HMGB1 Level in Cerebrospinal Fluid as a Marker of Treatment Outcome in Patients with Acute Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

Sokół, Bartosz; Woźniak, Anna; Jankowski, Ron; Jurga, Stefan; Wąsik, Norbert; Shahid, Hinna; Grześkowiak, Bartosz F.

doi:10.1016/j.jstrokecerebrovasdis.2015.05.002

Cited by 38 publications

(29 citation statements)

References 26 publications

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“…The expression of HMGB1 in cerebral vessels following experimental SAH [13] and in the CSF of patients with SAH [25] has been demonstrated to be significantly increased. Since our primary data did not show any significant implication of HMGB1 in the development of an impaired cerebral artery response after SAH, we did not further determine the changes in the expression of HMGB1 in the cerebral vessels and brain tissues.…”

Section: Discussionmentioning

confidence: 99%

The Role of HMGB1 in Pial Arteriole Dilating Reactivity following Subarachnoid Hemorrhage in Rats

Changyaleket

Vályi-Nagy³

et al. 2016

J Vasc Res

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High-mobility group box 1 protein (HMGB1) has been implicated in inflammatory responses, and is also associated with cerebral vasospasm after subarachnoid hemorrhage (SAH). However, there are no direct evident links between HMGB1 and cerebral vasospasm. We therefore investigated the effects of HMGB1 on pial arteriole reactivity following SAH in rats. We initially found that SAH induced a significant decrease in pial arteriole dilating responses to sciatic nerve stimulation (SNS), hypercapnia (CO₂), and the topical suffusion of acetylcholine (ACh), adenosine (ADO), and s-nitroso-N-acetylpenicillamine (SNAP) over a 7-day period after SAH. The percent change of arteriolar diameter was decreased to the lowest point at 48 h after SAH, in response to dilating stimuli (i.e., it decreased from 41.0 ± 19.0% in the sham group to 11.00 ± 0.70% after SNS) (n = 5, p < 0.01). HMGB1 infusion in the lateral ventricle in normal rats for 48 h did not change the pial arteriole dilating response. In addition, inhibitors of HMGB1-receptor for advanced glycation end-product or HMGB1-toll-like receptor 2/4 interaction, or the HMBG1 antagonist did not improve pial arteriole reactivity 48 h after SAH. These findings suggest that HMGB1 may not be a major player in cerebral vascular dilating dysfunction after SAH.

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Section: Discussionmentioning

confidence: 99%

The Role of HMGB1 in Pial Arteriole Dilating Reactivity following Subarachnoid Hemorrhage in Rats

Changyaleket

Vályi-Nagy³

et al. 2016

J Vasc Res

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“…Another clinical study described elevated CSF HMGB1 levels in acute hydrocephalus after the aSAH and strong correlations with different scores of aSAH severity, including Hunt and Hess grades, the World Federation of Neurological Surgeons (WFNS) score, and the Glasgow Coma Scale (GCS). Furthermore, HMGB1 levels were correlated with the duration of stay in the intensive care unit and poor outcomes after 3 months [22]. Wang and colleagues confirmed the association between CSF HMGB1 levels and poor outcomes after 3 months in a larger cohort of aSAH patients.…”

Section: Hmgb1 Is Released In Cerebrospinal Fluid (Csf) and Systemic mentioning

confidence: 85%

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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“…HMGB1 increases in the cerebrospinal fluid (CSF) of SAH patients with a poor functional outcome. The upregulation of HMGB1 correlates significantly with IL-6, IL-8, and TNF-α expression in CSF, developing towards a pro-inflammatory response after SAH [42][43][44] . While another study suggests no correlation between HMGB1 and IL-6 concentrations in plasma, which may indicate the acute activation of HMGB1 occurs only in the CNS [45] .…”

Section: Microglial M1 Polarizationmentioning

confidence: 94%

Microglial activation and polarization after subarachnoid hemorrhage

Zheng¹,

Wong²

2019

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Subarachnoid hemorrhage (SAH) is a devastating stroke type, with high mortality and morbidity. The neuroinflammatory response evolves over time from early brain injury to delayed cerebral deterioration. Microglia, the resident immune cells of the central nervous system, respond to the acute brain injury through activation and polarization. Microglia are able to polarize along two pathways, classic M1 and alternative M2, towards tissue injury and tissue repair respectively. The modulation of microglial activation has gained appreciation as a means to prevent the detrimental effects. In this review, we describe the progression of microglial polarization after SAH and summarize the key studies on mediators of microglial activation, including M1 and M2 specific microglial markers, transcription factors and key signaling pathways. Interactions between microglia and other cells are critical in modulating microglial activation and function, which are discussed as well. The preclinical application of microgliadependent treatments is presented, aiming for a better understanding of modulating microglial function and suggesting future investigation for therapeutic approaches.

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HMGB1 Level in Cerebrospinal Fluid as a Marker of Treatment Outcome in Patients with Acute Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

Cited by 38 publications

References 26 publications

The Role of HMGB1 in Pial Arteriole Dilating Reactivity following Subarachnoid Hemorrhage in Rats

The Role of HMGB1 in Pial Arteriole Dilating Reactivity following Subarachnoid Hemorrhage in Rats

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

Microglial activation and polarization after subarachnoid hemorrhage

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