Robinson Bobby Darnell, Tharakan Binu, Lomas Angela, Wiggins-Dohlvik Katie, Alluri Himakarnika, Shaji Chinchusha Anasooya, Jupiter Daniel, Isbell Claire Larson
Department of Surgery, Baylor Scott and White Medical CenterTempleTexas.
School of Medicine, Texas A&M Health Sciences CenterTempleTexas.
Proc (Bayl Univ Med Cent). 2020 Apr 2;33(2):199-204. doi: 10.1080/08998280.2020.1727706. eCollection 2020 Apr.
Blood-brain barrier breakdown and associated vascular hyperpermeability leads to vasogenic edema in traumatic brain injury (TBI). Tight junctions maintain blood-brain barrier integrity; their disruption in TBI holds significant promise for diagnosis and treatment. A controlled cortical impactor was used for TBI in mouse studies. Blood was collected 1 h after injury and sent for antibody microarray analysis. Twenty human subjects with radiographic evidence of TBI were enrolled and blood collected within 48 h of admission. Control subjects were individuals with nontrauma diagnoses. The subjects were matched by age and gender. Enzyme-linked immunosorbent assays were performed on each TBI and control sample for tight junction-associated proteins (TJPs), inflammatory markers, and S100β. Plasma was used to conduct in vitro monolayer permeability studies with human brain endothelial cells. S100β and the TJP occludin were significantly elevated in TBI plasma in both the murine and human studies. Monolayer permeability studies showed increased hyperpermeability in TBI groups. Plasma from TBI subjects increases microvascular hyperpermeability in vitro. TJPs in the blood may be a potential biomarker for TBI.
血脑屏障破坏及相关的血管通透性增加会导致创伤性脑损伤（TBI）中的血管源性水肿。紧密连接维持血脑屏障的完整性；其在TBI中的破坏对诊断和治疗具有重要意义。在小鼠研究中，使用可控皮质撞击器造成TBI。损伤后1小时采集血液并送去进行抗体微阵列分析。招募了20名有TBI影像学证据的人类受试者，并在入院后48小时内采集血液。对照受试者为非创伤性诊断的个体。受试者按年龄和性别匹配。对每个TBI和对照样本进行酶联免疫吸附测定以检测紧密连接相关蛋白（TJPs）、炎症标志物和S100β。使用血浆对人脑内皮细胞进行体外单层通透性研究。在小鼠和人类研究中TBI血浆中的S100β和TJP封闭蛋白均显著升高。单层通透性研究显示TBI组的通透性增加。TBI受试者的血浆在体外增加微血管通透性。血液中的TJPs可能是TBI的潜在生物标志物。
