Jinling Hospital Department of Neurology, Nanjing University, School of Medicine, Nanjing, 210002, PR China; Department of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221006, China.
Jinling Hospital Department of Neurology, Nanjing Medical University, Nanjing, 210002, PR China.
Biochem Biophys Res Commun. 2020 Jun 4;526(3):799-804. doi: 10.1016/j.bbrc.2020.03.159. Epub 2020 Apr 5.
AIM/BACKGROUND: CD99 participate in neutrophil infiltration after inflammatory events; however, despite the important role of inflammation in ischemic stroke, the role of CD99 in ischemic stroke remains unclear.
In the present study, we detected the protein expression of CD99, ICAM-1, and CD31 (PECAM-1) in oxygen-glucose deprivation (OGD)-induced bEnd.3 cells and neutrophils and explored the influence of HIF-1α and IL-1β on their expression. We also explored the role of CD99 in the OGD-induced transmigration of neutrophils.
Our results showed that OGD induction upregulated CD99 in bEnd.3 cells and that this effect could be abolished by the preadministration of IL-1β and was not mediated by HIF-1α. However, the activation of ICAM-1 by OGD remained activated with IL-1β treatment. No significant influence of IL-1β on OGD-induced CD31. Finally, we found a significant increase in infiltrated neutrophils after OGD induction compared with the control and OGD + anti-CD99 groups.
Our results indicated that CD99 mediates neutrophil infiltration and transmigration via OGD induction and thus constitutes a potential therapeutic target for anti-inflammatory treatment after ischemic stroke.
目的/背景：CD99 参与炎症事件后的中性粒细胞浸润；然而，尽管炎症在缺血性中风中起重要作用，但 CD99 在缺血性中风中的作用仍不清楚。
在本研究中，我们检测了氧葡萄糖剥夺（OGD）诱导的 bEnd.3 细胞和中性粒细胞中 CD99、ICAM-1 和 CD31（PECAM-1）的蛋白表达，并探讨了 HIF-1α 和 IL-1β 对其表达的影响。我们还探讨了 CD99 在 OGD 诱导的中性粒细胞迁移中的作用。
我们的结果表明，OGD 诱导上调了 bEnd.3 细胞中的 CD99，而这种作用可以被 IL-1β 预处理所消除，并且不受 HIF-1α 的介导。然而，OGD 诱导的 ICAM-1 的激活在 IL-1β 处理后仍然保持激活。IL-1β 对 OGD 诱导的 CD31 没有显著影响。最后，我们发现与对照组和 OGD+抗-CD99 组相比，OGD 诱导后中性粒细胞浸润显著增加。
我们的结果表明，CD99 通过 OGD 诱导介导中性粒细胞浸润和迁移，因此构成了缺血性中风后抗炎治疗的潜在治疗靶点。
