4.6 Article

Changes in Adhesion and the Expression of Adhesion Molecules in PBMCs after Aneurysmal Subarachnoid Hemorrhage: Relation to Cerebral Vasospasm

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TRANSLATIONAL STROKE RESEARCH
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SPRINGER
DOI: 10.1007/s12975-023-01136-6

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Aneurysmal subarachnoid hemorrhage (aSAH); Peripheral blood mononuclear cells (PBMCs); Vasospasm (VSP); Adhesion to the endothelium; Adhesion molecules

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Aneurysmal subarachnoid hemorrhage (aSAH) is a neurovascular disease caused by blood leakage into the subarachnoid space after rupture of cerebral vessels. This study analyzed the changes in peripheral blood mononuclear cells (PBMCs) and their interaction with endothelium in aSAH patients, with a focus on adhesion and expression of adhesion molecules. The study found increased adhesion of PBMCs, particularly monocytes, in patients with aSAH, especially those who developed vasospasm. The expression of several adhesion molecules in T lymphocytes and monocytes was altered, providing insights for predicting vasospasm and improving treatment.
Aneurysmal subarachnoid hemorrhage (aSAH) is a neurovascular disease produced by extravasation of blood to the subarachnoid space after rupture of the cerebral vessels. After bleeding, the immune response is activated. The role of peripheral blood mononuclear cells (PBMCs) in this response is a current subject of research. We have analysed the changes in PBMCs of patients with aSAH and their interaction with the endothelium, focusing on their adhesion and the expression of adhesion molecules. Using an in vitro adhesion assay, we observed that the adhesion of PBMCs of patients with aSAH is increased. Flow cytometry analysis shows that monocytes increased significantly in patients, especially in those who developed vasospasm (VSP). In aSAH patients, the expression of CD162, CD49d, CD62L and CD11a in T lymphocytes and of CD62L in monocytes increased. However, the expression of CD162, CD43, and CD11a decreased in monocytes. Furthermore, monocytes from patients who developed arteriographic VSP had lower expression of CD62L. In conclusion, our results confirm that after aSAH, monocyte count and adhesion of PBMCs increase, especially in patients with VSP, and that the expression of several adhesion molecules is altered. These observations can help predict VSP and to improve the treatment of this pathology.

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