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

Kōyama, Yutaka

doi:10.3390/ijms22094333

Cited by 26 publications

(17 citation statements)

References 124 publications

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“…The expression of cyclin D1 can be observed in reactive astrocytes after cerebral ischemia ( Di Giovanni et al, 2005 ; Zhu et al, 2007 ). Interestingly, some studies have found that endothelin-1 (ET-1) can also induce astrocyte activation after brain injury ( Koyama and Michinaga, 2012 ; Koyama, 2021 ). After the intervention with ET-1, the phosphorylation of SP1 and the activity of Cyclin D1 were increased.…”

Section: The Changes Of Astrocytes After Ischemiamentioning

confidence: 99%

Activation and Role of Astrocytes in Ischemic Stroke

Shen

Gao

Han

et al. 2021

Front. Cell. Neurosci.

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Ischemic stroke refers to the disorder of blood supply of local brain tissue caused by various reasons. It has high morbidity and mortality worldwide. Astrocytes are the most abundant glial cells in the central nervous system (CNS). They are responsible for the homeostasis, nutrition, and protection of the CNS and play an essential role in many nervous system diseases’ physiological and pathological processes. After stroke injury, astrocytes are activated and play a protective role through the heterogeneous and gradual changes of their gene expression, morphology, proliferation, and function, that is, reactive astrocytes. However, the position of reactive astrocytes has always been a controversial topic. Many studies have shown that reactive astrocytes are a double-edged sword with both beneficial and harmful effects. It is worth noting that their different spatial and temporal expression determines astrocytes’ various functions. Here, we comprehensively review the different roles and mechanisms of astrocytes after ischemic stroke. In addition, the intracellular mechanism of astrocyte activation has also been involved. More importantly, due to the complex cascade reaction and action mechanism after ischemic stroke, the role of astrocytes is still difficult to define. Still, there is no doubt that astrocytes are one of the critical factors mediating the deterioration or improvement of ischemic stroke.

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Section: The Changes Of Astrocytes After Ischemiamentioning

confidence: 99%

Activation and Role of Astrocytes in Ischemic Stroke

Shen

Gao

Han

et al. 2021

Front. Cell. Neurosci.

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“…Besides this, Off signals from neurons appear important in maintaining tissue homeostasis and limiting microglia activity under inflammatory conditions, presumably preventing damage to intact parts of the brain [ 143 ]. Endothelin B-receptor-mediated regulation of astrocytic activation was reported to improve brain disorders, such as neuropathic pain [ 144 ]. SP also directly activates microglia and astrocytes and contributes to microglial activation [ 145 , 146 ], initiating signaling via the nuclear factor kappa B pathway, leading to pro-inflammatory cytokines production [ 147 ] ( Figure 2 E).…”

Section: Neurogenic Inflammationmentioning

confidence: 99%

Neurogenic Inflammation: The Participant in Migraine and Recent Advancements in Translational Research

et al. 2021

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Migraine is a primary headache disorder characterized by a unilateral, throbbing, pulsing headache, which lasts for hours to days, and the pain can interfere with daily activities. It exhibits various symptoms, such as nausea, vomiting, sensitivity to light, sound, and odors, and physical activity consistently contributes to worsening pain. Despite the intensive research, little is still known about the pathomechanism of migraine. It is widely accepted that migraine involves activation and sensitization of the trigeminovascular system. It leads to the release of several pro-inflammatory neuropeptides and neurotransmitters and causes a cascade of inflammatory tissue responses, including vasodilation, plasma extravasation secondary to capillary leakage, edema, and mast cell degranulation. Convincing evidence obtained in rodent models suggests that neurogenic inflammation is assumed to contribute to the development of a migraine attack. Chemical stimulation of the dura mater triggers activation and sensitization of the trigeminal system and causes numerous molecular and behavioral changes; therefore, this is a relevant animal model of acute migraine. This narrative review discusses the emerging evidence supporting the involvement of neurogenic inflammation and neuropeptides in the pathophysiology of migraine, presenting the most recent advances in preclinical research and the novel therapeutic approaches to the disease.

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“…The involvement of the serotonergic Animal studies are one of the most important arenas for pain research. The endothelin receptor mediates the alteration of astrocyte functions, leading to the alleviation of neuropathic pain [124]. The dissociative anesthetics ketamine induces analgesic effects in models of acute pain and relieves thermal and mechanical allodynia in a chronic neuropathic pain model [125].…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway

et al. 2021

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Chronic pain is an unpleasant sensory and emotional experience that persists or recurs more than three months and may extend beyond the expected time of healing. Recently, nociplastic pain has been introduced as a descriptor of the mechanism of pain, which is due to the disturbance of neural processing without actual or potential tissue damage, appearing to replace a concept of psychogenic pain. An interdisciplinary task force of the International Association for the Study of Pain (IASP) compiled a systematic classification of clinical conditions associated with chronic pain, which was published in 2018 and will officially come into effect in 2022 in the 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the World Health Organization. ICD-11 offers the option for recording the presence of psychological or social factors in chronic pain; however, cognitive, emotional, and social dimensions in the pathogenesis of chronic pain are missing. Earlier pain disorder was defined as a condition with chronic pain associated with psychological factors, but it was replaced with somatic symptom disorder with predominant pain in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) in 2013. Recently clinical nosology is trending toward highlighting neurological pathology of chronic pain, discounting psychological or social factors in the pathogenesis of pain. This review article discusses components of the pain pathway, the component-based mechanisms of pain, central and peripheral sensitization, roles of chronic inflammation, and the involvement of tryptophan-kynurenine pathway metabolites, exploring the participation of psychosocial and behavioral factors in central sensitization of diseases progressing into the development of chronic pain, comorbid diseases that commonly present a symptom of chronic pain, and psychiatric disorders that manifest chronic pain without obvious actual or potential tissue damage.

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

Cited by 26 publications

References 124 publications

Activation and Role of Astrocytes in Ischemic Stroke

Activation and Role of Astrocytes in Ischemic Stroke

Neurogenic Inflammation: The Participant in Migraine and Recent Advancements in Translational Research

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway

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