Gołąb-Janowska Monika, Paczkowska Edyta, Machaliński Bogusław, Kotlęga Dariusz, Meller Agnieszka, Safranow Krzysztof, Maj Michał, Nowacki Przemysław
Department of Neurology, Pomeranian Medical University, Szczecin, Poland.
Department of General Pathology, Pomeranian Medical University, Szczecin, Poland.
Stem Cells Int. 2018 Apr 26;2018:2827580. doi: 10.1155/2018/2827580. eCollection 2018.
Therapeutic neovascularization might represent an important strategy to salvage tissue after ischemia. Circulating bone marrow-derived endothelial progenitor cells (EPCs) were previously shown to augment the neovascularization of ischemic tissue. Angiotensin-converting enzyme inhibitors (ACEIs) might modulate EPC mobilization. We evaluated populations of circulating stem cells and early EPCs in acute ischemic stroke (AIS) patients and the effect of ACEI on circulating EPCs in these patients with respect to aspects of stroke pathogenesis.
We studied 43 AIS patients (group I), comprising 33 treated with ACEI (group Ia) and 10 untreated (group Ib). Risk factor controls (group II) included 22 subjects. EPCs were measured by flow cytometry.
In AIS patients, the number of circulating stem cells and early EPCs upon admission was similar to that in control group individuals. There were no significant differences in the numbers of stem cells and early EPCs over subsequent days after AIS. There were also no significant differences in stem cell and early EPC numbers over the first 3 days between group Ia and group Ib. However, on day 7, these numbers were significantly higher in group Ib than in group Ia ( < 0.05). In AIS patients chronically treated with ACEI, there was a negative correlation between CD133 cell number and neurological deficit on the first, third, and seventh days ( < 0.005).
An increased number of circulating stem cells and early EPCs were not observed in stroke patients chronically treated with ACEI. In patients chronically treated with ACEI, a significant correlation was observed between decreased neurological deficit and higher levels of CD133 cells; this could be due to the positive influence of these cells on the regeneration of the endothelium and improved circulation in the ischemic penumbra.
治疗性血管新生可能是缺血后挽救组织的一项重要策略。先前研究表明,循环血中的骨髓源性内皮祖细胞(EPC)可增强缺血组织的血管新生。血管紧张素转换酶抑制剂(ACEI)可能调节EPC的动员。我们评估了急性缺血性卒中(AIS)患者循环干细胞和早期EPC的数量,以及ACEI对这些患者循环EPC的影响及其与卒中发病机制的关系。
我们研究了43例AIS患者(I组),其中33例接受ACEI治疗(Ia组),10例未接受治疗(Ib组)。危险因素对照组(II组)包括22名受试者。通过流式细胞术检测EPC。
在AIS患者中,入院时循环干细胞和早期EPC的数量与对照组个体相似。AIS发病后的后续几天,干细胞和早期EPC的数量无显著差异。Ia组和Ib组在发病后的前3天,干细胞和早期EPC的数量也无显著差异。然而,在第7天,Ib组的这些细胞数量显著高于Ia组(<0.05)。在长期接受ACEI治疗的AIS患者中,第1天、第3天和第7天CD133细胞数量与神经功能缺损呈负相关(<0.005)。
长期接受ACEI治疗的卒中患者未观察到循环干细胞和早期EPC数量增加。在长期接受ACEI治疗的患者中,神经功能缺损减轻与CD133细胞水平升高之间存在显著相关性;这可能是由于这些细胞对内皮再生的积极影响以及改善了缺血半暗带的血液循环。