Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz.
Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main.
J Vis Exp. 2024 Sep 27(211). doi: 10.3791/67264.
Intestinal ischemia-reperfusion (I/R) injury is an acute condition characterized by tissue damage resulting from restricted blood flow to the mesenteric vessels, leading to both local and systemic pathologies with a poor prognosis. Both ischemia and reperfusion trigger a series of cellular and molecular responses, with inflammatory cells serving as key regulators of the pathology. These interactions with the ischemic endothelium are mediated by multiple adhesion receptors. Several animal models have been established to mimic this pathology and investigate the involved molecular pathways. In this study, a microsurgical model of I/R injury is combined with intravital microscopy to visualize leukocyte rolling, adhesion, and neutrophil extracellular trap (NET) formation. This model is applied to transgenic mice deficient in endothelial PAR1 (F2r) to assess the impact of PAR1 on leukocyte rolling and NET formation 1 h after ischemia and immediately following reperfusion. In vivo, Acridine Orange leukocyte staining was employed, and NETs were visualized using a nucleic acid stain. Interestingly, reduced leukocyte adhesion and NET formation were observed in mice lacking the endothelial PAR1 receptor. This model enables the in vivo analysis of key regulators involved in I/R injury.
肠缺血再灌注(I/R)损伤是一种急性病症,其特征是肠系膜血管血流受限导致组织损伤,从而引发局部和全身病理变化,预后不良。缺血和再灌注均会引发一系列细胞和分子反应,炎症细胞是病理变化的关键调节因子。这些与缺血内皮细胞的相互作用是通过多种黏附受体介导的。已经建立了几种动物模型来模拟这种病理变化,并研究涉及的分子途径。在这项研究中,将 I/R 损伤的显微外科模型与活体显微镜结合使用,以可视化白细胞滚动、黏附和中性粒细胞胞外陷阱(NET)的形成。该模型应用于内皮细胞 PAR1 缺陷的转基因小鼠(F2r),以评估 PAR1 在缺血后 1 小时和再灌注后即刻对白细胞滚动和 NET 形成的影响。在体内,采用吖啶橙白细胞染色,并使用核酸染色来可视化 NET。有趣的是,缺乏内皮细胞 PAR1 受体的小鼠观察到白细胞黏附和 NET 形成减少。该模型可用于体内分析 I/R 损伤中涉及的关键调节因子。