Bone marrow-derived cells that home to acoustic deafened cochlea preserved their hematopoietic identity
Bone marrow-derived cells that home to acoustic deafened cochlea preserved their hematopoietic identity
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DOI：
10.1002/cne.21729
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发表时间：
2008-07-10
影响因子：
2.5
通讯作者：
Ruan, Runsheng
中科院分区：
文献类型：
--
作者：
Tan, Brian Tiong Gee;Lee, Myranda Mui Gek;Ruan, Runsheng
骨髓细胞（BMC）的高度可塑性促使我们测试其在内耳修复中的恢复可能性。我们的目的是确定这些细胞转分化成专门的耳蜗细胞类型后，声损伤和BMC动员的潜力。将来自绿色荧光蛋白（GFP）转基因小鼠的BMCs移植到致死辐射小鼠，并在3个月后进行声致聋。在单独的实验中，给予干细胞因子和粒细胞集落刺激因子以测试BMC动员对骨髓衍生细胞（BMDQ转分化）的影响。所有小鼠在骨髓移植后3个月表现出几乎完全的嵌合体。在声损伤后，观察到强大的BMDC迁移的耳蜗。GFP（+）细胞迁移在声聋后第一周最为显著，这些细胞在螺旋韧带、外淋巴室壁和利姆布斯区域显著聚集。大多数BMDC表达CD 45和CD 68，并被鉴定为巨噬细胞。在声致聋后的第一周，在螺旋韧带中也观察到基质衍生因子1（SDF-1）的上调。细胞因子治疗导致体循环中BMC动员增加。然而，任何干细胞祖细胞的存在或BMDC分化成表达耳蜗感觉，支持，纤维细胞，或神经元标记的任何细胞类型中未检测到的耳蜗。总之，我们已经证明了归巢能力的BMDCs的remaened耳蜗，这些细胞显示成熟的造血特性没有自发转分化的任何耳蜗细胞类型后，声创伤或骨髓动员。
The high degree of bone marrow cell (BMC) plasticity has prompted us to test its restoration possibility in inner ear repair. Our aim was to determine the potential of these cells to transdifferentiate into specialized cochlea cell types after acoustic injury and BMC mobilization. Lethally irradiated mice were transplanted with BMCs from green fluorescent protein (GFP) transgenic mice and subjected to acoustic deafening 3 months later. In a separate experiment, stem cell factor and granulocyte colony-stimulating factor were administered to test the effect of BMC mobilization on bone marrow-derived cell (BMDQ transdifferentiation. All mice showed almost complete chimerism 3 months after bone marrow transplantation. Upon acoustic trauma, robust BMDC migration was observed in the deafened cochlea. GFP(+) cell migration was most prominent during the first week after acoustic deafening, and these cells accumulated significantly at the spiral ligament, perilymphatic compartment walls, and limbus regions. Most of the BMDCs expressed CD45 and CD68 and were identified as macrophages. Upregulation of stromal-derived factor 1 (SDF-1) was also observed in the spiral ligament during the first week after acoustic deafening. Cytokine treatment resulted in increased BMC mobilization in the systemic circulation. However, the presence of any stem cell progenitors or the differentiation of BMDCs into any cell types expressing cochlea sensory, supporting, fibrocytic, or neuronal markers were not detected in the deafened cochlea. In conclusion, we have demonstrated the homing capability of BMDCs to the deafened cochlea, and these cells displayed mature hematopoietic properties without spontaneous transdifferentiation to any cochlea cell types after acoustic trauma or bone marrow mobilization.