Neuroprotective Effects of Endogenous Secretory Receptor for Advanced Glycation End-products in Brain Ischemia

Yu, Shun; Harashima, Ai; Oishi, Masahiro; Hattori, Tsuyoshi; Hori, Osamu; Kitao, Yasuko; Yamamoto, Hiroshi; Leerach, Nontaphat; Nakada, Mitsutoshi; Yamamoto, Yasuhiko; Hayashi, Yasuhiko

doi:10.14336/ad.2019.0715

Cited by 19 publications

(20 citation statements)

References 51 publications

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“…Mechanisms underlying DM may worsen consequence including vascular damage with stenosis of cerebral arteries leading to impairment of cerebral collateral flow [ 104 ]. Patients with DM presented an increased recurrence of stroke, especially IS, leading to neuronal cell death and infarction that accounts for about 87% of all strokes [ 63 , 105 , 106 ] when compared to non-DM patients [ 107 , 108 ]. Patients suffering from acute ischemic stroke (AIS) with a history of prior stroke and DM could have increased serious cerebral injury [ 109 ].…”

Section: Potential Dm-induced Mechanisms Leading To Diabetic Strokmentioning

confidence: 99%

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Xing¹,

Tang²,

Lei³

et al. 2020

Aging and disease

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The goal of this review was to summarize current biochemical mechanisms of and risk factors for diabetic brain injury. We mainly summarized mechanisms published in the past three years and focused on diabetes induced cognitive impairment, diabetes-linked Alzheimer's disease, and diabetic stroke. We think there is a need to conduct further studies with increased sample sizes and prolonged period of follow-ups to clarify the effect of DM on brain dysfunction. Additionally, we also think that enhancing experimental reproducibility using animal models in conjunction with application of advanced devices should be considered when new experiments are designed. It is expected that further investigation of the underlying mechanisms of diabetic cognitive impairment will provide novel insights into therapeutic approaches for ameliorating diabetes-associated injury in the brain.

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Section: Potential Dm-induced Mechanisms Leading To Diabetic Strokmentioning

confidence: 99%

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Xing¹,

Tang²,

Lei³

et al. 2020

Aging and disease

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“…In this study, blood endogenous secretory RAGE (esRAGE), a truncated variant of RAGE isoforms, remarkably inhibited transient brain ischemia-induced neuronal cell damage and apoptosis in the mouse bilateral common carotid artery occlusion model (Shimizu et al, 2020). The neuroprotective effects of esRAGE in ischemia are associated with its transfer into the brain through the BBB by RAGE on endothelial cells (Shimizu et al, 2020). These findings indicate that endothelial RAGE has two distinct roles in ischemia, namely, as an inducer of vascular and neuronal injury and as a transporter of esRAGE, a neuroprotector, to the brain (Shimizu et al, 2020).…”

Section: Receptor For Advanced Glycation End Products (Rage)mentioning

confidence: 93%

“…A previous study further assessed the role of RAGE in cerebral ischemic injury. In this study, blood endogenous secretory RAGE (esRAGE), a truncated variant of RAGE isoforms, remarkably inhibited transient brain ischemia-induced neuronal cell damage and apoptosis in the mouse bilateral common carotid artery occlusion model (Shimizu et al, 2020). The neuroprotective effects of esRAGE in ischemia are associated with its transfer into the brain through the BBB by RAGE on endothelial cells (Shimizu et al, 2020).…”

Section: Receptor For Advanced Glycation End Products (Rage)mentioning

confidence: 93%

“…The neuroprotective effects of esRAGE in ischemia are associated with its transfer into the brain through the BBB by RAGE on endothelial cells (Shimizu et al, 2020). These findings indicate that endothelial RAGE has two distinct roles in ischemia, namely, as an inducer of vascular and neuronal injury and as a transporter of esRAGE, a neuroprotector, to the brain (Shimizu et al, 2020).…”

Section: Receptor For Advanced Glycation End Products (Rage)mentioning

confidence: 99%

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The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury

Gou

Ying

Yan

et al. 2020

Front. Cell. Neurosci.

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High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that plays an important role in stabilizing nucleosomes and DNA repair. HMGB1 can be passively released from necrotic neurons or actively secreted by microglia, macrophages/monocytes, and neutrophils. Cerebral ischemia is a major cause of mortality and disability worldwide, and its outcome depends on the number of neurons dying due to hypoxia in the ischemic area. HMGB1 contributes to the pathogenesis of cerebral ischemia via mediating neuroinflammatory responses to cerebral ischemic injury. Extracellular HMGB1 regulates many neuroinflammatory events by interacting with its different cell surface receptors, such as receptors for advanced glycation end products, toll-like receptor (TLR)-2, and TLR-4. Additionally, HMGB1 can be redox-modified, thus exerting specific cellular functions in the ischemic brain and has different roles in the acute and late stages of cerebral ischemic injury. However, the role of HMGB1 in cerebral ischemia is complex and remains unclear. Herein, we summarize and review the research on HMGB1 in cerebral ischemia, focusing especially on the role of HMGB1 in hypoxic ischemia in the immature brain and in white matter ischemic injury. We also outline the possible mechanisms of HMGB1 in cerebral ischemia and the main strategies to inhibit HMGB1 pertaining to its potential as a novel critical molecular target in cerebral ischemic injury.

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“…This point should be further examined. Interestingly, it is also found that circulating esRAGE is transported into the brain through the BBB by mRAGE on endothelial cells, potentially contributing to the oxytocin transfer into the brain 28 .…”

Section: Possible Routes and Functions Of Oxytocinmentioning

confidence: 99%

RAGE regulates oxytocin transport into the brain

Yamamoto

Higashida

2020

Commun Biol

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Oxytocin, a nonapeptide hormone, has a key role in female reproductive functions as well as in social memory in the brain. In our recent Communications Biology article, we reported that oxytocin is transported from the peripheral blood into the brain by the receptor for advanced glycation end-products (RAGE) in endothelial cells at the blood−brain barrier. Additionally, we found that oral oxytocin is absorbed by RAGE on intestinal epithelial cells at the blood−intestinal barrier. From a physiological perspective, we herein outline the continuing research regarding oxytocin and social behaviour. Oxytocin in female reproduction and beyond Oxytocin is primarily synthesized in the oxytocinergic neurons in the hypothalamus within the brain 1,2. Oxytocin in brain neurons is secreted somato-axono-dendritically into the brain 3,4 and released from the nerve terminals in the posterior pituitary into the circulation 1-4. Within the past decade, oxytocin in the brain has attracted increasing attention because of the importance of oxytocin in species-specific social memory functioning 5-7. Oxytocin in the blood circulation has a primary hormonal role in female reproduction but was not thought to re-enter the brain. Recently, however, based on the practical nasal administration of large doses of oxytocin to humans with and without social deficit-related psychiatric disorders, such as autism spectrum disorders and schizophrenia 8,9 , oxytocin has been thought to cross the blood−brain barrier (BBB) 3,10. However, there is little or no direct evidence for this transport process, with the exception of two reports that examined human cerebrospinal fluid (CSF) and microdialysates from the mouse and rat hippocampus and amygdala 11,12. They found that peak levels of oxytocin were observed 30-60 min after the nasal administration of oxytocin in three species 12,13 , which is confirmed in our study as well 14. Furthermore, if oxytocin is indeed transferred from the blood to the brain, the underlying molecular mechanism is unclear. How oxytocin crosses the blood−brain barrier The transport of peptides across the BBB requires specific or nonspecific interactions with proteins or receptors that are expressed on the luminal and/or abluminal surfaces of brain

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Neuroprotective Effects of Endogenous Secretory Receptor for Advanced Glycation End-products in Brain Ischemia

Cited by 19 publications

References 51 publications

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus

The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury

RAGE regulates oxytocin transport into the brain

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