the progression to chronic inflammatory disease.
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The immunological and neuroendocrine properties of macrophage migration inhibitory factor (MIF) are diverse. In this article we review the known cellular, molecular and genetic properties of MIF that place it as a key regulatory cytokine, acting within both the innate and adaptive immune responses.The unexpected and paradoxical induction of MIF secretion by low concentrations of glucocorticoids is explored. The role of MIF as a locally acting modulator of glucocorticoid sensitivity within foci of inflammation is also discussed. MIF has no homology with any other pro-inflammatory cytokine and until recently lacked a recognised transmembrane receptor. MIF has also been shown to be directly taken up into target cells and to interact with intracellular signalling molecules, including the Jun activation domain-binding protein Jab-1.Comprehensive analysis of the MIF gene has identified important functional polymorphisms and a series of genetic studies has revealed both association and linkage of MIF with inflammatory diseases. Altered MIF regulation may therefore be pivotal to acquiring chronic inflammation following an innate immune response.