Mature and Myelinating Oligodendrocytes Are Specifically Vulnerable to Mild Fluid Percussion Injury in Mice.
Mature and Myelinating Oligodendrocytes Are Specifically Vulnerable to Mild Fluid Percussion Injury in Mice.
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DOI：
10.1089/neur.2023.0037
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发表时间：
2023
影响因子：
2.4
通讯作者：
Kim, Haesun A.
中科院分区：
文献类型：
--
作者：
Adams, Alexandra A.;Wood, Teresa L.;Kim, Haesun A.
髓磷脂丢失和少突胶质细胞死亡在创伤性脑损伤（TBI）患者以及中重度TBI后的实验动物模型中都有充分的记录。相比之下，轻度TBI （mTBI）不一定导致髓磷脂丢失或少突胶质细胞死亡，但会导致髓磷脂的结构改变。为了更深入地了解mTBI对成年大脑少突胶质细胞谱系的影响，我们对小鼠进行了轻度外侧液体撞击损伤（mFPI），并使用多种少突胶质细胞谱系标记物(血小板衍生生长因子受体[PDGFR]-α，谷胱甘肽s -转移酶[GST]-π， CC1，乳腺癌扩增序列1 [BCAS1]，髓鞘碱性蛋白[MBP]，髓磷脂相关糖蛋白（MAG）、蛋白脂蛋白（PLP）和FluoroMyelin™)。分析了与撞击部位相关的胼胝体的两个区域：撞击部位附近（病灶）和前方（远端）的区域。mFPI不会导致局灶或远端胼胝体少突胶质细胞死亡，也不会影响少突胶质细胞前体（PDGFR-α+）和GST-π+少突胶质细胞数量。在局灶性而非远端胼胝体中，mFPI导致CC1+和BCAS1+活性髓鞘少突胶质细胞减少，并降低了FluoroMyelin强度，但未改变髓鞘蛋白表达（MBP、PLP和MAG）。在病灶区和远端区，甚至在没有明显轴突损伤的区域，都观察到节点-副阳极组织的破坏和Nav1.6+节点的丢失。总之，我们的研究显示成熟和髓鞘少突胶质细胞对mFPI的反应存在区域差异。此外，mFPI对节点-副阳极组织产生广泛影响，影响距离损伤部位近或远的区域。
Myelin loss and oligodendrocyte death are well documented in patients with traumatic brain injury (TBI), as well as in experimental animal models after moderate-to-severe TBI. In comparison, mild TBI (mTBI) does not necessarily result in myelin loss or oligodendrocyte death, but causes structural alterations in the myelin. To gain more insight into the impact of mTBI on oligodendrocyte lineage in the adult brain, we subjected mice to mild lateral fluid percussion injury (mFPI) and characterized the early impact (1 and 3 days post-injury) on oligodendrocytes in the corpus callosum using multiple oligodendrocyte lineage markers (platelet-derived growth factor receptor [PDGFR]-α, glutathione S-transferase [GST]-π, CC1, breast carcinoma-amplified sequence 1 [BCAS1], myelin basic protein [MBP], myelin-associated glycoprotein [MAG], proteolipid protein [PLP], and FluoroMyelin™). Two regions of the corpus callosum in relation to the impact site were analyzed: areas near (focal) and anterior (distal) to the impact site. mFPI did not result in oligodendrocyte death in either the focal or distal corpus callosum, nor impact on oligodendrocyte precursors (PDGFR-α+) and GST-π+ oligodendrocyte numbers. In the focal but not distal corpus callosum, mFPI caused a decrease in CC1+ as well as BCAS1+ actively myelinating oligodendrocytes and reduced FluoroMyelin intensity without altering myelin protein expression (MBP, PLP, and MAG). Disruption in node-paranode organization and loss of Nav1.6+ nodes were observed in both the focal and distal regions, even in areas without obvious axonal damage. Altogether, our study shows regional differences in mature and myelinating oligodendrocyte in response to mFPI. Further, mFPI elicits a widespread impact on node-paranode organization that affects regions both close to and remotely located from the site of injury.
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影响因子：
17.1
作者：
Fard MK;van der Meer F;Sánchez P;Cantuti-Castelvetri L;Mandad S;Jäkel S;Fornasiero EF;Schmitt S;Ehrlich M;Starost L;Kuhlmann T;Sergiou C;Schultz V;Wrzos C;Brück W;Urlaub H;Dimou L;Stadelmann C;Simons M
通讯作者：
Simons M
影响因子：
3.2
作者：
Flygt, Johanna;Gumucio, Astrid;Marklund, Niklas
通讯作者：
Marklund, Niklas
影响因子：
5.3
作者：
Reeves, TM;Phillips, LL;Povlishock, JT
通讯作者：
Povlishock, JT
影响因子：
4.7
作者：
Kim, Jihyun;Elias, Anthony;Kim, Haesun A.
通讯作者：
Kim, Haesun A.
影响因子：
1.2
作者：
Lotocki G;de Rivero Vaccari J;Alonso O;Molano JS;Nixon R;Dietrich WD;Bramlett HM
通讯作者：
Bramlett HM