Anti-high mobility group box-1 antibody attenuated vascular smooth muscle cell phenotypic switching and vascular remodelling after subarachnoid haemorrhage in rats

Wang, Liang; Zhang, Zhaosi; Liang, Luodan; Wu, Yue; Zhong, Jian; Sun, Xiaochuan

doi:10.1016/j.neulet.2019.134338

Cited by 16 publications

(18 citation statements)

References 25 publications

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“…Similarly to the aforementioned study, the anti-HMGB1 antibody also significantly reduced the expression of receptors for vasoconstrictive substances and reduced the threshold for a thrombin-or KCl-induced vasospasm in isolated basilar arteries after SAH [39]. Furthermore, authors demonstrated that the phenotypic and vascular remodeling reversal to partly depend upon PI3K/Akt activity [39]. These evidences indicate not only the reversal of vasospastic changes, but also the prevention against vascular remodeling and phenotypic switching, which result in the vessel wall thickening and reduced luminal diameters, which pave the way to delayed cerebral ischemia and neurological decline.…”

Section: Anti-hmgb1 Antibodies Confer Protection Against Cvssupporting

confidence: 57%

“…Furthermore, anti-HMGB1 antibody administration was associated with an improvement in cortical blood flow, reduction in cerebral edema, cortical apoptosis, microglial activation and neurological impairments (assessed by modified Garcia scoring and beam balance test) [39]. Similarly to the aforementioned study, the anti-HMGB1 antibody also significantly reduced the expression of receptors for vasoconstrictive substances and reduced the threshold for a thrombin-or KCl-induced vasospasm in isolated basilar arteries after SAH [39]. Furthermore, authors demonstrated that the phenotypic and vascular remodeling reversal to partly depend upon PI3K/Akt activity [39].…”

Section: Anti-hmgb1 Antibodies Confer Protection Against Cvsmentioning

confidence: 99%

“…The increased HMGB1 expression in the basilar artery was found to be associated with the overexpression of embryonic smooth muscle myosin heavy chain (Smemb) and osteopontin (OPN) and with a reduced expression of adult α-smooth muscle actin (α-SMA) and smooth muscle-myosin heavy chain (SM-MHC), but these changes were reversed by anti-HMGB1 antibodies [39]. Furthermore, anti-HMGB1 antibody administration was associated with an improvement in cortical blood flow, reduction in cerebral edema, cortical apoptosis, microglial activation and neurological impairments (assessed by modified Garcia scoring and beam balance test) [39]. Similarly to the aforementioned study, the anti-HMGB1 antibody also significantly reduced the expression of receptors for vasoconstrictive substances and reduced the threshold for a thrombin-or KCl-induced vasospasm in isolated basilar arteries after SAH [39].…”

Section: Anti-hmgb1 Antibodies Confer Protection Against Cvsmentioning

confidence: 99%

“…Another study aimed at the antibody-mediated antagonism of HMGB1 after SAH has shown that the prevention of vascular smooth muscle cell (VSMC) phenotypic switching and vascular remodeling may underlie the relieving of vasospasms [39]. The increased HMGB1 expression in the basilar artery was found to be associated with the overexpression of embryonic smooth muscle myosin heavy chain (Smemb) and osteopontin (OPN) and with a reduced expression of adult α-smooth muscle actin (α-SMA) and smooth muscle-myosin heavy chain (SM-MHC), but these changes were reversed by anti-HMGB1 antibodies [39]. Furthermore, anti-HMGB1 antibody administration was associated with an improvement in cortical blood flow, reduction in cerebral edema, cortical apoptosis, microglial activation and neurological impairments (assessed by modified Garcia scoring and beam balance test) [39].…”

Section: Anti-hmgb1 Antibodies Confer Protection Against Cvsmentioning

confidence: 99%

“…After aSAH, it has been shown that the early brain injury caused due to cerebral edema, which stems from early BBB disruption, leads to a poor clinical outcome [44]. The BBB disruption has been shown to be reduced after antagonizing HMGB1 and reducing cerebral edema in SAH animal models [39].…”

Section: Subarachnoid Hemorrhage and Blood-brain Barriermentioning

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: Anti-hmgb1 Antibodies Confer Protection Against Cvssupporting

confidence: 57%