期刊
NEUROSURGERY
卷 73, 期 2, 页码 317-331出版社
OXFORD UNIV PRESS INC
DOI: 10.1227/01.neu.0000430323.24623.de
关键词
Craniocerebral trauma; Fibrinolysis; Fibrosis; Glycosylation; Inflammation
资金
- Oulu University Hospital
- Maire Taponen Foundation
- National Graduate School of Clinical Investigation (CLIGS)
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 (alpha, beta, gamma), hemoglobin (alpha, beta), malate dehydrogenase, peroxiredoxin 2, and transforming growth factor-beta-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-beta-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.
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