Cerebrospinal fluid macrophage migration inhibitory factor: a potential predictor of cerebral vasospasm and clinical outcome after aneurysmal subarachnoid hemorrhage

Kwan, Kevin; Arapi, Orseola; Wagner, Katherine; Schneider, Júlia; Sy, Heustein; Ward, M.F.; Sison, Cristina; Li, Chunyan; Eisenberg, Mark; Chalif, David J.; Narayan, Raj K.; Miller, Edmund J.; Ledoux, Didier

doi:10.3171/2019.6.jns19613

Cited by 14 publications

(17 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Compared to intracerebral microdialysis, CSF analysis may reflect a more general picture of brain injury. CSF analysis basing on lumbar puncture is cornerstone for aSAH diagnosis, which means that changes of proteins can be detected quickly and conveniently to clarify the correlation between these changes and SAH pathology (Wasik et al, 2017 ; Papa et al, 2018 ; Kwan et al, 2019 ). To our knowledge, this study is the first to report the change of CSF HSP27 in patients with aSAH as compared with patients with NPH, showing a trend of increasing first and then decreasing in the early days.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage

Zhou

Sun

Wang

et al. 2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Cell apoptosis plays an important role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Heat shock protein 27 (HSP27), a member of the small heat shock protein (HSP) family, is induced by various stress factors and exerts protective role on cells. However, the role of HSP27 in brain injury after SAH needs to be further clarified. Here, we reported that HSP27 level of cerebrospinal fluid (CSF) is increased obviously at day 1 in patients with aneurysmal SAH (aSAH) and related to the grades of Hunt and Hess (HH), World Federation of Neurological Surgeons (WFNS), and Fisher score. In rat SAH model, HSP27 of CSF is first increased and then obviously declined; overexpression of HSP27, not knockdown of HSP27, attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex; and overexpression of HSP27 effectively suppresses SAH-elevated activation of mitogen-activated protein Kinase Kinase 4 (MKK4), the c-Jun N-terminal kinase (JNK), c-Jun, and caspase-3. In an in vitro hemolysate-damaged cortical neuron model, HSP2765−90 peptide effectively inhibits hemolysate-induced neuron death. Furthermore, TAT-HSP2765−90 peptide, a fusion peptide consisting of trans-activating regulatory protein (TAT) of HIV and HSP2765−90 peptide, effectively attenuates SAH-induced neurological deficit and cell apoptosis in the basal cortex of rats. Altogether, our results suggest that TAT-HSP27 peptide improves neurologic deficits via reducing apoptosis.

show abstract

Section: Discussionmentioning

confidence: 99%

“…CSF samples were collected in sterile tubes or catheter and stored at −80°C. CSF samples of patients with normal pressure hydrocephalus (NPH) were as the experimental control because CSF is difficult to obtain from healthy individuals (Kwan et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage

Zhou

Sun

Wang

et al. 2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Our results suggest a limited role for inflammatory cytokines in the palmitate-dependent and independent induction of Npy gene expression, and other mechanisms likely underlie this effect. While the concentrations of cytokines used in this study were somewhat higher than reported circulating or CSF concentrations in vivo (Friebe et al, 2011;Herder et al, 2008;Jain et al, 2015;Kwan et al, 2019;Niino et al, 2000;Panidis et al, 2008;von Vietinghoff & Ley, 2009), these levels are commonly used for cell line studies. Based on the efficacy of triacsin C to block the induction of Npy, palmitate metabolism appears to be an upstream mediator of the effect.…”

Section: Discussionmentioning

confidence: 80%

Palmitate‐mediated induction of neuropeptide Y expression occurs through intracellular metabolites and not direct exposure to proinflammatory cytokines

Tran

Chen

et al. 2021

Journal of Neurochemistry

View full text Add to dashboard Cite

A contributing factor to the development of obesity is the consumption of a diet high in saturated fatty acids, such as palmitate. These fats induce hypothalamic neuroinflammation, which dysregulates neuronal function and induces orexigenic neuropeptide Y (Npy) to promote food intake. An inflammatory cytokine array identified multiple candidates that could mediate palmitate-induced up-regulation of Npy mRNA levels. Of these, visfatin or nicotinamide phosphoribosyltransferase (NAMPT), macrophage migratory inhibitory factor (MIF), and IL-17F were chosen for further study. Direct treatment of the neuropeptide Y/agouti-related peptide (NPY/AgRP)-expressing mHypoE-46 neuronal cell line with the aforementioned cytokines demonstrated that visfatin could directly induce Npy mRNA expression. Preventing the intracellular metabolism of palmitate through long-chain acyl-CoA synthetase (ACSL) inhibition was sufficient to block the palmitate-mediated increase in Npy gene expression.Furthermore, thin-layer chromatography revealed that in neurons, palmitate is readily incorporated into ceramides and defined species of phospholipids. Exogenous C16 ceramide, dipalmitoyl-phosphatidylcholine, and dipalmitoyl-phosphatidylethanolamine were sufficient to significantly induce Npy expression. This study suggests that the intracellular metabolism of palmitate and elevation of metabolites, including ceramide and phospholipids, are responsible for the palmitate-mediated induction of the potent orexigen Npy. Furthermore, this suggests that the regulation of Npy expression is less reliant on inflammatory cytokines per se than palmitate metabolites in a model of NPY/AgRP neurons. These lipid species likely induce detrimental downstream cellular signaling events ultimately causing an increase in feeding, resulting in an overweight phenotype and/or obesity.

show abstract

“…Meanwhile, peripheral circulating macrophages are recruited by monocyte chemotactic protein-1 to enter the site of injury (Lu et al, 2009;Niwa et al, 2016). Similar to microglia, monocytes and macrophages are likely to be involved in the inflammatory response or oxidative damage after SAH and lead to poor prognosis (Kwan et al, 2019;Unda et al, 2020). Therefore, further research on its mechanism will help to develop more effective treatment regimens.…”

Section: Monocytes/macrophagesmentioning

confidence: 99%

Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage

Liu

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Subarachnoid hemorrhage (SAH) has a high mortality rate and causes long-term disability in many patients, often associated with cognitive impairment. However, the pathogenesis of delayed brain dysfunction after SAH is not fully understood. A growing body of evidence suggests that neuroinflammation and oxidative stress play a negative role in neurofunctional deficits. Red blood cells and hemoglobin, immune cells, proinflammatory cytokines, and peroxidases are directly or indirectly involved in the regulation of neuroinflammation and oxidative stress in the central nervous system after SAH. This review explores the role of various cellular and acellular components in secondary inflammation and oxidative stress after SAH, and aims to provide new ideas for clinical treatment to improve the prognosis of SAH.

show abstract

Cerebrospinal fluid macrophage migration inhibitory factor: a potential predictor of cerebral vasospasm and clinical outcome after aneurysmal subarachnoid hemorrhage

Cited by 14 publications

References 16 publications

TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage

TAT-HSP27 Peptide Improves Neurologic Deficits via Reducing Apoptosis After Experimental Subarachnoid Hemorrhage

Palmitate‐mediated induction of neuropeptide Y expression occurs through intracellular metabolites and not direct exposure to proinflammatory cytokines

Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage

Contact Info

Product

Resources

About