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Protein microarray analysis identifies key cytokines associated with malignant middle cerebral artery infarction
Zhonghe Zhou1, Jinghua Zhang1, Xiaoqiu Li1
1Department of Neurology General Hospital of Shen-Yang Military Region Shenyang China.
Insights
Researchers identified 10 key cytokines, including NCAM1 and LCN2, involved in malignant middle cerebral artery infarction (MMI). These molecules and the cytokine-cytokine receptor pathway may offer new diagnostic biomarkers and therapeutic targets for MMI.
Area of Science:
- Biochemistry
- Immunology
- Neuroscience
Background:
- Malignant middle cerebral artery infarction (MMI) is a severe form of stroke with high mortality.
- Understanding the molecular mechanisms, particularly the role of cytokines, is crucial for developing effective treatments.
Purpose of the Study:
- To identify differentially expressed cytokines in patients with MMI.
- To elucidate the regulatory mechanisms and pathways involved in MMI pathogenesis.
Main Methods:
- Serum samples from MMI and non-acute cerebral infarction (NACI) patients were analyzed using a Human Cytokine Antibody Array.
- Statistical analyses (t-test, Fisher's Exact Test) identified differentially expressed cytokines.
- Gene Ontology, pathway enrichment, and protein-protein interaction network analyses were performed.
Main Results:
- Ten differentially expressed cytokines were identified, with four upregulated (NCAM1, IGFBP-6, LYVE1, LCN2) and six downregulated (TGFB1, EGF, PDGFA, MMP-10, IL-27, CCL2).
- The cytokine-cytokine receptor interaction pathway was significantly enriched.
- These cytokines showed altered expression levels in MMI compared to NACI.
Conclusions:
- The identified cytokines (NCAM1, LCN2, IGFBP-6, LYVE1, MMP-10, IL-27, PDGFA, EGF, CCL2, TGFB1) are potentially involved in MMI development.
- The cytokine-cytokine receptor interaction pathway may play a significant role in MMI.
- These cytokines represent potential diagnostic biomarkers and therapeutic targets for MMI.
Introduction:
We aimed to explore potential cytokines involved in the malignant middle cerebral artery infarction (MMI) and elucidate their underlying regulatory mechanisms.
Methods:
We first developed a cytokine profile by Quantibody® Human Cytokine Antibody Array7000 using serum samples from eight patients with MMI and eight patients with non-acute cerebral infarction (NACI). The differentially expressed cytokines were then identified in patients with MMI using two-tailed Student's t-test and Fisher's Exact Test compared with patients with NACI. Gene Ontology and pathway enrichment analyses were performed using DAVID. Protein-protein interaction (PPI) network was constructed based on STRING database.
Results:
A total of 10 differentially expressed cytokines were identified from 320 unique inflammatory cytokines in serums. Among them, four cytokines, like NCAM1 (neural cell adhesion molecule 1), IGFBP-6 (insulin-like growth factor binding protein 6), LYVE1 (lymphatic vessel endothelial hyaluronan receptor 1), and LCN2 (Lipocalin2), were up-regulated, while another six cytokines, such as TGFB1 (transforming growth factor, beta 1, also known as LAP), EGF (epidermal growth factor), PDGFA (platelet-derived growth factor alpha polypeptide), MMP-10 (matrix metallopeptidase 10), IL-27 (interleukin 27), and CCL2 (chemokine (C-C motif) receptor 2), were down-regulated. Moreover, cytokine-cytokine receptor interaction pathway was significantly enriched.
Conclusions:
Our findings indicate that 10 differentially expressed cytokines, such as NCAM1, LCN2, IGFBP-6, LYVE1, MMP-10, IL-27, PDGFA, EGF, CCL2, and TGFB1 may participate in the development of MMI. Moreover, cytokine-cytokine receptor interaction pathway may be an important mechanism involved in this disease. These differentially expressed cytokines may serve as diagnostic biomarkers or drug targets for MMI.
