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首页> 外文期刊>Brain research >Axl-/- mice have delayed recovery and prolonged axonal damage following cuprizone toxicity.
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Axl-/- mice have delayed recovery and prolonged axonal damage following cuprizone toxicity.

机译：Axl //-小鼠在铜氮磷中毒后具有延迟的恢复和延长的轴突损伤。

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摘要

Activation of the receptor tyrosine kinase Axl recruits signaling molecules that regulate cell growth and survival. To evaluate Axl's role in brain during cuprizone toxicity, mice were fed cuprizone and evaluated at 3-, 4-, and 6-week cuprizone treatment and 3- and 5-week post-cuprizone withdrawal. At 4-week cuprizone treatment, the corpora callosa of wildtype (WT) mice had robust Oil Red O+ staining indicative of ongoing phagocytosis. Axl-/- mice had minimal Oil Red O+ staining, fewer microglia, and significantly more TUNEL+/ASPA+ mature oligodendrocytes than the WT. At 6-week cuprizone treatment, there was significantly more Oil Red O+ staining in the Axl-/- corpora callosa than in the WT indicating a lag in the clearance of cellular and myelin debris. Relative to WT mice, there were fewer mature oligodendrocytes and significantly more SMI-32+ axons at 3-week post-cuprizone withdrawal, indicative of axonal damage in the Axl-/- corpora callosa. Electron microscopy determined that at 3-week post-cuprizone withdrawal the number of dystrophic axons and axons containing autophagosome-like vacuoles/mouse was increased in the Axl-/- mice relative to the WT mice. In Axl-/- corpora callosa, 5-week post-cuprizone withdrawal, the number of mature oligodendrocytes was comparable to the WT mice, but axons in the Axl-/- mice were SMI-32+, suggesting that Axl-/- mice have delayed clearance of apoptotic oligodendrocytes and myelin debris resulting in prolonged axonal damage and recovery from cuprizone toxicity.
机译：受体酪氨酸激酶Axl的激活募集了调节细胞生长和存活的信号分子。为了评估在cuprizone毒性期间Axl在大脑中的作用，给小鼠喂食cuprizone，并在3、4和6周cuprizone治疗以及3和5周后停用cuprizone进行评估。在4周的铜酮治疗中，野生型（WT）小鼠的体具有强烈的油红O +染色，表明正在进行吞噬作用。与WT相比，Axl-/-小鼠的油红O +染色极少，小胶质细胞少，并且TUNEL + / ASPA +成熟少突胶质细胞明显更多。在6周的铜酮治疗中，Axl-/-体的油红O +染色明显多于WT，这表明细胞和髓磷脂碎片的清除滞后。相对于WT小鼠，停药后3周成熟的少突胶质细胞少，SMI-32 +轴突明显多，表明轴突损伤了Axl //-体。电子显微镜检查确定，在停药后三周，相对于WT小鼠，营养不良性轴突和含有自噬体样空泡/小鼠的轴突的数量增加了。在Axl-/-corpcorp愈伤组织撤药5周后，成熟的少突胶质细胞的数量与WT小鼠相当，但Axl-/-小鼠的轴突为SMI-32 +，表明Axl-/-小鼠具有延缓凋亡性少突胶质细胞和髓磷脂碎片清除的作用，从而导致轴突损伤时间延长，并从铜酮毒性中恢复过来。

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