scholarly journals Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation: A Promoter or a Suppressor?

2018 ◽  
Vol 20 (1) ◽  
pp. 124 ◽  
Author(s):  
Apoorva Iyer ◽  
Svetlana Chapoval
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Fine Tuning ◽  
Breast Cancers ◽  
Immune Functions ◽  
Immune Cell Activation ◽  
Important Regulator ◽  
And Function ◽  
Axon Guidance Molecule ◽  
Guidance Molecule

Neuroimmune semaphorin 4A (Sema4A), a member of semaphorin family of transmembrane and secreted proteins, is an important regulator of neuronal and immune functions. In the nervous system, Sema4A primarily regulates the functional activity of neurons serving as an axon guidance molecule. In the immune system, Sema4A regulates immune cell activation and function, instructing a fine tuning of the immune response. Recent studies have shown a dysregulation of Sema4A expression in several types of cancer such as hepatocellular carcinoma, colorectal, and breast cancers. Cancers have been associated with abnormal angiogenesis. The function of Sema4A in angiogenesis and cancer is not defined. Recent studies have demonstrated Sema4A expression and function in endothelial cells. However, the results of these studies are controversial as they report either pro- or anti-angiogenic Sema4A effects depending on the experimental settings. In this mini-review, we discuss these findings as well as our data on Sema4A regulation of inflammation and angiogenesis, which both are important pathologic processes underlining tumorigenesis and tumor metastasis. Understanding the role of Sema4A in those processes may guide the development of improved therapeutic treatments for cancer.

scholarly journals Neuroimmune Semaphorin 4A in Cancer Angiogenesis and Inflammation

2018 ◽  
Author(s):  
Apoorva Iyer ◽  
Svetlana P. Chapoval
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Fine Tuning ◽  
Breast Cancers ◽  
Immune Functions ◽  
Immune Cell Activation ◽  
Important Regulator ◽  
And Function ◽  
Axon Guidance Molecule ◽  
Guidance Molecule

Neuroimmune semaphorin 4A (Sema4A), a member of semaphorin family of transmembrane and secreted proteins, is an important regulator of neuronal and immune functions. In the nervous system, Sema4A primarily regulates the functional activity of neurons serving as an axon guidance molecule. In the immune system, Sema4A regulates immune cell activation and function granting a fine tuning of immune response. Recent studies have shown a dysregulation of Sema4A expression in several types of cancer such as hepatocellular carcinoma, colorectal and breast cancers. Cancers have been associated with abnormal angiogenesis. The function of Sema4A in angiogenesis and cancer is not defined. Recent studies have demonstrated Sema4A expression and function in endothelial cells. However, the results of these studies are controversial as they report either pro – or anti-angiogenic Sema4A effects depending on the experimental settings. In this mini-review, we discuss these findings as well as our data on Sema4A regulation of inflammation and angiogenesis, which both are important pathologic processes underlining tumorigenesis and tumor metastasis. Understanding the role of Sema4A in those processes may guide the development of improved therapeutic treatments for cancer.

Biology of the Heparanase–Heparan Sulfate Axis and Its Role in Disease Pathogenesis

2021 ◽  
Vol 47 (03) ◽  
pp. 240-253 ◽  
Author(s):  
Israel Vlodavsky ◽  
Uri Barash ◽  
Hien M. Nguyen ◽  
Shi-Ming Yang ◽  
Neta Ilan
Keyword(s):  
Cell Proliferation ◽  
Heparan Sulfate ◽  
Cell Activation ◽  
Immune Cell ◽  
Enzyme Activation ◽  
Cell Of Origin ◽  
Immune Cell Activation ◽  
Cytokines And Chemokines ◽  
And Function ◽  
Multiple Signaling

AbstractCell surface proteoglycans are important constituents of the glycocalyx and participate in cell–cell and cell–extracellular matrix (ECM) interactions, enzyme activation and inhibition, and multiple signaling routes, thereby regulating cell proliferation, survival, adhesion, migration, and differentiation. Heparanase, the sole mammalian heparan sulfate degrading endoglycosidase, acts as an “activator” of HS proteoglycans, thus regulating tissue hemostasis. Heparanase is a multifaceted enzyme that together with heparan sulfate, primarily syndecan-1, drives signal transduction, immune cell activation, exosome formation, autophagy, and gene transcription via enzymatic and nonenzymatic activities. An important feature is the ability of heparanase to stimulate syndecan-1 shedding, thereby impacting cell behavior both locally and distally from its cell of origin. Heparanase releases a myriad of HS-bound growth factors, cytokines, and chemokines that are sequestered by heparan sulfate in the glycocalyx and ECM. Collectively, the heparan sulfate–heparanase axis plays pivotal roles in creating a permissive environment for cell proliferation, differentiation, and function, often resulting in the pathogenesis of diseases such as cancer, inflammation, endotheliitis, kidney dysfunction, tissue fibrosis, and viral infection.

Modulation of innate immune cell activation and function by Polysaccharide Krestin (PSK)

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
CA Wenner ◽  
H Wang ◽  
A Hill-Force ◽  
MR Martzen ◽  
MR Verneris
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Immune Cell Activation ◽  
And Function

Neuroinflammation and Neurodegenerative Diseases

2016 ◽  
Author(s):  
Taylor R. Jay ◽  
Shane M. Bemiller ◽  
Lee E. Neilson ◽  
Paul J. Cheng-Hathaway ◽  
Bruce T. Lamb
Keyword(s):  
Neurodegenerative Diseases ◽  
Immune Cells ◽  
Cell Activation ◽  
Immune Cell ◽  
Active Role ◽  
Immune Cell Activation ◽  
Excitotoxic Damage ◽  
And Function ◽  
Inflammatory Molecules ◽  
The Brain

Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic damage in surrounding neurons, and aberrantly clear healthy cells and structures from the brain. In turn, the cells within the brain play important roles in determining the phenotype and function of these immune cells, and changes in the interaction among these cells in the context of disease can lead to detrimental immune cell activation. There has been recent interest in developing inflammation-related biomarkers to help diagnose NDDs and immune-targeted therapeutics.

scholarly journals Renal sensing of bacterial metabolites in the gut-kidney axis

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0000292021
Author(s):  
Orestes Foresto-Neto ◽  
Bruno Ghirotto ◽  
Niels Olsen Saraiva Câmara
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Cell Metabolism ◽  
Kidney Injury ◽  
Intestinal Bacteria ◽  
Short Chain Fatty Acids ◽  
Renal Diseases ◽  
Immune Functions ◽  
Immune Cell Activation ◽  
G Protein Coupled

Seminal works have now revealed the microbiota is connected with several diseases, including renal disorders. The balance between optimal and dysregulated host-microbiota interactions has changed completely our understanding of immunity and inflammation. Kidney injury is associated with accumulation of uremic toxins in the intestine, augmented intestinal permeability and systemic inflammation. Intestinal bacteria can signal through innate receptors and induce immune cell activation in lamina propria and release of inflammatory mediators into bloodstream. But gut microbiota can also modulate immune functions through soluble products as short chain fatty acids (SCFAs). The three most common SCFAs are propionate, butyrate and acetate which can signal through specific G-protein coupled receptors (GPCRs) such as GPR43, GPR41 and GPR109a, expressed on the surface of epithelial, myeloid, endothelial and immune cells, among others. The triggered signaling can change cell metabolism, immune cell activation and cell death. Here, we reviewed gut-kidney axis, how kidney cells can sense SCFAs and its implication in renal diseases.

scholarly journals Myeloid Krüppel-Like Factor 2 Critically Regulates K/BxN Serum-Induced Arthritis

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 908 ◽  
Author(s):  
Manjusri Das ◽  
Moonmoon Deb ◽  
Dipranjan Laha ◽  
Matthew Joseph ◽  
Suman Kanji ◽  
...  
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Histone Acetyltransferases ◽  
Immune Cell Activation ◽  
Immune Mediated ◽  
Activated Monocytes ◽  
Osteoclastic Differentiation ◽  
And Function ◽  
Deficient Mice

Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease, and Krüppel-like factor 2 (KLF2) regulates immune cell activation and function. Herein, we show that in our experiments 50% global deficiency of KLF2 significantly elevated arthritic inflammation and pathogenesis, osteoclastic differentiation, matrix metalloproteinases (MMPs), and inflammatory cytokines in K/BxN serum-induced mice. The severities of RA pathogenesis, as well as the causative and resultant cellular and molecular factors, were further confirmed in monocyte-specific KLF2 deficient mice. In addition, induction of RA resulted in a decreased level of KLF2 in monocytes isolated from both mice and humans along with higher migration of activated monocytes to the RA sites in humans. Mechanistically, overexpression of KLF2 decreased the level of MMP9; conversely, knockdown of KLF2 increased MMP9 in monocytes along with enrichment of active histone marks and histone acetyltransferases on the MMP9 promoter region. These findings define the critical regulatory role of myeloid KLF2 in RA pathogenesis.

scholarly journals Carbohydrate and Amino Acid Metabolism as Hallmarks for Innate Immune Cell Activation and Function

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 562 ◽  
Author(s):  
Haoxin Zhao ◽  
Lydia N. Raines ◽  
Stanley Ching-Cheng Huang
Keyword(s):  
Amino Acids ◽  
Immune Cells ◽  
Amino Acid Metabolism ◽  
Cell Activation ◽  
Acid Metabolism ◽  
Immune Cell ◽  
Innate Immune ◽  
Effector Functions ◽  
Immune Cell Activation ◽  
And Function

Immune activation is now understood to be fundamentally linked to intrinsic and/or extrinsic metabolic processes which are essential for immune cells to survive, proliferate, and perform their effector functions. Moreover, disruption or dysregulation of these pathways can result in detrimental outcomes and underly a number of pathologies in both communicable and non-communicable diseases. In this review, we discuss how the metabolism of carbohydrates and amino acids in particular can modulate innate immunity and how perturbations in these pathways can result in failure of these immune cells to properly function or induce unfavorable phenotypes.

Oxidized Haemoglobin–Driven Endothelial Dysfunction and Immune Cell Activation: Novel Therapeutic Targets for Atherosclerosis

2013 ◽  
Vol 20 (37) ◽  
pp. 4806-4814 ◽  
Author(s):  
Brigitta Buttari ◽  
Elisabetta Profumo ◽  
Rita Businaro ◽  
Luciano Saso ◽  
Raffaele Capoano ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Cell Activation ◽  
Immune Cell ◽  
Therapeutic Targets ◽  
Immune Cell Activation ◽  
Novel Therapeutic

scholarly journals Neuronal guidance proteins in cardiovascular inflammation

2021 ◽  
Vol 116 (1) ◽  
Author(s):  
Marius Keller ◽  
Valbona Mirakaj ◽  
Michael Koeppen ◽  
Peter Rosenberger
Keyword(s):  
Cell Activation ◽  
Immune Cell ◽  
Vascular Endothelial ◽  
Therapeutic Approaches ◽  
Immune Cell Activation ◽  
Cytokines And Chemokines ◽  
The Future ◽  
Cardiovascular Pathologies ◽  
Neuronal Guidance

AbstractCardiovascular pathologies are often induced by inflammation. The associated changes in the inflammatory response influence vascular endothelial biology; they complicate the extent of ischaemia and reperfusion injury, direct the migration of immune competent cells and activate platelets. The initiation and progression of inflammation is regulated by the classical paradigm through the system of cytokines and chemokines. Therapeutic approaches have previously used this knowledge to control the extent of cardiovascular changes with varying degrees of success. Neuronal guidance proteins (NGPs) have emerged in recent years and have been shown to be significantly involved in the control of tissue inflammation and the mechanisms of immune cell activation. Therefore, proteins of this class might be used in the future as targets to control the extent of inflammation in the cardiovascular system. In this review, we describe the role of NGPs during cardiovascular inflammation and highlight potential therapeutic options that could be explored in the future.

scholarly journals Oxidative stress and immune cell activation quantification in sepsis and non-sepsis critical care patients by neopterin/7,8-dihydroneopterin analysis

Pteridines ◽  
2020 ◽  
Vol 31 (1) ◽  
pp. 68-82
Author(s):  
Gregory Baxter-Parker ◽  
Ravinder Reddy Gaddam ◽  
Elena Moltchanova ◽  
Anitra Carr ◽  
Geoff Shaw ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Function ◽  
Cell Activation ◽  
Immune Cell ◽  
Intensive Care Patients ◽  
Immune Cell Activation ◽  
Immune System Activation ◽  
System Activation ◽  
Urinary Neopterin ◽  
Critical Care Patients

AbstractIntroduction: Neopterin and 7,8-dihydroneopterin are used as biomarkers of oxidative stress and inflammation, but the effect of kidney function on these measurements has not been extensively explored. We examine the levels of oxidative stress, inflammation and kidney function in intensive patients and compare them to equivalent patients without sepsis.Methods: 34 Intensive care patients were selected for the study, 14 without sepsis and 20 with. Both groups had equivalent levels of trauma, assessed by SAPS II, SOFA, and APACHE II and III scores. Plasma and urinary neopterin and total neopterin (neopterin + 7,8-dihydroneopterin) values were measured.Results: Neopterin and total neopterin were significantly elevated in urine and plasma for multiple days in sepsis versus non-sepsis patients. Plasma neopterin and total neopterin have decreasing relationships with increased eGFR (p<0.008 and p<0.001, respectively). Plasma/urinary neopterin and total neopterin ratios demonstrate that total neopterin flux is more influenced by eGFR than neopterin, with significantce of p<0.02 and p<0.0002 respectively.Conclusion: Sepsis patients present with greater levels of oxidative stress and immune system activation than non-sepsis patients of equal levels of trauma, as measured by neopterin and total neopterin. eGFR may need to be taken into account when accessing the level of inflammation from urinary neopterin measurements.

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