Rescue of retinal ganglion cells from axotomy-induced apoptosis through TRK oncogene transfer.
Rescue of retinal ganglion cells from axotomy-induced apoptosis through TRK oncogene transfer.
复制标题
通过 TRK 癌基因转移拯救视网膜神经节细胞免于轴切术诱导的细胞凋亡。
DOI：
10.1097/00001756-199810050-00008
复制
发表时间：
1998
期刊：
影响因子：
1.7
通讯作者：
Sharma,SC
中科院分区：
文献类型：
--
作者：
GarciaValenzuela,E;Sharma,SC
轴突损伤后，中枢神经元通过程序性细胞死亡而死亡。通过特异性基因转移修饰细胞内机制可能提供一种生存机制。在这里，我们提出了拯救大鼠视网膜神经节细胞（RGCs）通过基因转移的TRK癌基因。在上级丘视轴突终末处给予质粒DNA导致逆行转运至其索马并显著表达外源DNA。使用这种转染方法，将含有TRK癌基因的质粒引入RGC中。质粒注射后三天，切断视神经。TRK癌基因转染诱导轴突切断的神经元的延长存活，持续超过10天。将基因传递到特定的细胞类型是开发受损神经系统再生治疗策略的第一步。
FOLLOWING axonal injury, central neurons die through programmed cell death. Modification of intracellular mechanisms through specific gene transfer might provide a mechanism for survival. Here we present rescue of rat retinal ganglion cells (RGCs) through gene transfer of TRK oncogenes. Administration of plasmid DNA at the optic axon terminals in the superior colliculus results in retrograde transport to their soma and significant expression of the exogenous DNA. Using this approach for transfection, a TRK oncogene containing plasmid was introduced in RGCs. Three days after plasmid injection, optic nerves were transected. TRK oncogene transfection induced extended survival of the axotomized neurons, lasting over 10 days. Gene delivery to specific cell types is an initial step in the development of therapeutic strategies for regeneration of the damaged nervous system.