Enhanced cortical expression of myeloid differentiation primary response protein 88 (Myd88) in patients with traumatic brain injury

Li, Wei; Liu, Huan-Dong; You, Wanchun; Zhou, Meifang; Ling, Hai-Ping; Shen, Wei; Zhu, Lin; Hang, Chun-Hua

doi:10.1016/j.jss.2012.10.928

Cited by 17 publications

(6 citation statements)

References 23 publications

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“…Double staining was performed following the procedures of our laboratory (Li et al, ). Briefly, frozen tissue sections of the occipital cortex (4 μm) were used for double staining of NF‐κB (p65)/neuronal nuclei (NeuN).…”

Section: Methodsmentioning

confidence: 99%

Nuclear factor‐κB/Bcl‐XL pathway is involved in the protective effect of hydrogen‐rich saline on the brain following experimental subarachnoid hemorrhage in rabbits

Zhuang

Sun

Zhang

et al. 2013

J of Neuroscience Research

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Early brain injury (EBI), a significant contributor to poor outcome after subarachnoid hemorrhage (SAH), is intimately associated with neuronal apoptosis. Recently, the protective role of hydrogen (H2 ) in the brain has been widely studied, but the underlying mechanism remains elusive. Numerous studies have shown nuclear factor-κB (NF-κB) as a crucial survival pathway in neurons. Here we investigated the role of H2 in EBI following SAH, focusing on the NF-κB pathway. A double blood injection model was used to produce experimental SAH, and H2 -rich saline was injected intraperitoneally. NF-κB activity within the occipital cortex was measured. Immunofluorescence was performed to demonstrate the activation of NF-κB; Bcl-xL and cleaved caspase-3 were determined via Western blot. Gene expression of Bcl-xL was detected by real-time PCR, and TUNEL and Nissl staining were performed to illustrate brain injury in the occipital cortex. SAH induced a significant increase of cleaved caspase-3. Correspondingly, TUNEL staining demonstrated obvious neuronal apoptosis following SAH. In contrast, H2 treatment markedly increased NF-κB activity and the expression of Bcl-xL and decreased the level of cleaved caspase-3. Additionally, H2 treatment significantly reduced post-SAH neuronal apoptosis. The current study shows that H2 treatment alleviates EBI in the rabbits following SAH and that NF-κB/Bcl-xL pathway is involved in the protective role of H2 .

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Section: Methodsmentioning

confidence: 99%

Nuclear factor‐κB/Bcl‐XL pathway is involved in the protective effect of hydrogen‐rich saline on the brain following experimental subarachnoid hemorrhage in rabbits

Zhuang

Sun

Zhang

et al. 2013

J of Neuroscience Research

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“…, is upregulated in neural and immune cells following TBI (Lee et al, 2013). Brain injury in humans also induces expression of the TLR adaptor protein, myeloid differentiation primary response gene 88 (MyD88) (Li et al, 2013). After recognition of endogenous proteins released by damaged cells (such as alarmins (Bianchi, 2007) and other DAMPs), a cellular response is triggered that involves several kinases, including NFκB-inducing kinase (Lee et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift

Jassam

Izzy

Whalen

et al. 2017

Neuron

562

496

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SUMMARY Traumatic brain injury (TBI) is a leading cause of morbidity and disability, with a considerable socioeconomic burden. Heterogeneity of pathoanatomical subtypes and diversity in the pathogenesis and extent of injury contribute to differences in the course and outcome of TBI. Following the primary injury, extensive and lasting damage is sustained through a complex cascade of events referred to as “secondary injury”. Neuroinflammation is proposed as an important manipulable aspect of secondary injury in animal and human studies. Because neuroinflammation can be detrimental or beneficial, before developing immunomodulatory therapies, it is necessary to better understand the timing and complexity of the immune responses that follows TBI. With a rapidly increasing body of literature, there is a need for a clear summary of TBI neuroimmunology. This review presents our current understanding of the immune response to TBI in a chronological and compartment-based manner, highlighting early changes in gene expression and initial signaling pathways that lead to activation of innate and adaptive immunity. Based on recent advances in our understanding of innate immune cell activation, we propose a new paradigm to study innate immune cells following TBI that moves away from the existing M1/M2 classification of activation states towards a stimulus and disease-specific understanding of polarization state based on transcriptomic and proteomic profiling.

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“…[7–9] Myeloid differentiation factor 88 (MyD88) is a key adaptor of TLR4, which leads to activation of downstream NF-κB and subsequent production of pro-inflammatory cytokines associated with neurotoxicity. [10–12]…”

Section: Introductionmentioning

confidence: 99%

TLR4/NF-κB signaling pathway gene single nucleotide polymorphisms alter gene expression levels and affect ARDS occurrence and prognosis outcomes

Ding

Feng²,

Chen

et al. 2019

Medicine

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Background: To study the occurrence and prognosis of acute respiratory distress syndrome (ARDS) using single nucleotide polymorphisms (SNPs) of TNF-α rs1800629, IL-6 rs1800796, and MyD88 rs7744 loci in the TLR4/NF-κB pathway. Methods: Genotypes were analyzed for TNF-α rs1800629, IL-6 rs1800796, and MyD88 rs7744 loci. Plasma TNF-α and IL-6 levels and MyD88 mRNA expression in peripheral blood mononuclear cells (PBMCs) of 300 ARDS patients and 300 non-ARDS patients (control group) were examined. The patients were followed up for 60 days, and the prognosis outcome was recorded. Results: The TNF-α rs1800629 locus A allele and the IL-6 rs1800796 locus G allele were found to be risk factors for ARDS (adjusted OR = 1.452, 95% CI: 1.211–1.689, P < .001 and adjusted OR = 1.205, 95% CI: 1.058–1.358, P = .005, respectively). The G allele at MyD88 rs7744 locus was a protective factor against ARDS (adjusted OR = 0.748, 95% CI: 0.631–0.876, P < .001). Compared with the other groups, homozygotes for TNF-α rs1800629, IL-6 rs1800796, and MyD88 rs7744 loci had higher expression levels, of which homozygotes for TNF-α rs1800629 and IL-6 rs1800796 loci had lower 60-day survival rates, while MyD88 rs7744 locus homozygotes had a higher 60-day survival rate. Conclusion: The effect of TNF-α rs1800629, IL-6 rs1800796, and MyD88 rs7744 SNPs on gene expression level is a likely cause of ARDS occurrence and poor prognosis.

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Enhanced cortical expression of myeloid differentiation primary response protein 88 (Myd88) in patients with traumatic brain injury

Cited by 17 publications

References 23 publications

Nuclear factor‐κB/Bcl‐XL pathway is involved in the protective effect of hydrogen‐rich saline on the brain following experimental subarachnoid hemorrhage in rabbits

Nuclear factor‐κB/Bcl‐XL pathway is involved in the protective effect of hydrogen‐rich saline on the brain following experimental subarachnoid hemorrhage in rabbits

Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift

TLR4/NF-κB signaling pathway gene single nucleotide polymorphisms alter gene expression levels and affect ARDS occurrence and prognosis outcomes

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