The Role of High Mobility Group Box 1 in Ischemic Stroke

Ye, Yingze; Zeng, Zhi; Jin, Tong‐Shou; Zhang, Hongfei; Xiong, Xiaoxing; Gu, Lijuan

doi:10.3389/fncel.2019.00127

Cited by 69 publications

(59 citation statements)

References 117 publications

(165 reference statements)

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“…The results of studies on IS suggest the important role of HMGB1 in stroke-induced immunosuppression, which is similar to a phenomenon observed in SAH [28][29][30][31]. The levels of this protein were increased in IS patients and correlated with the number of circulating leukocytes, stroke severity, and inflammatory markers [32].…”

Section: Discussionsupporting

confidence: 66%

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Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

et al. 2019

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Influence of an intracranial aneurysm (IA) rupture on the expression of miRNAs and the potential significance of the resulting changes remains poorly understood. We aimed to characterize the response to the IA rupture through the analysis of miRNAs in peripheral blood cells. Expression of small RNAs was investigated using deep transcriptome sequencing in patients in the acute phase of an IA rupture (first 72 h), in the chronic phase (3-15 months), and controls. A functional analysis and the potential interactions between miRNAs and target genes were investigated. We also measured the levels of proteins that were influenced by regulated miRNAs. We found that 106 mature miRNAs and 90 miRNA precursors were differentially expressed among the groups. The regulated miRNAs were involved in a variety of pathways, and the top pathway involved cytokine-cytokine receptor interactions. The identified miRNAs targeted the inflammatory factors HMGB1 and FASLG. Changes in their expression were detected at the mRNA and protein levels. IA rupture strongly influences the transcription profiles in peripheral blood cells. The regulated miRNAs were involved in the control of immune cell homeostasis. In summary, these results may aid in the elucidation of the molecular mechanisms that orchestrate the inflammatory response to IA rupture.

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Section: Discussionsupporting

confidence: 66%

“…RNAs were isolated from peripheral blood cells, whereas protein was measured in plasma. Circulating HMGB1 can be released from various cells, including activated platelets [31,37]. The activation of platelets is a known phenomenon in SAH and is associated with early brain injury after SAH [3,38].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

et al. 2019

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“…There has been an ongoing research finding connections between HMGB1 and immunopathology of disorders and traumas in various body systems. Its role in ischemic stroke was described by Ye et al [16]. Its complex function in cardiomyocyte senescence and cardiac inflammatory injury was described by Lu et al [17].…”

Section: Introductionmentioning

confidence: 98%

Alarmins HMGB1, IL-33, S100A7, and S100A12 in Psoriasis Vulgaris

Borský

Fiala

Andrýs

et al. 2020

Mediators of Inflammation

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Background. Psoriasis vulgaris is a chronic autoimmune disease associated with systemic inflammation. Increased levels of numerous cytokines, chemokines, growth factors, and other molecules were found in the skin and in the circulation of psoriatic patients. Alarmins, also known as danger signals, are intracellular proteins, which are released to an extracellular space after infection or damage. They are the markers of cell destructive processes. Objective. The aim of the present study was to evaluate the suitability of selected alarmins (HMGB1, IL-33, S100A7, and S100A12) as potential biomarkers of severity of psoriasis and to explore possible relationships between these proteins for the purpose of better understanding their roles in the immunopathology of psoriasis. Methods. The serum levels of selected alarmins were measured in 63 psoriatic patients and 95 control individuals. The levels were assessed by the ELISA technique using commercial kits. The data were statistically processed with MedCalc version 19.0.5. Results. In psoriatic patients, we found significantly increased levels of HMGB1 (p<0.05), IL-33 (p<0.01), S100A7 (p<0.0001), and S100A12 (p<0.0001). In addition, we found a significant relationship between HMGB1 and S100A7 (Spearman’s rho=0.276, p<0.05) in the patients and significant relationship between HMGB1 and IL-33 in the controls (Spearman’s rho=0.416, p<0.05). We did not find any relationship between observed alarmins and the disease severity. Conclusions. The alarmins HMGB1, IL-33, S100A7, and S100A12 were significantly elevated in the serum of patients, which states the hypothesis that they play specific roles in the immunopathology of psoriasis. However, we have not yet found a relationship between observed alarmins and the disease severity. The discovery of the relationship between HMGB1 and S100A7 is a novelty that should be studied in the future to further clarify its role and importance.

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“…Both experimental and clinical studies indicate that HMGB1 is released from injured brain tissues as well as activated microglia within the ischemic tissues and activates an early inflammatory response after AIS [109]. HMGB1signals via TLR2 and TLR4 signaling activate the NF-κB pathway and induce a proinflammatory response [110]. Several studies have shown that plasma levels of HMGB1 increase in ischemic stroke and correlate with poor outcome [111][112][113].…”

Section: Tlr9mentioning

confidence: 99%

The role of Toll-like receptor signaling pathways in cerebrovascular disorders: the impact of spreading depolarization

Ahmadabad

Ghadiri

Gorji

2020

J Neuroinflammation

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Cerebral vascular diseases (CVDs) are a group of disorders that affect the blood supply to the brain and lead to the reduction of oxygen and glucose supply to the neurons and the supporting cells. Spreading depolarization (SD), a propagating wave of neuroglial depolarization, occurs in different CVDs. A growing amount of evidence suggests that the inflammatory responses following hypoxic-ischemic insults and after SD plays a double-edged role in brain tissue injury and clinical outcome; a beneficial effect in the acute phase and a destructive role in the late phase. Toll-like receptors (TLRs) play a crucial role in the activation of inflammatory cascades and subsequent neuroprotective or harmful effects after CVDs and SD. Here, we review current data regarding the pathophysiological role of TLR signaling pathways in different CVDs and discuss the role of SD in the potentiation of the inflammatory cascade in CVDs through the modulation of TLRs.

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The Role of High Mobility Group Box 1 in Ischemic Stroke

Cited by 69 publications

References 117 publications

Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

Alarmins HMGB1, IL-33, S100A7, and S100A12 in Psoriasis Vulgaris

The role of Toll-like receptor signaling pathways in cerebrovascular disorders: the impact of spreading depolarization

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