Human Traumatic Brain Injury Results in Oligodendrocyte Death and Increases the Number of Oligodendrocyte Progenitor Cells
Human Traumatic Brain Injury Results in Oligodendrocyte Death and Increases the Number of Oligodendrocyte Progenitor Cells
复制标题
DOI：
10.1093/jnen/nlw025
复制
发表时间：
2016-06-01
影响因子：
3.2
通讯作者：
Marklund, Niklas
中科院分区：
文献类型：
--
作者：
Flygt, Johanna;Gumucio, Astrid;Marklund, Niklas
少突胶质细胞(OL)的死亡可能导致白质病理，这是创伤性脑损伤(TBI)患者网络功能障碍和持续性认知问题的常见原因。少突胶质前体细胞(OPC)在成体中枢神经系统中持续存在，并可能替代死亡的OCs。对10例重型颅脑损伤患者(年龄51.7±18.5岁)伤后60.6±75小时(4~192小时)因严重脑挫伤和/或局灶性脑肿胀而手术切除的脑组织标本进行OPC和OL死亡的免疫组织化学分析。对照组脑组织取自5例年龄匹配的无中枢神经系统疾病患者。TUNEL和CC1联合标记用于分析损伤脑组织中增加的凋亡OL(p<；0.05)，与从损伤到手术的时间无关。OPC标记物Opol2、A2B5、NG2和PDGFR-α被使用。与单一标记的Orig2、A2B5、NG2和PDGFR-α阳性细胞的数量相比，联合标记细胞的数量在颅脑损伤标本中增加(p<；0.05)；这与从损伤到手术的时间呈负相关(r=-0.8，p<；0.05)。这些结果表明，严重的局灶性人脑损伤导致损伤后OL死亡和OPC增加，这可能影响脑损伤后的脑白质功能。
Oligodendrocyte (OL) death may contribute to white matter pathology, a common cause of network dysfunction and persistent cognitive problems in patients with traumatic brain injury (TBI). Oligodendrocyte progenitor cells (OPCs) persist throughout the adult CNS and may replace dead OLs. OL death and OPCs were analyzed by immunohistochemistry of human brain tissue samples, surgically removed due to life-threatening contusions and/or focal brain swelling at 60.6 +/- 75 hours (range 4-192 hours) postinjury in 10 severe TBI patients (age 51.7 +/- 18.5 years). Control brain tissue was obtained postmortem from 5 age-matched patients without CNS disorders. TUNEL and CC1 co-labeling was used to analyze apoptotic OLs, which were increased in injured brain tissue (p < 0.05), without correlation with time from injury until surgery. The OPC markers Olig2, A2B5, NG2, and PDGFR-alpha were used. In contrast to the number of single-labeled Olig2, A2B5, NG2, and PDGFR-alpha-positive cells, numbers of Olig2 and A2B5 co-labeled cells were increased in TBI samples (p < 0.05); this was inversely correlated with time from injury to surgery (r = -0.8, p < 0.05). These results indicate that severe focal human TBI results in OL death and increases in OPCs postinjury, which may influence white matter function following TBI.