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Article: Mechanisms of neuregulin action.

Talmage, David A

2008 Volume 289, Page(s) 74–84; discussion 84–93

Abstract: Neuregulin 1 (Nrg1) and ErbB receptor tyrosine kinase signalling is essential for the formation and ... neuronal connectivity. Recent studies have identified novel signalling mechanisms and revealed unexpected ...

Abstract	Neuregulin 1 (Nrg1) and ErbB receptor tyrosine kinase signalling is essential for the formation and proper functioning of multiple organ systems and inappropriate Nrgl/ErbB signalling severely compromises health, contributing to such diverse pathologies as cancer and neuropsychiatric disorders. Numerous genetic modelling studies in mice demonstrate that Nrg1 signalling is important in the development of normal neuronal connectivity. Recent studies have identified novel signalling mechanisms and revealed unexpected roles of Nrg1 isoforms in both the developing and adult nervous system. Of particular interest to this discussion are findings linking deficits in Nrg1-ErbB4 signalling to perturbations of synaptic transmission, myelination, and the survival of particular sets of neurons and glia.
MeSH term(s)	Animals ; Brain/physiology ; Brain/physiopathology ; Disease Models, Animal ; ErbB Receptors/physiology ; Gene Expression Regulation ; Genetic Variation ; Humans ; Mice ; Myelin Sheath/physiology ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Neuregulin-1 ; Neuroglia/physiology ; Neurons/physiology ; Receptor, ErbB-4 ; Schizophrenia/genetics ; Schizophrenia/pathology ; Schizophrenia/physiopathology ; Signal Transduction ; Synaptic Transmission/physiology
Chemical Substances	NRG1 protein, human ; Nerve Tissue Proteins ; Neuregulin-1 ; ERBB4 protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Erbb4 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-4 (EC 2.7.10.1)
Language	English
Publishing date	2008-05-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1528-2511
ISSN	1528-2511
DOI	10.1002/9780470751251.ch6
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Article ; Online: Molecular mechanisms of endothelial remodeling under doxorubicin treatment.

Podyacheva, Ekaterina / Danilchuk, Maria / Toropova, Yana

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 162, Page(s) 114576

Abstract: ... of information about the known molecular mechanisms of endothelial remodeling under the action of DOX. ... Moreover, DOX can impair the production of nitric oxide, endothelin-1, neuregulin, thrombomodulin ... mechanisms underlying DOX-induced cardiotoxicity are not fully understood, but recent studies have shown ...

Abstract	Doxorubicin (DOX) is an effective antineoplastic agent used to treat various types of cancers. However, its use is limited by the development of cardiotoxicity, which may result in heart failure. The exact mechanisms underlying DOX-induced cardiotoxicity are not fully understood, but recent studies have shown that endothelial-mesenchymal transition (EndMT) and endothelial damage play a crucial role in this process. EndMT is a biological process in which endothelial cells lose their characteristics and transform into mesenchymal cells, which have a fibroblast-like phenotype. This process has been shown to contribute to tissue fibrosis and remodeling in various diseases, including cancer and cardiovascular diseases. DOX-induced cardiotoxicity has been demonstrated to increase the expression of EndMT markers, suggesting that EndMT may play a critical role in the development of this condition. Furthermore, DOX-induced cardiotoxicity has been shown to cause endothelial damage, leading to the disruption of the endothelial barrier function and increased vascular permeability. This can result in the leakage of plasma proteins, leading to tissue edema and inflammation. Moreover, DOX can impair the production of nitric oxide, endothelin-1, neuregulin, thrombomodulin, thromboxane B2 etc. by endothelial cells, leading to vasoconstriction, thrombosis and further impairing cardiac function. In this regard, this review is devoted to the generalization and structuring of information about the known molecular mechanisms of endothelial remodeling under the action of DOX.
MeSH term(s)	Humans ; Cardiotoxicity/metabolism ; Endothelial Cells/metabolism ; Doxorubicin ; Cardiovascular Diseases ; Fibrosis ; Neoplasms
Chemical Substances	Doxorubicin (80168379AG)
Language	English
Publishing date	2023-03-28
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.114576
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Article: [Mechanism of action of neuregulin protecting the myocardium against daunorubicin-caused damage in rats].

Jiang, Sha-yi / Ma, Pei-ran / Xie, Xiao-tian

Zhonghua er ke za zhi = Chinese journal of pediatrics

2006 Volume 44, Issue 7, Page(s) 541–543

MeSH term(s)	Animals ; Antibiotics, Antineoplastic/administration & dosage ; Antibiotics, Antineoplastic/toxicity ; Apoptosis/drug effects ; Daunorubicin/administration & dosage ; Daunorubicin/toxicity ; Disease Models, Animal ; Female ; In Situ Nick-End Labeling ; Male ; Myocardium/cytology ; Myocardium/metabolism ; Myocardium/pathology ; Myocardium/ultrastructure ; Neuregulins/metabolism ; Neuregulins/pharmacology ; RNA, Messenger/metabolism ; Rats ; Rats, Wistar ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Antibiotics, Antineoplastic ; Neuregulins ; RNA, Messenger ; Erbb2 protein, rat (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Daunorubicin (ZS7284E0ZP)
Language	Chinese
Publishing date	2006-07
Publishing country	China
Document type	Journal Article
ZDB-ID	784523-6
ISSN	0578-1310
ISSN	0578-1310
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Article ; Online: Availability of neuregulin-1beta1 protects neurons in spinal cord injury and against glutamate toxicity through caspase dependent and independent mechanisms.

Shahsavani, Narjes / Alizadeh, Arsalan / Kataria, Hardeep / Karimi-Abdolrezaee, Soheila

Experimental neurology

2021 Volume 345, Page(s) 113817

Abstract: ... adult spinal cord. However, despite this pivotal role, Nrg-1β1 specific effects and mechanisms of action ... after SCI. In rat SCI, we previously uncovered that the tissue levels of neuregulin-1beta 1 (Nrg-1β1 ... signaling pathways. Altogether, our work provides novel insights into the role and mechanisms of Nrg-1β1 in neuronal ...

Abstract	Spinal cord injury (SCI) causes sensorimotor and autonomic impairment that partly reflects extensive, permanent loss of neurons at the epicenter and penumbra of the injury. Strategies aimed at enhancing neuronal protection are critical to attenuate neurodegeneration and improve neurological recovery after SCI. In rat SCI, we previously uncovered that the tissue levels of neuregulin-1beta 1 (Nrg-1β1) are acutely and persistently downregulated in the injured spinal cord. Nrg-1β1 is well-known for its critical roles in the development, maintenance and physiology of neurons and glia in the developing and adult spinal cord. However, despite this pivotal role, Nrg-1β1 specific effects and mechanisms of action on neuronal injury remain largely unknown in SCI. In the present study, using a clinically-relevant model of compressive/contusive SCI in rats and an in vitro model of glutamate toxicity in primary neurons, we demonstrate Nrg-1β1 provides early neuroprotection through attenuation of reactive oxygen species, lipid peroxidation, necrosis and apoptosis in acute and subacute stages of SCI. Mechanistically, availability of Nrg-1β1 following glutamate challenge protects neurons from caspase-dependent and independent cell death that is mediated by modulation of mitochondria associated apoptotic cascades and MAP kinase and AKT signaling pathways. Altogether, our work provides novel insights into the role and mechanisms of Nrg-1β1 in neuronal injury after SCI and introduces its potential as a new neuroprotective target for this debilitating neurological condition.
MeSH term(s)	Animals ; Caspases/metabolism ; Cells, Cultured ; Female ; Glutamic Acid/toxicity ; Neuregulin-1/administration & dosage ; Neuregulin-1/metabolism ; Neuroprotection/drug effects ; Neuroprotection/physiology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries/metabolism ; Spinal Cord Injuries/prevention & control
Chemical Substances	Neuregulin-1 ; Nrg1 protein, rat ; Glutamic Acid (3KX376GY7L) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2021-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2021.113817
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Article ; Online: Effect of age onset on schizophrenia-like phenotypes and underlying mechanisms in model mice.

Ju, Jun / Liu, Luping / Zhang, Yujie / Zhou, Qiang

Progress in neuro-psychopharmacology & biological psychiatry

2018 Volume 89, Page(s) 465–474

Abstract: ... whether schizophrenia with either adolescence- or adult-onset have distinct phenotypes and cellular mechanisms ... onset model mice, there are distinct differences in cellular mechanisms between them. We suggest ...

Abstract	In humans, schizophrenia with onset in adolescence or adult has distinct features. To understand whether schizophrenia with either adolescence- or adult-onset have distinct phenotypes and cellular mechanisms in schizophrenia model mice, we altered Nrg1 signaling during either adolescence or adult mice via injection of anti-Nrg1 antibodies. We found that in either early-onset schizophrenia (EOS)- or late-onset schizophrenia (LOS)-like mice, certain behavior phenotypes are shared including hyperlocomotion, impaired working memory and impaired fear conditioning. Anxiety appears to be largely unaffected. In vitro electrophysiology in brain slices showed altered excitation/inhibition balance in EOS-like mice towards enhanced synaptic excitation, but intrinsic excitability of the fast-spiking GABAergic neurons was elevated in the LOS-like mice. Thus, although schizophrenia-like main phenotypes appear to be preserved in both age onset model mice, there are distinct differences in cellular mechanisms between them. We suggest that these differences are important for more precise diagnosis and more effective treatment of schizophrenia.
MeSH term(s)	Action Potentials/physiology ; Age of Onset ; Animals ; Behavior, Animal/physiology ; Cognition Disorders/physiopathology ; Disease Models, Animal ; Male ; Memory/physiology ; Mice, Inbred C57BL ; Motor Activity ; Neuregulin-1/antagonists & inhibitors ; Neuregulin-1/metabolism ; Neurons/physiology ; Phenotype ; Schizophrenia/epidemiology ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; Tissue Culture Techniques
Chemical Substances	Neuregulin-1 ; Nrg1 protein, mouse
Language	English
Publishing date	2018-07-17
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	781181-0
ISSN	1878-4216 ; 0278-5846
ISSN (online)	1878-4216
ISSN	0278-5846
DOI	10.1016/j.pnpbp.2018.07.015
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Article ; Online: Molecular signaling mechanisms of axon-glia communication in the peripheral nervous system.

Grigoryan, Tamara / Birchmeier, Walter

BioEssays : news and reviews in molecular, cellular and developmental biology

2015 Volume 37, Issue 5, Page(s) 502–513

Abstract: ... shown that during development, neuronally provided signals, such as Neuregulin, Jagged, and Wnt interact ... neuronal survival and allow efficient transduction of action potentials. Deregulation of neuron ... In this article we discuss the molecular signaling mechanisms that coordinate interactions between ...

Abstract	In this article we discuss the molecular signaling mechanisms that coordinate interactions between Schwann cells and the neurons of the peripheral nervous system. Such interactions take place perpetually during development and in adulthood, and are critical for the homeostasis of the peripheral nervous system (PNS). Neurons provide essential signals to control Schwann cell functions, whereas Schwann cells promote neuronal survival and allow efficient transduction of action potentials. Deregulation of neuron-Schwann cell interactions often results in developmental abnormalities and diseases. Recent investigations have shown that during development, neuronally provided signals, such as Neuregulin, Jagged, and Wnt interact to fine-tune the Schwann cell lineage progression. In adult, the signal exchange between neurons and Schwann cells ensures proper nerve function and regeneration. Identification of the mechanisms of neuron-Schwann cell interactions is therefore essential for our understanding of the development, function and pathology of the peripheral nervous system as a whole.
MeSH term(s)	Animals ; Axons/metabolism ; Humans ; Neuroglia/cytology ; Neuroglia/metabolism ; Peripheral Nervous System/cytology ; Peripheral Nervous System/metabolism ; Signal Transduction/physiology ; Wnt Proteins/metabolism
Chemical Substances	Wnt Proteins
Language	English
Publishing date	2015-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201400172
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Article ; Online: Erythropoietin Restores Long-Term Neurocognitive Function Involving Mechanisms of Neuronal Plasticity in a Model of Hyperoxia-Induced Preterm Brain Injury.

Hoeber, Daniela / Sifringer, Marco / van de Looij, Yohan / Herz, Josephine / Sizonenko, Stéphane V / Kempe, Karina / Serdar, Meray / Palasz, Joanna / Hadamitzky, Martin / Endesfelder, Stefanie / Fandrey, Joachim / Felderhoff-Müser, Ursula / Bendix, Ivo

Oxidative medicine and cellular longevity

2016 Volume 2016, Page(s) 9247493

Abstract: ... in an experimental model of preterm brain injury. In search of the putative mechanisms of action we evaluated ...

Abstract	Cerebral white and grey matter injury is the leading cause of an adverse neurodevelopmental outcome in prematurely born infants. High oxygen concentrations have been shown to contribute to the pathogenesis of neonatal brain damage. Here, we focused on motor-cognitive outcome up to the adolescent and adult age in an experimental model of preterm brain injury. In search of the putative mechanisms of action we evaluated oligodendrocyte degeneration, myelination, and modulation of synaptic plasticity-related molecules. A single dose of erythropoietin (20,000 IU/kg) at the onset of hyperoxia (24 hours, 80% oxygen) in 6-day-old Wistar rats improved long-lasting neurocognitive development up to the adolescent and adult stage. Analysis of white matter structures revealed a reduction of acute oligodendrocyte degeneration. However, erythropoietin did not influence hypomyelination occurring a few days after injury or long-term microstructural white matter abnormalities detected in adult animals. Erythropoietin administration reverted hyperoxia-induced reduction of neuronal plasticity-related mRNA expression up to four months after injury. Thus, our findings highlight the importance of erythropoietin as a neuroregenerative treatment option in neonatal brain injury, leading to improved memory function in adolescent and adult rats which may be linked to increased neuronal network connectivity.
MeSH term(s)	Animals ; Animals, Newborn ; Behavior, Animal/drug effects ; Brain Injuries/etiology ; Brain Injuries/metabolism ; Brain Injuries/pathology ; Cell Survival/drug effects ; Cognition/drug effects ; Diffusion Tensor Imaging ; Disease Models, Animal ; Down-Regulation/drug effects ; Erythropoietin/pharmacology ; Hyperoxia ; Immunohistochemistry ; Microscopy, Confocal ; Mitochondria/metabolism ; Myelin Basic Protein/metabolism ; Neuregulin-1/genetics ; Neuregulin-1/metabolism ; Neuronal Plasticity/drug effects ; Neuropilin-1/genetics ; Neuropilin-1/metabolism ; Neuroprotective Agents/pharmacology ; Oligodendroglia/cytology ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Rats ; Rats, Wistar ; Synaptophysin/genetics ; Synaptophysin/metabolism ; White Matter/drug effects ; White Matter/metabolism
Chemical Substances	Myelin Basic Protein ; Neuregulin-1 ; Neuroprotective Agents ; Synaptophysin ; Erythropoietin (11096-26-7) ; Neuropilin-1 (144713-63-3)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2016/9247493
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Article: Schizophrenia: neural mechanisms for novel therapies.

Sawa, Akira / Snyder, Solomon H

Molecular medicine (Cambridge, Mass.)

2003 Volume 9, Issue 1-2, Page(s) 3–9

Abstract: ... dysbindin, and neuregulin. ... their actions may facilitate new drug discovery. Agents influencing glutamate neurotransmission and N-methyl-D ...

Abstract	Although valuable antischizophrenic drugs exist, they only partially ameliorate symptoms and elicit substantial side effects. Classic neuroleptic drugs act by blocking dopamine receptors. They can relieve some symptoms but not behavioral withdrawal features that are designated "negative" symptoms. Clozapine and related newer atypical neuroleptics may be more efficacious in relieving negative symptoms. Understandng their actions may facilitate new drug discovery. Agents influencing glutamate neurotransmission and N-methyl-D-aspartate receptors, especially the cotransmitter D-serine, are promising. Stimulation of the alpha7 subtype of nicotinic acetylcholine receptor may also be efficacious. The search for genes linked to schizophrenia has revealed several leads that may permit development of novel therapeutic agents. Promising genes include disrupted-in-schizophrenia-1, dysbindin, and neuregulin.
MeSH term(s)	Antipsychotic Agents/therapeutic use ; Humans ; Neural Pathways/drug effects ; Neural Pathways/metabolism ; Receptors, Neurotransmitter/genetics ; Receptors, Neurotransmitter/metabolism ; Schizophrenia/drug therapy ; Schizophrenia/metabolism
Chemical Substances	Antipsychotic Agents ; Receptors, Neurotransmitter
Language	English
Publishing date	2003-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1283676-x
ISSN	1076-1551
ISSN	1076-1551
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Article ; Online: Analysis of Gpr126 function defines distinct mechanisms controlling the initiation and maturation of myelin.

Glenn, Thomas D / Talbot, William S

Development (Cambridge, England)

2013 Volume 140, Issue 15, Page(s) 3167–3175

Abstract: ... cAMP does not initiate myelination in the absence of functional Neuregulin 1 (Nrg1) signaling ... of action potentials along axons. The transcription factor Krox20 regulates the initiation of myelination ... we define two distinct mechanisms controlling the initiation and maturation of myelin. We show that gpr126 ...

Abstract	In peripheral nerves, Schwann cells form the myelin sheath, which allows the efficient propagation of action potentials along axons. The transcription factor Krox20 regulates the initiation of myelination in Schwann cells and is also required to maintain mature myelin. The adhesion G protein-coupled receptor (GPCR) Gpr126 is essential for Schwann cells to initiate myelination, but previous studies have not addressed the role of Gpr126 signaling in myelin maturation and maintenance. Through analysis of Gpr126 in zebrafish, we define two distinct mechanisms controlling the initiation and maturation of myelin. We show that gpr126 mutant Schwann cells elaborate mature myelin sheaths and maintain krox20 expression for months, provided that the early signaling defect is bypassed by transient elevation of cAMP. At the onset of myelination, Gpr126 and protein kinase A (PKA) function as a switch that allows Schwann cells to initiate krox20 expression and myelination. After myelination is initiated, krox20 expression is maintained and myelin maturation proceeds independently of Gpr126 signaling. Transgenic analysis indicates that the Krox20 cis-regulatory myelinating Schwann cell element (MSE) becomes active at the onset of myelination and that this activity is dependent on Gpr126 signaling. Activity of the MSE declines after initiation, suggesting that other elements are responsible for maintaining krox20 expression in mature nerves. We also show that elevated cAMP does not initiate myelination in the absence of functional Neuregulin 1 (Nrg1) signaling. These results indicate that the mechanisms regulating the initiation of myelination are distinct from those mediating the maturation and maintenance of myelin.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Early Growth Response Protein 2/genetics ; Early Growth Response Protein 2/metabolism ; Gene Expression ; Genes, erbB-2 ; Lateral Line System/embryology ; Lateral Line System/physiology ; Mutation ; Myelin Basic Protein/genetics ; Myelin Basic Protein/metabolism ; Myelin Sheath/physiology ; Myelin Sheath/ultrastructure ; Neuregulin-1/genetics ; Neuregulin-1/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Schwann Cells/physiology ; Schwann Cells/ultrastructure ; Signal Transduction ; Zebrafish/embryology ; Zebrafish/genetics ; Zebrafish/physiology ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	EGR2 protein, Xenopus ; Early Growth Response Protein 2 ; Myelin Basic Protein ; Neuregulin-1 ; Receptors, G-Protein-Coupled ; Zebrafish Proteins ; stx7l protein, zebrafish ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2013-06-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.093401
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Article: Epidermal growth factor receptor: mechanisms of activation and signalling.

Jorissen, Robert N / Walker, Francesca / Pouliot, Normand / Garrett, Thomas P J / Ward, Colin W / Burgess, Antony W

Experimental cell research

2003 Volume 284, Issue 1, Page(s) 31–53

Abstract: ... the neuregulins. We review the structure and function of the EGFR, from ligand binding to the initiation ... that mediate the actions of a family of growth factors including EGF, transforming growth factor-alpha, and ...

Abstract	The epidermal growth factor (EGF) receptor (EGFR) is one of four homologous transmembrane proteins that mediate the actions of a family of growth factors including EGF, transforming growth factor-alpha, and the neuregulins. We review the structure and function of the EGFR, from ligand binding to the initiation of intracellular signalling pathways that lead to changes in the biochemical state of the cell. The recent crystal structures of different domains from several members of the EGFR family have challenged our concepts of these processes.
MeSH term(s)	Animals ; Cell Movement ; ErbB Receptors/metabolism ; Humans ; Models, Molecular ; Protein Conformation ; Signal Transduction ; Transforming Growth Factors/metabolism
Chemical Substances	Transforming Growth Factors (76057-06-2) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2003-03-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/s0014-4827(02)00098-8
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