Protein microarray analysis identifies key cytokines associated with malignant middle cerebral artery infarction

Zhou, Zhonghe; Zhang, Jinghua; Li, Xiaoqiu; Xia, Cheng; Han, Yaling; Chen, Hui‐Sheng

doi:10.1002/brb3.746

Cited by 15 publications

(13 citation statements)

References 44 publications

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“…This aspect is of major importance for the usability of LCN2 as a biomarker to predict disease outcome or severity as suggested by Hochmeister et al [10]. In stroke, blood levels of LCN2 correlate with disease severity and unfavorable clinical outcome [10,43,44]. In a vascular dementia model, astrocyte-derived LCN2 mediated cognitive impairment and hippocampal damage [45].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke

Taklimie

Gasterich

Scheld

et al. 2019

IJMS

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Ischemic stroke causes rapid hypoxic damage to the core neural tissue which is followed by graded chronological tissue degeneration in the peri-infarct zone. The latter process is mainly triggered by neuroinflammation, activation of inflammasomes, proinflammatory cytokines, and pyroptosis. Besides microglia, astrocytes play an important role in the fine-tuning of the inflammatory network in the brain. Lipocalin-2 (LCN2) is involved in the control of innate immune responses, regulation of excess iron, and reactive oxygen production. In this study, we analyzed LCN2 expression in hypoxic rat brain tissue after ischemic stroke and in astrocyte cell cultures receiving standardized hypoxic treatment. Whereas no LCN2-positive cells were seen in sham animals, the number of LCN2-positive cells (mainly astrocytes) was significantly increased after stroke. In vitro studies with hypoxic cultured astroglia revealed that LCN2 expression is significantly increased after only 2 h, then further increased, followed by a stepwise decline. The expression pattern of several proinflammatory cytokines mainly followed that profile in wild type (WT) but not in cultured LCN2-deficient astrocytes. Our data revealed that astrocytes are an important source of LCN2 in the peri-infarct region under hypoxic conditions. However, we must also stress that brain-intrinsic LCN2 after the initial hypoxia period might come from other sources such as invaded immune cells and peripheral organs via blood circulation. In any case, secreted LCN2 might have an influence on peripheral organ functions and the innate immune system during brain hypoxia.

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Section: Discussionmentioning

confidence: 99%

Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke

Taklimie

Gasterich

Scheld

et al. 2019

IJMS

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“…Its treatment with aspirin and clopidogrel is one of the commonly used methods. As a predictive diagnostic index for cerebral infarction (17), the expression level of relevant cytokines is upregulated in the brain after stroke, and the brain plug area is enlarged by infiltrating ischemic areas (18).…”

Section: Discussionmentioning

confidence: 99%

Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its effect on serum hs-CRP, sICAM-1 and TNF-α

Wang

et al. 2019

Exp Ther Med

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Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its influence on serum high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-α (TNF-α) were explored. Ninety patients with acute cerebral infarction treated in Yidu Central Hospital of Weifang were analyzed, and those treated with aspirin alone were group A (n=40) and those treated with aspirin and clopidogrel were group B (n=50) according to the different treatment plans. The NIHSS score, total effective rate and incidence rate of adverse reactions after treatment and admission were compared between the two groups. The expression level of hs-CRP was detected by enzymelinked immunosorbent assay, and the expression levels of sICAM-1 and TNF-α were analyzed by radioimmunoassay before treatment and three weeks after surgery, respectively, and they were analyzed and compared. After treatment, the total effective rate of patients in group B was significantly higher than that of group A (P<0.05). The general clinical baseline information, NIHSS score, and the expression levels of hs-CRP, sICAM-1, and TNF-α of patients in group B were significantly improved after treatment compared with those before treatment (P<0.05), and the NIHSS score and the expression levels of serum hs-CRP, sICAM-1, and TNF-α of those in group B were significantly lower than those in group A (P<0.05). Combination therapy of aspirin and clopidogrel can improve cerebral infarction effectively, and inhibit the expression levels of hs-CRP, sICAM-1 and TNF-α more effectively than aspirin alone.

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“…[24], was identified as a potential Research Shuli Liang MD pathway component of PNKD pathogenic mechanism. Another potential biomarker in CSF of PNKD diagnosis was PDGFA, which regulates the proliferation and self-renewal in stem cells such as skin adipocyte stem cell and glioblastoma stem cell [25,26],and may participate in the development of malignant middle cerebral artery infarction (MMI) [27].…”

Section: Discussionmentioning

confidence: 99%

Indentification of Novel Biomarkers for Paroxysmal Non- Kinesigenic Dyskinesia Diagnosis Via Cerebrospinal Fluid and Plasma Proteomic Analysis

Cui¹,

Yu²,

Zhang³

et al. 2018

Neuropsychiatry

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Purpose: Paroxysmal non-kinesigenic dyskinesia (PNKD) is a rare autosomal dominant movement disorder characterized by spontaneous attacks. The purpose of this study was to find and analyze the differentially expressed proteins between PNKD patients and their healthy family members with matched age and gender, thus providing potential biomarkers for early diagnosis of patients with PNKD. Methods: Four PNKD patients and four healthy family members were selected. Isobaric tags for relative and absolute quantitation (iTRAQ) coupled with LC-MS/MS were used to identify the differential proteins obtained from CSF and plasma of PNDK patients and healthy family members. Bioinformatic analyses of differential proteins were performed included Gene Ontology (GO) enrichment, pathway enrichment and protein-protein interaction network analysis. Results: A total of 1242 and 512 unique proteins were identified in CSF and plasma respectively. The numbers of proteins that were differentially expressed between PNKD patients and their healthy family members were 42 in CSF and 57 in plasma respectively. Proteins that were differentially expressed were further analyzed based on bioinformatics. Two differentially expressed proteins in the CSF, CALML5 and PDGFA, and one in the plasma, ACTB, showed close links with the PNKD protein in the protein-protein interaction network. Conclusion: CALML5 and PDGFA in the CSF and ACTB in the plasma may take part in PNKD pathogenesis and act as the potential biomarkers for PNKD diagnosis.

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Protein microarray analysis identifies key cytokines associated with malignant middle cerebral artery infarction

Cited by 15 publications

References 44 publications

Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke

Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke

Clinical efficacy of aspirin combined with clopidogrel in treating cerebral infarction and its effect on serum hs-CRP, sICAM-1 and TNF-α

Indentification of Novel Biomarkers for Paroxysmal Non- Kinesigenic Dyskinesia Diagnosis Via Cerebrospinal Fluid and Plasma Proteomic Analysis

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