HMGB1 promotes neurovascular remodeling via Rage in the late phase of subarachnoid hemorrhage

Tian, Xiaojie; Sun, Liang; Feng, Dongxia; Sun, Qing; Dou, Yang; Liu, Cheng‐Lin; Zhou, Feng; Li, Haiying; Shen, Haitao; Wang, Zhong

doi:10.1016/j.brainres.2017.06.001

Cited by 39 publications

(34 citation statements)

References 26 publications

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“…Intriguingly, an oxidized form of HMGB1 has been shown to play a neuroprotective role during the recovery phase of the SAH (day 14 after the SAH), depicted by an inability to stimulate serum and CSF TNF-α upsurge and enhancing neurotrophin expression, as opposed to a reduced form of HMGB1 [56]. Furthermore, the inhibition of HMGB1 and RAGE signaling during this delayed recovery phase after the SAH (day 14 after the SAH) was associated with a decline in the neurotrophic growth factors (Nerve growth factor (NGF), Brain derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF)) and a reduction in neurogenesis as assessed by BrdU and DCX positive neurons [56]. The inhibition of RAGE by FPS-ZM1 and HMGB1 by ethyl pyruvate and glycyrrhizin also enhanced brain water content and the functional neurological impairment during this delayed recovery phase after SAH [56].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the inhibition of HMGB1 and RAGE signaling during this delayed recovery phase after the SAH (day 14 after the SAH) was associated with a decline in the neurotrophic growth factors (Nerve growth factor (NGF), Brain derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF)) and a reduction in neurogenesis as assessed by BrdU and DCX positive neurons [56]. The inhibition of RAGE by FPS-ZM1 and HMGB1 by ethyl pyruvate and glycyrrhizin also enhanced brain water content and the functional neurological impairment during this delayed recovery phase after SAH [56]. It would be quite interesting to study the dynamics of these distinct isoforms over the course of early brain injury and CVS after the SAH, and the impact of modulating these HMGB1 isoforms on inflammatory changes and neurological function after an experimental SAH.…”

Section: Discussionmentioning

confidence: 99%

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Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Muhammad

Chaudhry

Kahlert

et al. 2020

IJMS

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Aneurysmal subarachnoid hemorrhage (aSAH) is a complex and potentially deadly disease. Neurosurgical clipping or endovascular coiling can successfully obliterate ruptured aneurysms in almost every case. However, despite successful interventions, the clinical outcomes of aSAH patients are often poor. The reasons for poor outcomes are numerous, including cerebral vasospasm (CVS), post-hemorrhagic hydrocephalus, systemic infections and delayed cerebral ischemia. Although CVS with subsequent cerebral ischemia is one of the main contributors to brain damage after aSAH, little is known about the underlying molecular mechanisms of brain damage. This review emphasizes the importance of pharmacological interventions targeting high mobility group box 1 (HMGB1)-mediated brain damage after subarachnoid hemorrhage (SAH) and CVS. We searched Pubmed, Ovid medline and Scopus for “subarachnoid hemorrhage” in combination with “HMGB1”. Based on these criteria, a total of 31 articles were retrieved. After excluding duplicates and selecting the relevant references from the retrieved articles, eight publications were selected for the review of the pharmacological interventions targeting HMGB1 in SAH. Damaged central nervous system cells release damage-associated molecular pattern molecules (DAMPs) that are important for initiating, driving and sustaining the inflammatory response following an aSAH. The discussed evidence suggested that HMGB1, an important DAMP, contributes to brain damage during early brain injury and also to the development of CVS during the late phase. Different pharmacological interventions employing natural compounds with HMGB1-antagonizing activity, antibody targeting of HMGB1 or scavenging HMGB1 by soluble receptors for advanced glycation end products (sRAGE), have been shown to dampen the inflammation mediated brain damage and protect against CVS. The experimental data suggest that HMGB1 inhibition is a promising strategy to reduce aSAH-related brain damage and CVS. Clinical studies are needed to validate these findings that may lead to the development of potential treatment options that are much needed in aSAH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Muhammad

Chaudhry

Kahlert

et al. 2020

IJMS

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“…In a systematic review on the role of HMGB1 danger signaling in TBI, HMGB1 was found to be released from damaged neurons, and furthermore, it was elevated in patient's serum and cerebrospinal fluid (CSF) [108]. Moreover, HMGB1 increased in CSF associated with neuronal death in subarachnoid hemorrhage [109,110]. The elaborated studies show that HMGB1 may serve as a prognostic biomarker and therapeutic target in patients with TBI [108].…”

Section: High-mobility Group Box Proteinmentioning

confidence: 99%

Damage-associated molecular patterns in trauma

Relja

Land

2019

Eur J Trauma Emerg Surg

131

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In 1994, the "danger model" argued that adaptive immune responses are driven rather by molecules released upon tissue damage than by the recognition of "strange" molecules. Thus, an alternative to the "self versus non-self recognition model" has been provided. The model, which suggests that the immune system discriminates dangerous from safe molecules, has established the basis for the future designation of damage-associated molecular patterns (DAMPs), a term that was coined by Walter G. Land, Seong, and Matzinger. The pathological importance of DAMPs is barely somewhere else evident as in the posttraumatic or post-surgical inflammation and regeneration. Since DAMPs have been identified to trigger specific immune responses and inflammation, which is not necessarily detrimental but also regenerative, it still remains difficult to describe their "friend or foe" role in the posttraumatic immunogenicity and healing process. DAMPs can be used as biomarkers to indicate and/or to monitor a disease or injury severity, but they also may serve as clinically applicable parameters for optimized indication of the timing for, i.e., secondary surgeries. While experimental studies allow the detection of these biomarkers on different levels including cellular, tissue, and circulatory milieu, this is not always easily transferable to the human situation. Thus, in this review, we focus on the recent literature dealing with the pathophysiological importance of DAMPs after traumatic injury. Since dysregulated inflammation in traumatized patients always implies disturbed resolution of inflammation, so-called model of suppressing/inhibiting inducible DAMPs (SAMPs) will be very briefly introduced. Thus, an update on this topic in the field of trauma will be provided.

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“…In the recovery phase of SAH, Tian et al ( 52 ) suggested that HMGB1 can promote neurological recovery and blood vessel regeneration via RAGE mediation, which further demonstrated that HMGB1 serves different roles at different disease stages.…”

Section: Hmgb1 and Acute Cerebrovascular Diseasementioning

confidence: 99%

The role of high mobility group box 1 protein in acute cerebrovascular diseases (Review)

Dang

Wang

et al. 2018

biom rep

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The occurrence and development of acute cerebrovascular diseases involves an inflammatory response, and high mobility group box protein 1 (HMGB1) is a pro-inflammatory factor that is expressed not only in the early-injury stage of disease, but also during the post-repair process. In the initial stage of disease, HMGB1 is released into the outside of the cell to participate in the cascade amplification reaction of inflammation, causing vasospasm, destruction of the blood-brain barrier and apoptosis of nerve cells. In the recovery stage of disease, HMGB1 can promote tissue repair and remodeling, which can aid in nerve function recovery. This review summarizes the biological characteristics of HMGB1, and the role of HMGB1 in ischemic and hemorrhagic cerebrovascular disease, and cerebral venous thrombosis.

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HMGB1 promotes neurovascular remodeling via Rage in the late phase of subarachnoid hemorrhage

Cited by 39 publications

References 26 publications

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

Damage-associated molecular patterns in trauma

The role of high mobility group box 1 protein in acute cerebrovascular diseases (Review)

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