Decreased levels of cell-division cycle 42 (Cdc42) protein in peripheral lymphocytes from ischaemic stroke patients are associated with Golgi apparatus function
Objectives To investigate levels of cell-division cycle 42 (Cdc42) protein, and their relationship with Golgi apparatus function in peripheral lymphocytes, in patients following ischaemic stroke. Methods Patients with acute cerebral ischaemic stroke (within 24–72 h of the onset of focal neurological...
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Published in | Journal of international medical research Vol. 41; no. 3; pp. 642 - 653 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.06.2013
Sage Publications |
Subjects | |
Online Access | Get full text |
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Summary: | Objectives
To investigate levels of cell-division cycle 42 (Cdc42) protein, and their relationship with Golgi apparatus function in peripheral lymphocytes, in patients following ischaemic stroke.
Methods
Patients with acute cerebral ischaemic stroke (within 24–72 h of the onset of focal neurological symptoms) and healthy control subjects were enrolled in this prospective case–control study. The cellular location of Cdc42 in peripheral lymphocytes was demonstrated using immunofluorescence. Protein levels of Cdc42 and trans-golgi network protein 2 (TGN46) in peripheral lymphocytes were determined by immunocytochemical staining and Western blotting.
Results
A total of 38 patients with stroke and 38 control subjects were studied. The mean ± SD percentage of Cdc42-positive lymphocytes from patients with stroke was significantly lower than that in control subjects (39.53 ± 13.55% versus 66.61 ± 23.30%, respectively). Similar findings were demonstrated for TGN46. Cdc42 levels were positively correlated with TGN46 levels (r = 0.92).
Conclusions
Acute ischaemic stroke was associated with reduced levels of Cdc42 protein. These findings might lead to the development of drugs that could have therapeutic benefits in patients with acute ischaemic stroke. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0300-0605 1473-2300 1473-2300 |
DOI: | 10.1177/0300060513480093 |