High Mobility Group Box 1 and Traumatic Brain Injury

Richard, Seidu A.; Wu, Min; Su, Zhaoliang; Xu, Huji

doi:10.4236/jbbs.2017.72006

Cited by 20 publications

(16 citation statements)

References 51 publications

(72 reference statements)

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“…TBI is an insult to the brain through any external mechanical force ( Webster et al, 2017 ), which makes TBI a devastating and intractable cause of worldwide morbidity and mortality. Survivors live the rest of their lives with cognitive, motor, behavioral or speech and language disabilities ( Richard et al, 2017 ). However, the pathophysiology of TBI is still elusive and a tremendous research must be made to explore the progression of neurodegeneration and the ensuing inflammatory processes ( Parker et al, 2017 ).…”

Section: Role Of Hmgb1 In Tbimentioning

confidence: 99%

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HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

et al. 2018

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High mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein released by glia and neurons upon inflammasome activation and activates receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR) 4 on the target cells. HMGB1/TLR4 axis is a key initiator of neuroinflammation. In recent days, more attention has been paid to HMGB1 due to its contribution in traumatic brain injury (TBI), neuroinflammatory conditions, epileptogenesis, and cognitive impairments and has emerged as a novel target for those conditions. Nevertheless, HMGB1 has not been portrayed as a common prognostic biomarker for these HMGB1 mediated pathologies. The current review discusses the contribution of HMGB1/TLR4/RAGE signaling in several brain injury, neuroinflammation mediated disorders, epileptogenesis and cognitive dysfunctions and in the light of available evidence, argued the possibilities of HMGB1 as a common viable biomarker of the above mentioned neurological dysfunctions. Furthermore, the review also addresses the result of preclinical studies focused on HMGB1 targeted therapy by the HMGB1 antagonist in several ranges of HMGB1 mediated conditions and noted an encouraging result. These findings suggest HMGB1 as a potential candidate to be a common biomarker of TBI, neuroinflammation, epileptogenesis, and cognitive dysfunctions which can be used for early prediction and progression of those neurological diseases. Future study should explore toward the translational implication of HMGB1 which can open the windows of opportunities for the development of innovative therapeutics that could prevent several associated HMGB1 mediated pathologies discussed herein.

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Section: Role Of Hmgb1 In Tbimentioning

confidence: 99%

“…During TBI, HMGB1 is released via the N -methyl D -aspartate receptor subtype 2B (NR2B)-mediated mechanism from necrotic neurons ( Richard et al, 2017 ). HMGB1 mediates sterile inflammation and provokes macrophages and endothelial cells to release TNF-α, IL-1, and IL-6 by binding with RAGE and TLR4.…”

Section: Role Of Hmgb1 In Tbimentioning

confidence: 99%

HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

et al. 2018

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“…Several studies have demonstrated that HMGB1 is vigorously expressed by activated leukocytes or inactively secreted from stressed and necrotic cells [82,83]. It is also evidenced that HMGB1 is momentously raised in the circulation of traumatic injury and peaks up within first 6 h post injury [84,85]. Numerous studies have shown that extracellular HMGB1 can attract myeloid derived cells such as PMN-MDSCs, macrophages, DCs and Immature Myeloid Cells(IMC) [59,86] (Fig.…”

Section: Mdscs High Mobility Group Box 1 and Cancermentioning

confidence: 99%

Myeloid-derived Suppressor Cells in Cancer: A Review on the Pathogenesis and Therapeutic Potentials

Richard¹

2018

TOCIJ

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Myeloid-Derived Suppressor Cells (MDSCs) are multifarious group of immature cells that arise from the myeloid and amass in individuals with cancer, sepsis, burns, or chronic inflammation. It has been evidenced that these group of cells are efficient in modifying adaptive and innate immune responses, coherent with their assumed key biological roles. It is evidenced that MDSCs inter-communicate with Tumor-Associated Macrophages (TAM), Tumor-Associated Neutrophils (TAN), Dendritic Cells (DCs), Receptor for Advanced Glycation End-products (RAGE), Toll-Like Receptors (TLRs), Matrix Metalloproteinase (MMPs) as well as High Mobility Group Box 1 (HMGB1) during carcinogenesis. This interaction although elaborated in various studies and reviews still does not explain in details as to how their interplay results in cancer pathogenesis. We noted that MDSC contributed to cancer immune suppressionviaTLR-4 receptor and lipopolysaccharideas (LPS). Furthermore, MDSC contributed to cancer developmentviaMMPs (MMP-9 and MMP1-12) as well as RAGE. In the cancer microenvironment, HMGB1-driven MDSC amassment expedites cancer development and metastasisviaPMN-MDSCs, macrophages, DCs and Immature Myeloid Cells (IMC). Also, HMGB1 intermediation with MDSCsviaRAGE and/or TLR-4 leading to cancer development. Nevertheless, MDSCs have already proven potent in some cancers and are currently been used as treatment options although further studies are needed in some other cancers. Our review, therefore, explores the pivotal pathogenic and therapeutic roles of MDSCs in cancer.

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“…Studies have shown that the translocation of HMGB1 out of the nucleus is initiated by it acetylation resulting in its relocation. Advance studies have proven that HMGB1 after translocation in the cytoplasm binds to receptors like toll-like receptor 2 (TLR2), TLR4 or receptor for advanced glycation end products (RAGE), resulting the stimulation of numerous complexes of inflammatory responses (104,107,168). Studies have demonstrated RSV blocks HMGB1 translocation out of the nucleus, via the stimulation of sirtuin 1 (Sirt1), a NA-D + -dependent class III protein deacetylase (78,162,168).…”

Section: Resveratrol and Hmgb1 In Gliomamentioning

confidence: 99%

The Therapeutic Potential of Resveratrol in Gliomas

Richard¹

2019

ABCMed

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Resveratrol (RSV) is found in most human foods especially fruits such as grapes, peanuts, strawberry, blueberry, cranberry, mulberry, lingberry, sparkleberry, bilberry and in flowers as well as leaves like butterfly orchid tree, eucalyptus, spruce, lily, gnetum and so many others. Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair. RSV is precipitously metabolized in the liver via phase-II detoxification enzymes leading to its principal urine excretion. RSV steered growth inhibition, induction of apoptosis and G0/G1phase cell cycle arrest in an experiment involving glioma cells. RVS can block the triggering of signal transducer and activator of transcription (STAT3) signaling of glioma cells. RSV subdues STAT3 signaling via the inhibition of SRC or Janus kinase (JAK2) induction, thereby inducing growth inhibitory and apoptotic properties. RSV explicitly blocks both COX-1 and COX-2 invitro. In the cancer inflammatory milieu, the blockade effects of RSV on NF-κB could also lead to the blockade of TNF-α resulting in inhibition of cancer advancement as well as metastasis.Individually, RSV has proven to very potent in glioma cells. It is able to down-regulate glioma angiogenesis as well as metastasis. In combination with other agents, RVS augment its potency in glioma. RVS is able to cross the blood brain barrier (BBB) via gap junctions making it very efficient central nervous system medication. RVS after oral administration peaks in the blood stream after one hour meaning it acts very fast. This review focuses on the neuropharmacological role of RVS in glioma.proven to have chemo-preventive effects on numerous human ailments like osteoporosis and gastric ulcers besides the cardioprotective effect mentioned above (27,32). STRUCTURE AND FUNCTIONS OF RESVERATROLRSV is a white powder with a feeble yellow cast. It is a stilbene with a natural polyphenol configuration analogous to diethylstilbestrol and estradiol (32,86). Its molecular formula is C 14 H 12 O 3 and it is commonly referred to as 3,5,4'thihydroxystilbene. Other unconventional terms use to describe this compound are: 3,4',5-stilbenetriol, (E)-5-(7-hydroxystyryl) resorcinol, (E)-5-(4-hydroxystyryl) benzene-1,3-diol. RSV occurs innately as both cis-and trans-isomers. The trans-isomer is often used in classic laboratory studies because its more physical available have has higher biological activity than the cis-isomer. On the other hand, the cis-isomer is unstably and not commercial accessible (32,144).Functionally, RSV has the propensity to safeguard DNA as well as the induction of DNA repair (17,89). Studies have proven that, at high dose, RSV does not only suppress cancer advancement but also inhibits the synthesis of RNA, DNA and

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High Mobility Group Box 1 and Traumatic Brain Injury

Cited by 20 publications

References 51 publications

HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

Myeloid-derived Suppressor Cells in Cancer: A Review on the Pathogenesis and Therapeutic Potentials

The Therapeutic Potential of Resveratrol in Gliomas

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