Characterization of chronic subdural hematoma fluid proteome
Related Experiment Video
Updated: May 11, 2026

Sample Preparation for Endopeptidomic Analysis in Human Cerebrospinal Fluid
Published on: December 4, 2017
Anna-Leena Heula1, Steffen Ohlmeier, Juha Sajanti
1‡Department of Clinical Medicine, Neurosurgery, University of Oulu, Oulu, Finland; §Department of Neurosurgery, Oulu University Hospital, Oulu, Finland; ¶Department of Clinical Medicine, Neurology, University of Oulu, Oulu, Finland; ‖Department of Neurology, Oulu University Hospital, Oulu, Finland; #Clinical Research Center, Oulu University Hospital, Oulu, Finland; **Proteomics Core Facility, Biocenter Oulu, Department of Biochemistry, University of Oulu, Oulu, Finland; ‡‡Department of Surgery and Department of Neurology, Seinäjoki Central Hospital, Seinäjoki, Finland.
Insights
This study analyzed chronic subdural hematoma (CSDH) fluid proteins, identifying key molecules involved in CSDH pathogenesis and inflammation. Findings reveal potential targets for future CSDH treatment strategies.
Area of Science:
- Neuroscience
- Biochemistry
- Medical Research
Background:
- Chronic subdural hematoma (CSDH) progression involves inflammation, but its protein composition and role in enlargement are unclear.
- Understanding CSDH fluid proteins is crucial for elucidating pathogenesis.
Purpose of the Study:
- To characterize CSDH fluid proteins.
- To compare CSDH fluid and serum protein profiles.
- To identify proteins involved in CSDH pathogenesis.
Main Methods:
- Proteomic analysis of CSDH fluid and serum from 5 patients.
- Utilized 2D gel electrophoresis, glycosylation staining, and mass spectrometry.
Main Results:
- Identified 57 different proteins in CSDH fluid, many glycosylated.
- Found elevated levels of carbonic anhydrase I, fibrinogen, hemoglobin, and TGF-β-induced protein ig-h3 in CSDH fluid.
- Observed decreased haptoglobin and altered complement C3/C4 components.
Conclusions:
- CSDH fluid is primarily blood-derived, involving coagulation and fibrinolysis.
- Carbonic anhydrase I, TGF-β-induced protein ig-h3, and complement system alterations are implicated in CSDH pathogenesis.
- Inflammation and fibrosis pathways present potential therapeutic targets.
Background:
Chronic subdural hematoma (CSDH) is commonly caused by head injury, but the progression of CSDH is recognized as an inflammatory process. The protein composition of the CSDH fluid has not been fully elucidated, nor has the contribution of its components to the enlargement of the hematoma cavity and to its chronic manifestation.
Objective:
To characterize the protein content of CSDH fluid and study the differences between CSDH fluid and serum to identify proteins putatively involved in the pathogenesis of CSDH.
Methods:
CSDH fluid and serum of 5 patients were investigated with 2-dimensional gel electrophoresis followed by glycosylation-specific fluorescence staining and mass spectrometry.
Results:
Two-dimensional gel electrophoresis revealed approximately 1100 protein spots in the CSDH fluid. We identified 213 spots representing 57 different proteins, most of which were glycosylated. The comparison with serum revealed 11 proteins with elevated levels in the CSDH fluid including carbonic anhydrase I, catalase, ferritin light chain, fibrinogen (α, β, γ), hemoglobin (α, β), malate dehydrogenase, peroxiredoxin 2, and transforming growth factor-β-induced protein ig-h3. The levels of haptoglobin and a fragment of complement C4 were decreased. Changes in spot positions were detected for apolipoprotein A1 and a fragment of complement C3.
Conclusion:
The hematoma fluid originates mainly from blood and the results suggest the involvement of coagulation and fibrinolysis cascades. However, proteins with a potential role in CSDH pathogenesis were detected including carbonic anhydrase I, transforming growth factor-β-induced protein ig-h3, and the altered components of the complement system. Inflammation and fibrosis indicate targets for further studies in the pathogenesis of CSDH.
Related Concept Videos
Cerebral Edema ll: Pathophysiology
Hemorrhagic Stroke ll: Pathophysiology