The effect of an anti-inflammatory pentapeptide produced by Entamoeba histolytica on gene expression in the U-937 monocytic cell line

Silva-García, Raúl; Estrada-Garcia, Iris Citlalli; Ramos‐Payán, Rosalío; Torres, Amada; Morales-Martínez, M. E.; Arenas‐Aranda, Diego; Giménez-Scherer, Juan Antonio; Blanco-Favéla, Francisco; Rico-Rosillo, María Guadalupe

doi:10.1007/s00011-007-6199-y

Cited by 17 publications

(13 citation statements)

References 33 publications

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“…The ability of MLIF to regulate and normalize genes (downregulating the upregulated genes and upregulating the downregulated genes, Table 2) involved in the inflammatory process in the CIA model suggests that it has an immunomodulatory effect. This is in agreement with the previously reported [20,21] role of MLIF and suggests a potential mechanism for amelioration of arthritis in the CIA model.…”

Section: Discussionsupporting

confidence: 82%

“…As in other studies [1][2][3][4]21], MLIF exhibited an immune-modulating effect in the inflammatory process, presumably acting on mobilization, adherence, and recruitment of immune cells, as well as extracellular matrix modeling in the development of arthritis. The modulatory capacity of MLIF on genes that were upregulated or downregulated by CIA-associated inflammation when it is administered in a preventive scheme encourages research into MLIF as a therapeutic agent in RA and other inflammatory diseases.…”

Section: Discussionmentioning

confidence: 74%

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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

et al. 2010

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 74%

Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

et al. 2010

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“…It is also reported that MLIF can inhibit the expression of interleukin-1␤, interferon-␥, interleukin-5, and interleukin-6 and increase the expression of interleukin-10 in macrophages. [11][12][13][14][15][16] The anti-inflammatory effect of MLIF led us to the initial interest to test whether it can act inflammatory response in brain ischemia. We 17 and other laboratories 18 have found MLIF can remarkably protect brain ischemic injury with decreased ischemic volume changes.…”

mentioning

confidence: 99%

A Pentapeptide Monocyte Locomotion Inhibitory Factor Protects Brain Ischemia Injury by Targeting the eEF1A1/Endothelial Nitric Oxide Synthase Pathway

Zhang

Fan

Liu

et al. 2012

Stroke

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Background and Purpose-Ischemic stroke is a major cause of death worldwide but lacks viable treatment or treatment targets. Monocyte locomotion inhibitory factor (MLIF) is a small heat-stable pentapeptide produced by Entamoeba histolytica in axenic culture, which is supposed to protect the brain from ischemic injury; the mechanism, however, remains unknown. In this study, we further investigated the mechanism underlying the protective role of MLIF in brain ischemia. Methods-A middle cerebral artery occlusion model in rats was used for detecting the effect of MLIF in the brain ischemia in vivo. To identify targets of MLIF in brain endothelial cells, we performed immunoprecipitation of biotin-conjugated MLIF and mass spectrometry. Results-MLIF can protect the brain from ischemic injury in vivo, yielding decreased ischemic volume, prolonged survival, and improved neurological outcome. In vitro studies showed that MLIF displayed protective effects through inhibition of expression of pathological inflammatory adhesion molecules and enhancing endothelial nitric oxide synthase expression and nitric oxide release in the cerebrovascular endothelium. The target screening experiments demonstrated binding of MLIF to the ribosomal protein translation elongation factor eEF1A1. MLIF enhanced endothelial nitric oxide synthase expression through stabilization of endothelial nitric oxide synthase mRNA, and eEF1A1 was shown to be necessary for this enhanced expression. Knockdown of eEF1A1 or inhibition of endothelial nitric oxide synthase attenuated MLIF-mediated inhibition of adhesion molecule expression. Conclusions-In this study, we identified a new potential pharmacologically targetable mechanism underlying MLIF's protective effects in brain ischemia through the eEF1A1/endothelial nitric oxide synthase pathway. (Stroke. 2012;43:2764-2773.)

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“…The MLIF favors the Th2 response; modulates the synthesis of pro-/anti-inflammatory cytokines and the expression of genes involved in inflammation, proliferation, angiogenesis, synthesis/degradation of extracellular matrix, angiogenesis, and axonal guidance, among others; and acts mainly through the signaling pathways: NF-kB, MAPKinases, and eEF1A1/endothelial nitric oxide synthase [81][82][83][84].…”

Section: Monocyte Locomotion Inhibitory Factor (Mlif) Peptidementioning

confidence: 99%

Current Developments in Antioxidant Therapies for Spinal Cord Injury

Villa¹,

Villamar²,

Zapien³

et al. 2019

Spinal Cord Injury Therapy [Working Title]

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When spinal cord injury (SCI) occurs, numerous sources of reactive oxygen species and nitrogen species may be active within first minutes or hours and even reactivate few days later. Free radical formation and lipid peroxidation (LP) have been described as an important mechanism in the beginning and accelerated progress in the development of diverse pathologies, importantly in those related to central nervous system. The compromise of molecules and cellular structures due to the oxidative state of microenvironment in SCI may determinate survival or apoptosis of resident and infiltrating cells and polarization toward an inflammatory response, which lead to an extension of damaged tissue and loss of neuronal function, or a regulatory/regenerative response. The investigation of new antioxidant agents and their action at a molecular level begins to reveal mechanisms that, if correctly modulated, promise an improvement in recovery of functions with respect to conventional pharmacological therapies. In this chapter, we will review the general mechanisms of oxidative stress and lipid peroxidation, those antioxidant treatments in experimental development and clinical phase, as well as their achievements and limitations.

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The effect of an anti-inflammatory pentapeptide produced by Entamoeba histolytica on gene expression in the U-937 monocytic cell line

Abstract: Many modified genes are products regulated by the Nuclear Factor-kappaB and Mitogen Activated Protein Kinase pathways, suggesting MLIF involvement with these two major pathways for the modulation of the inflammation and immune responses.

Cited by 17 publications

References 33 publications

Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

A Pentapeptide Monocyte Locomotion Inhibitory Factor Protects Brain Ischemia Injury by Targeting the eEF1A1/Endothelial Nitric Oxide Synthase Pathway

Current Developments in Antioxidant Therapies for Spinal Cord Injury

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