Endothelin-induced protein tyrosine phosphorylation of cultured astrocytes: Its relationship to cytoskeletal actin organization

Kōyama, Yutaka; Baba, Akemichi

doi:10.1002/(sici)1098-1136(199906)26:4<324::aid-glia6>3.0.co;2-x

Cited by 13 publications

(3 citation statements)

References 37 publications

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“…In the same cells, ET-3 increases the number of cells that progress through G1/S phase, it enhances the gene expression of cyclins D, A and E and stimulates the activity of cyclin-dependent kinases Cdk2, Cdk4 and Cdk6 [132]. The addition of ET-3 to cultured astrocytes stimulates the expression of cyclooxygenase 2, the production of prostaglandin E 2 [85] and induces the formation of stress fibers, an organized F-actin structure, via a rho-dependent signal cascade [84] and tyrosine phosphorylation of astrocytic proteins [3,84]. In mouse embryo astrocytes that express predominantly ET B receptors, ET-1 induces phospholipase D activation [29], glutamate release [143], stimulation of c-fos and nerve growth factor expression [93], glucose uptake [165] as well as DNA synthesis [24].…”

Section: Signal Transduction Pathways Activated By Endothelins In Thementioning

confidence: 99%

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Schinelli¹

2006

CMC

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The endothelin system, consisting of three peptides, two peptidases and two G-protein coupled receptors, is widely expressed in the brain cell types and brain-derived tumor cell lines. The stimulation of endothelin receptors elicits a variety of short- and long-term changes at cellular level but the effects of the pharmacological modulation of the endothelin system in brain physiology and pathophysiology are, at the present time, poorly understood. Altered expression of endothelins (ETs) in reactive astrocytes has been observed in many pathological conditions of the human brain, such as infarcts, lacunae, traumatic conditions, Alzheimer's disease and inflammatory diseases of the brain. In addition, recent studies have shown that endothelin antagonists might inhibit growth and induce cell death in human melanoma cells in vitro and in vivo, and have emphasized a possible role of endothelin peptides as autocrine or paracrine factor in the proliferation and dissemination of tumor cell lines. Given the fact that brain cell and a variety of brain tumor cell lines express functional endothelin receptors, further studies are warranted to demonstrate a possible therapeutic role of endothelin agonists and antagonist in the pharmacological treatment of brain-related diseases and brain tumors.

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Section: Signal Transduction Pathways Activated By Endothelins In Thementioning

confidence: 99%

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Schinelli¹

2006

CMC

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“…With the conversion of the activated phenotype, astrocytes become hypertrophic and proliferative [ 3 , 4 ]. Stimulation of ET B receptors in cultured astrocytes causes morphological alterations accompanied by cytoskeletal actin reorganization [ 63 , 98 ] and stimulated cellular proliferation [ 64 , 69 , 70 ], which is consistent with the action of ET B receptors in vivo. These findings indicate that the activation of astrocytic ET B receptors promotes their conversion to activated astrocytes.…”

Section: Et B -Receptors-mediated Astrocytic Activationmentioning

confidence: 54%

Endothelin ETB Receptor-Mediated Astrocytic Activation: Pathological Roles in Brain Disorders

Kōyama

2021

IJMS

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In brain disorders, reactive astrocytes, which are characterized by hypertrophy of the cell body and proliferative properties, are commonly observed. As reactive astrocytes are involved in the pathogenesis of several brain disorders, the control of astrocytic function has been proposed as a therapeutic strategy, and target molecules to effectively control astrocytic functions have been investigated. The production of brain endothelin-1 (ET-1), which increases in brain disorders, is involved in the pathophysiological response of the nervous system. Endothelin B (ETB) receptors are highly expressed in reactive astrocytes and are upregulated by brain injury. Activation of astrocyte ETB receptors promotes the induction of reactive astrocytes. In addition, the production of various astrocyte-derived factors, including neurotrophic factors and vascular permeability regulators, is regulated by ETB receptors. In animal models of Alzheimer’s disease, brain ischemia, neuropathic pain, and traumatic brain injury, ETB-receptor-mediated regulation of astrocytic activation has been reported to improve brain disorders. Therefore, the astrocytic ETB receptor is expected to be a promising drug target to improve several brain disorders. This article reviews the roles of ETB receptors in astrocytic activation and discusses its possible applications in the treatment of brain disorders.

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“…Among these, chromatolysis is a hallmark feature (AldSkogius & Svensson, ), together with synaptic loss (Cullheim et al ., ; Oliveira et al ., ; Tiraihi & Rezaie, ). Simultaneously, close to the lesioned neurons, the glial cells become reactive (Derouiche & Frotsher, ), which has been related to the acceleration of neuronal and synaptic loss (Hermansson et al ., ; Koyama & Baba, ; Rogers et al ., ; Moran & Graeber, ; DeLeo et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection and reduction of glial reaction by cannabidiol treatment after sciatic nerve transection in neonatal rats

Perez

Ulian-Benitez

Cartarozzi

et al. 2013

Eur J of Neuroscience

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In neonatal rats, the transection of a peripheral nerve leads to an intense retrograde degeneration of both motor and sensory neurons. Most of the axotomy-induced neuronal loss is a result of apoptotic processes. The clinical use of neurotrophic factors is difficult due to side effects and elevated costs, but other molecules might be effective and more easily obtained. Among them, some are derived from Cannabis sativa. Cannabidiol (CBD) is the major non-psychotropic component found on the surface of such plant leaves. The present study aimed to investigate the neuroprotective potential of CBD. Thus, 2-day-old Wistar rats were divided into the following experimental groups: sciatic nerve axotomy + CBD treatment (CBD group), axotomy + vehicle treatment (phosphate buffer group) and a control group (no-treatment group). The results were analysed by Nissl staining, immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling at 5 days post-lesion. Neuronal counting revealed both motor and sensory neuron rescue following treatment with CBD (15 and 30 mg/kg). Immunohistochemical analysis (obtained by synaptophysin staining) revealed 30% greater synaptic preservation within the spinal cord in the CBD-treated group. CBD administration decreased the astroglial and microglial reaction by 30 and 27%, respectively, as seen by glial fibrillary acidic protein and ionised calcium binding adaptor molecule 1 immunolabeling quantification. In line with such results, the terminal deoxynucleotidyl transferase dUTP nick end labeling reaction revealed a reduction of apoptotic cells, mostly located in the spinal cord intermediate zone, where interneurons promote sensory-motor integration. The present results show that CBD possesses neuroprotective characteristics that may, in turn, be promising for future clinical use.

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Endothelin-induced protein tyrosine phosphorylation of cultured astrocytes: Its relationship to cytoskeletal actin organization

Cited by 13 publications

References 37 publications

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Pharmacology and Physiopathology of the Brain Endothelin System: An Overview

Endothelin ETB Receptor-Mediated Astrocytic Activation: Pathological Roles in Brain Disorders

Neuroprotection and reduction of glial reaction by cannabidiol treatment after sciatic nerve transection in neonatal rats

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