Concentration of neuron-specific enolase and S100 protein in the subretinal fluid of rhegmatogenous retinal detachment

Quintyn, J.–C.; Pereira, Fernanda T.; Hellot, M.-F.; Coquerel, Antoine

doi:10.1007/s00417-005-1175-0

Cited by 12 publications

(10 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…High NSE serum concentrations predicted poor neurological outcome in a majority of cardiac arrest patients [ 52 ]. NSE levels have also been used to predict neurological outcome in traumatic brain injury (TBI) [ 53 ] and retinal disease, such as retinal detachment [ 54 , 55 , 56 ]. Higher levels of NSE have been detected in Leber’s hereditary optic neuropathy (LHON), a mitochondrial disease affecting retinal ganglion cells (RGC) [ 56 ].…”

Section: Nse As Prognostic Factors In Patients During Neuroinflammmentioning

confidence: 99%

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

et al. 2018

View full text Add to dashboard Cite

Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells. While α-enolase is present in all neurological tissues, it can also be converted to neuron specific enolase (NSE). NSE is a glycolytic enzyme found in neuronal and neuroendocrine tissues that may play a dual role in promoting both neuroinflammation and neuroprotection in SCI and other neurodegenerative events. Elevated NSE can promote ECM degradation, inflammatory glial cell proliferation, and actin remodeling, thereby affecting migration of activated macrophages and microglia to the injury site and promoting neuronal cell death. Thus, NSE could be a reliable, quantitative, and specific marker of neuronal injury. Depending on the injury, disease, and microenvironment, NSE may also show neurotrophic function as it controls neuronal survival, differentiation, and neurite regeneration via activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways. This review discusses possible implications of NSE expression and activity in neuroinflammation, neurodegeneration, and neuroprotection in SCI and various neurodegenerative diseases for prognostic and therapeutic potential.

show abstract

Section: Nse As Prognostic Factors In Patients During Neuroinflammmentioning

confidence: 99%

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

et al. 2018

View full text Add to dashboard Cite

show abstract

“…27,28 Also, NSE has been defined as an effective marker of axonal injury within the CNS in its early stages 29 and of brain stress in general. 30 Both S100 and NSE are clinical biomarkers used in patients with TBI. S100 and NSE levels in cerebrospinal fluid and serum can be used more or less satisfactorily to predicate the existence, absence and severity of CNS injury or brain death and the outcome of TBI patients.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

Krohn

Dreßler

Bauer

et al. 2015

Journal of Neurotrauma

View full text Add to dashboard Cite

The availability of markers able to provide insight into protein changes in the central nervous system after fatal traumatic brain injury (TBI) is limited. The present study reports on the semi-quantitative assessments of the immunopositive neuroglial cells (both astrocytes and oligodendrocytes) and neurons for S100 protein (S100), as well as neuronal specific enolase (NSE), in the cerebral cortex, hippocampus, and cerebellum with regard to survival time and cause of death. Brain tissues of 47 autopsy cases with TBI (survival times ranged between several minutes and 34 d) and 10 age- and gender-matched controls (natural deaths) were examined. TBI cases were grouped according to their survival time in acute death after brain injury (ABI, n = 25), subacute death after brain injury (SBI, n = 18) and delayed death after brain injury (DBI, n = 4). There were no significant changes in the percentages of S100-stained astrocytes between TBI and control cases. The percentages of S100-positive oligodendrocytes in the pericontusional zone (PCZ) in cases with SBI were significantly lower than in controls (p < 0.05) and in the ABI group (p < 0.05). In the hippocampus, S100-positive oligodendrocytes were significantly lower in cases with ABI and SBI (both, p < 0.05), compared with controls. It is of particular interest that there were also S100-positive neurons in the PCZ and hippocampus in TBI cases after more than 2 h survival but not in ABI cases or controls. The percentages of NSE-positive neurons in the hippocampus were likewise significantly lower in cases with ABI, compared with controls (p < 0.05) but increased in cases with SBI in PCZ (p < 0.05). In conclusion, the present findings emphasize that S100 and NSE-immunopositivity might be useful for detecting the cause and process of death due to TBI. Further, S100-positivity in neurons may be helpful to estimate the survival time of fatal injuries in legal medicine.

show abstract

“…Breakdown of the blood-retinal barrier following RRD results in the leakage of blood, which may promote an inflammatory reaction and the proliferation of retinal glial and RPE cells. 24,25 In previous studies, various factors involved in the inflammation process, such as gelatinase activity, 26,27 connective tissue growth factor, 28 pigment-epithelium-derived factor, 29 IL-6, 30 s-100, 31 and TGF-b2 25 have been reported to be present in SRF. In our study, ARPE-19 cells cocultured with SRF showed elevated expression of ICAM-1 in vitro.…”

Section: Resultsmentioning

confidence: 98%

Subretinal fluid from rhegmatogenous retinal detachment and blood induces the expression of ICAM-1 in the human retinal pigment epithelium (ARPE-19) in vitro

Chen

et al. 2009

Eye

View full text Add to dashboard Cite

Purpose To evaluate the effect of subretinal fluid (SRF) from rhegmatogenous retinal detachment (RRD) and blood on the expression of intercellular adhesion molecule-1 (ICAM-1) in the retinal pigment epithelium. Methods The study included 22 patients who had experienced RRD within 1 month before the study and 14 patients with macular holes or pucker. SRF was collected during surgery to repair RRD and the vitreous was collected during vitrectomy. The SRF was cocultured with ARPE-19 cells with and without glucosamine sulphate (GS) and triamcinolone acetonide (TA). Blood from peripheral veins and blood components (red blood cells, platelet-poor plasma, and platelet-rich plasma) were also cocultured with ARPE-19 cells. Vitreous samples were cocultured with ARPE-19 cells in the control. The expression of ICAM-1 was detected and quantified by using flow cytometry. Results The expression of ICAM-1 in RPE cells was significantly higher (Po0.05) after 24-h incubation of 40% SRF with ARPE-19 cells. In addition, the expression of ICAM-1 in retinal pigment epithelium (RPE) cells significantly increased (Po0.01) when cocultured with blood and blood components. However, there were no differences (P40.05) in ICAM-1 expression when RPE cells were cocultured with or without GS or TA.Conclusions SRF and blood enhanced the expression of ICAM-1 in RPE cells in this study and the increased expression of ICAM-1 by SRF is not inhibited by GS or TA.

show abstract

Concentration of neuron-specific enolase and S100 protein in the subretinal fluid of rhegmatogenous retinal detachment

Abstract: Neuron-specific enolase (NSE) and S100 are known to be good markers of brain stress and, thus, are good markers of retinal stress.

Cited by 12 publications

References 25 publications

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

Immunohistochemical Investigation of S100 and NSE in Cases of Traumatic Brain Injury and Its Application for Survival Time Determination

Subretinal fluid from rhegmatogenous retinal detachment and blood induces the expression of ICAM-1 in the human retinal pigment epithelium (ARPE-19) in vitro

Contact Info

Product

Resources

About