Elucidating the novel biomarker and therapeutic potentials of High-mobility group box 1 in Subarachnoid hemorrhage: A review

Seidu A. Richard; Seidu A. Richard

doi:10.3934/Neuroscience.2019.4.316

AIMS Neuroscience

2019, Volume 6, Issue 4: 316-332. doi: 10.3934/Neuroscience.2019.4.316

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Review

Elucidating the novel biomarker and therapeutic potentials of High-mobility group box 1 in Subarachnoid hemorrhage: A review

Seidu A. Richard ^,

Department of Medicine, Princefield University, P. O. Box MA 128, Ho-Volta Region, Ghana West Africa

Received: 07 October 2019 Accepted: 21 November 2019 Published: 02 December 2019

Subarachnoid hemorrhage (SAH) frequently arises after an aneurysm in a cerebral artery ruptures, resulting into bleeding as well as clot formation. High-mobility group box 1 (HMGB1) is an extremely preserved, universal protein secreted in the nuclei of all cell varieties. This review explores the biomarker as well as therapeutic potentials of HMBG1 in SAH especially during the occurrence of cerebral vasospasms. Plasma HMGB1 levels have proven to be very useful prognosticators of effective outcome as well as death after SAH. Correspondingly, higher HMGB1 levels in the cerebrospinal fluid (CSF) of SAH patients correlated well with poor outcome; signifying that, CSF level of HMGB1 is a novel predictor of outcome following SAH. Nonetheless, the degree of angiographic vasospasm does not always correlate with the degree of neurological deficits in SAH patients. HMGB1 stimulated cerebral vasospasm, augmented gene as well as protein secretory levels of receptor for advance glycation end product (RAGE) in neurons following SAH; which means that, silencing HMGB1 during SAH could be of therapeutic value. Compounds like resveratrol, glycyrrhizin, rhinacanthin, purpurogallin, 4′-O-β-D-Glucosyl-5-O-Methylvisamminol (4OGOMV) as well as receptor-interacting serine/threonine-protein kinase 3 (RIPK3) gene are capable of interacting with HMGB1 resulting in therapeutic benefits following SAH.
- CSF,
- HMGB1,
- Plasma,
- Prognosis,
- SAH,
- Vasospasm
Citation: Seidu A. Richard. Elucidating the novel biomarker and therapeutic potentials of High-mobility group box 1 in Subarachnoid hemorrhage: A review[J]. AIMS Neuroscience, 2019, 6(4): 316-332. doi: 10.3934/Neuroscience.2019.4.316

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Abstract

Subarachnoid hemorrhage (SAH) frequently arises after an aneurysm in a cerebral artery ruptures, resulting into bleeding as well as clot formation. High-mobility group box 1 (HMGB1) is an extremely preserved, universal protein secreted in the nuclei of all cell varieties. This review explores the biomarker as well as therapeutic potentials of HMBG1 in SAH especially during the occurrence of cerebral vasospasms. Plasma HMGB1 levels have proven to be very useful prognosticators of effective outcome as well as death after SAH. Correspondingly, higher HMGB1 levels in the cerebrospinal fluid (CSF) of SAH patients correlated well with poor outcome; signifying that, CSF level of HMGB1 is a novel predictor of outcome following SAH. Nonetheless, the degree of angiographic vasospasm does not always correlate with the degree of neurological deficits in SAH patients. HMGB1 stimulated cerebral vasospasm, augmented gene as well as protein secretory levels of receptor for advance glycation end product (RAGE) in neurons following SAH; which means that, silencing HMGB1 during SAH could be of therapeutic value. Compounds like resveratrol, glycyrrhizin, rhinacanthin, purpurogallin, 4′-O-β-D-Glucosyl-5-O-Methylvisamminol (4OGOMV) as well as receptor-interacting serine/threonine-protein kinase 3 (RIPK3) gene are capable of interacting with HMGB1 resulting in therapeutic benefits following SAH.

Abbreviation BBB: Blood brain barrier; CSF: Cerebrospinal fluid; CVA: Cerebrovascular accidents; CT: Computer tomography; COX-2: Cyclooxygenase-2; eNOS: Endothelial nitric oxide synthase; ERK1: Extracellular regulated kinases; HMGB1: High-mobility group box 1; H&H: Hunt and Hess; Hb: Hemoglobin; GL: Glycyrrhizin; JAK: Janus kinase; IL: Interleukin; ICAM: Intercellular adhesion molecule; iNOS: Inducible nitric oxide synthase; D1: Lectin-like domain; NF-κB: Nuclear factor-κB; MyD88: Myeloid differentiation primary response protein 88; PAR1: Protease activated receptor 1; PI3K: Phosphoinositide 3-kinases; AKT: Protein Kinase B; PPG: Purpurogallin; D23: Proteoglycan-like domain; RAGE: Receptor for advance glycation end products; RSV: Resveratrol; RIPK3: Receptor-interacting serine/threonine-protein kinase 3; rHMGB1: Recombinant HMGB1; STAT: Signal transducer and activator of transcription; SMCs: Smooth muscle cells; SAH: Subarachnoid hemorrhage; TLRs: Toll-like receptors; TNF-α: Tumor necrosis factor-alpha; VCAM: Vascular cell-adhesion molecule; WFNS: World federation of neurosurgical societies;

Conflicts of interest

The author has no conflicts of interest.

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