Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke.
Microparticle Shedding from Neural Progenitor Cells and Vascular Compartment Cells Is Increased in Ischemic Stroke.
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DOI：
10.1371/journal.pone.0148176
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Badimon L
中科院分区：
文献类型：
--
作者：
Chiva-Blanch G;Suades R;Crespo J;Peña E;Padró T;Jiménez-Xarrié E;Martí-Fàbregas J;Badimon L
缺血性中风已被证明会诱导血小板和内皮微粒脱落，但中风是否会诱导额外的血液和血管室细胞中的微粒脱落尚不清楚。神经前体细胞已被证明可以替代脑损伤部位垂死的神经元；然而，神经前体细胞的激活是否与微粒脱落有关，以及这种激活是否能长期维持并与中风类型和严重程度相关仍然未知。我们分析了急性缺血性中风后神经前体细胞以及血液和血管室细胞微粒脱落的情况。中风发作后 48 小时内的 44 名患者被纳入研究。中风后 3-7 天评估脑损伤大小。在中风发作时以及 7 天和 90 天时，通过流式细胞术分析来自神经前体细胞以及血液和血管室细胞（血小板、内皮细胞、红细胞、白细胞、淋巴细胞、单核细胞和平滑肌细胞）的循环微粒。 44 名年龄匹配、无血管疾病记录的高心血管风险受试者被用作对照。与高心血管风险对照相比，患者在中风发作时以及 7 天和 90 天后表现出更高数量的神经前体细胞以及所有血液和血管室细胞衍生的微粒。 90 天时，与中风发作时的水平相比，神经前体细胞衍生的微粒减少，平滑肌细胞衍生的微粒增加，但仅限于中风引起的脑损伤最严重的患者。中风会增加血液和血管室细胞以及神经前体细胞微粒的脱落，这种效应会在缺血事件后长期维持长达 90 天。这些结果表明，中风诱导全身血液和血管细胞活化以及中风后神经元细胞修复过程的启动。较大的脑损伤与影响血管平滑肌细胞的较深的血管损伤相关。
Ischemic stroke has shown to induce platelet and endothelial microparticle shedding, but whether stroke induces microparticle shedding from additional blood and vascular compartment cells is unclear. Neural precursor cells have been shown to replace dying neurons at sites of brain injury; however, if neural precursor cell activation is associated to microparticle shedding, and whether this activation is maintained at long term and associates to stroke type and severity remains unknown. We analyzed neural precursor cells and blood and vascular compartment cells microparticle shedding after an acute ischemic stroke. Forty-four patients were included in the study within the first 48h after the onset of stroke. The cerebral lesion size was evaluated at 3–7 days of the stroke. Circulating microparticles from neural precursor cells and blood and vascular compartment cells (platelets, endothelial cells, erythrocytes, leukocytes, lymphocytes, monocytes and smooth muscle cells) were analyzed by flow cytometry at the onset of stroke and at 7 and 90 days. Forty-four age-matched high cardiovascular risk subjects without documented vascular disease were used as controls. Compared to high cardiovascular risk controls, patients showed higher number of neural precursor cell- and all blood and vascular compartment cell-derived microparticles at the onset of stroke, and after 7 and 90 days. At 90 days, neural precursor cell-derived microparticles decreased and smooth muscle cell-derived microparticles increased compared to levels at the onset of stroke, but only in those patients with the highest stroke-induced cerebral lesions. Stroke increases blood and vascular compartment cell and neural precursor cell microparticle shedding, an effect that is chronically maintained up to 90 days after the ischemic event. These results show that stroke induces a generalized blood and vascular cell activation and the initiation of neuronal cell repair process after stroke. Larger cerebral lesions associate with deeper vessel injury affecting vascular smooth muscle cells.