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Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 <t>DEPs</t> between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification <t>from</t> <t>HPA</t> database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.
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Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 <t>DEPs</t> between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification <t>from</t> <t>HPA</t> database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.
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Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 <t>DEPs</t> between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification <t>from</t> <t>HPA</t> database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.
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https://www.bioz.com/result/human protein atlas subcellular localization annotation/product/Human Protein Atlas
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Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 <t>DEPs</t> between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification <t>from</t> <t>HPA</t> database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.
Cell Atlas Subcellular Annotation, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 DEPs between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification from HPA database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Cerebrospinal Fluid Proteome Map Reveals Molecular Signatures of Reversible Cerebral Vasoconstriction Syndrome

doi: 10.1016/j.mcpro.2024.100794

Figure Lengend Snippet: Overview of the annotated brain cellular network or blood-brain barrier integrity and proposed pathological mechanism in RCVS patients. A , based on the 250 DEPs between RCVS patients and controls, we constructed the dysregulated biological processes and protein networks by integrating the protein–protein interactions and functional enrichment analysis with the tissue specificity classification from HPA database. Green color highlights brain-enriched proteins, while proteins that secreted to blood are labeled in pink color . Pain-related DEPs are presented in rhombuses . B , proposed pathogenesis of RCVS based on the RCVS-CSF proteome and literature knowledge. Susceptible subjects, when encountering precipitating factors, may exhibit sympathetic overactivity, endothelial dysfunction, and excessive oxidative stress. The vicious cycle of these components may lead to perivascular inflammation and peroxidative injury, which elicits the disruption of blood-brain barrier (BBB) and dysfunction of neurovascular units by damaging extracellular matrix (ECM), cell adhesions, and tight junctions. The disrupted BBB and dysfunctional neurovascular units may be phenotypically characterized by the clinical-radiological presentations within the RCVS disease spectrum, with accompanying proteins associated with neuronal injury or pain released into the CSF. CSF, cerebrospinal fluid; HPA, Human Protein Atlas; RVCS, reversible cerebral vasoconstriction syndrome.

Article Snippet: Thus, we annotated the composition details and potential sites of origin for all the DEPs by annotations from the Human Protein Atlas (HPA, v.19.3) ( ) to define the brain-specific proteins and proteins derived from blood.

Techniques: Construct, Protein-Protein interactions, Functional Assay, Labeling, Disruption