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Research Article
Weiwei Qin
Qingdao University
Corresponding Author
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Background
Cerebral ischemia-reperfusion (I/R) injury is the leading cause of death in severe hypotension caused by cardiac arrest, drowning, and excessive blood loss. Urine can sensitively reflect pathophysiological changes in the brain even at an early stage.
Methods
In this study, a rat model of global cerebral I/R injury was established via Pulsinelli’s four-vessel occlusion (4-VO) method. The proteomics techniques of data-independent acquisition (DIA) and parallel reaction monitoring (PRM) were applied to profile the urinary proteome. The differentially expressed proteins were subjected to Gene Ontology (GO) and protein-protein interaction (PPI) analysis.
Results
One hundred and sixty-four proteins significantly differed in the 4-VO rat urine samples compared to the control samples (1.5-fold change, p<0.05). GO analysis showed that the acute-phase response, the ERK1 and ERK2 cascade, endopeptidase activity, blood coagulation, and angiogenesis were overrepresented. After PRM validation, fifteen differentially expressed proteins were identified, and their expression was consistent with the DIA quantification. The abundance of FGG, COMP, TFF2, and HG2A was significantly changed only at 12 h after I/R injury. APOE, FAIM3, FZD1, IL1R2, UROK and CD48 were upregulated only at 48 h after I/R injury. KNG1, CATZ, PTGDS, PRVA and HEPC showed an overall trend of upregulation or downregulation at 12 and 48 h after I/R injury, reflecting the progression of cerebral I/R injury.
Conclusion
In this study, fifteen differentially expressed urinary proteins were identified and validated in a 4-VO rat model. Eight of these proteins were reported to be associated with cerebral I/R injury. These findings provide important clues to inform the monitoring of cerebral I/R injury and further the current understanding of its molecular biological mechanisms.
Keywords
global cerebral ischemia-reperfusion, 4-VO rats, urine, proteomics
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No competing interests reported.
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This preprint is under consideration at Scientific Reports. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Weiwei Qin
Qingdao University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 08 Nov, 2021
No community comments so far
Editor invited
On 02 Nov, 2021
Submission checks complete
On 02 Nov, 2021
First submitted
On 22 Oct, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Cerebral ischemia-reperfusion (I/R) injury is the leading cause of death in severe hypotension caused by cardiac arrest, drowning, and excessive blood loss. Urine can sensitively reflect pathophysiological changes in the brain even at an early stage.
Methods
In this study, a rat model of global cerebral I/R injury was established via Pulsinelli’s four-vessel occlusion (4-VO) method. The proteomics techniques of data-independent acquisition (DIA) and parallel reaction monitoring (PRM) were applied to profile the urinary proteome. The differentially expressed proteins were subjected to Gene Ontology (GO) and protein-protein interaction (PPI) analysis.
Results
One hundred and sixty-four proteins significantly differed in the 4-VO rat urine samples compared to the control samples (1.5-fold change, p<0.05). GO analysis showed that the acute-phase response, the ERK1 and ERK2 cascade, endopeptidase activity, blood coagulation, and angiogenesis were overrepresented. After PRM validation, fifteen differentially expressed proteins were identified, and their expression was consistent with the DIA quantification. The abundance of FGG, COMP, TFF2, and HG2A was significantly changed only at 12 h after I/R injury. APOE, FAIM3, FZD1, IL1R2, UROK and CD48 were upregulated only at 48 h after I/R injury. KNG1, CATZ, PTGDS, PRVA and HEPC showed an overall trend of upregulation or downregulation at 12 and 48 h after I/R injury, reflecting the progression of cerebral I/R injury.
Conclusion
In this study, fifteen differentially expressed urinary proteins were identified and validated in a 4-VO rat model. Eight of these proteins were reported to be associated with cerebral I/R injury. These findings provide important clues to inform the monitoring of cerebral I/R injury and further the current understanding of its molecular biological mechanisms.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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