Nikam S S, Tennekoon G I, Christy B A, Yoshino J E, Rutkowski J L
Department of Pediatrics, University of Michigan, Ann Arbor 48109, USA.
Mol Cell Neurosci. 1995 Aug;6(4):337-48. doi: 10.1006/mcne.1995.1026.
Nerve injury alters the function of Schwann cells from quiescent, myelin forming cells to proliferating cells that facilitate nerve repair. The transcription factor, Zif268, may be involved in transmitting injury-related signals since its expression is rapidly induced by nerve transection in vivo and without intervening protein synthesis by injury-related signals in vitro. Expression of the low-affinity p75 nerve growth factor receptor (NGFRp75) by Schwann cells after nerve injury closely correlated with the zif268 expression profile, and Zif268 transactivated the NGFRp75 promoter in transient transfection assays. Conversely, the NGFRp75 gene was not expressed when Zif268 protein was depleted by stable transfection of antisense cDNA. Moreover, nuclear proteins corresponding to Zif268 bound to the NGFRp75 promoter by Southwestern blotting, indicating that a direct interaction of Zif268 with the NGFR gene is required for its expression in Schwann cells.
神经损伤会使施万细胞的功能发生改变，从静止的、形成髓鞘的细胞转变为促进神经修复的增殖细胞。转录因子Zif268可能参与传递损伤相关信号，因为其表达在体内可被神经横断迅速诱导，且在体外无需损伤相关信号干预蛋白质合成。神经损伤后施万细胞低亲和力p75神经生长因子受体（NGFRp75）的表达与Zif268的表达谱密切相关，并且在瞬时转染实验中Zif268可反式激活NGFRp75启动子。相反，当通过反义cDNA稳定转染使Zif268蛋白缺失时，NGFRp75基因不表达。此外，通过蛋白质印迹法表明，与Zif268相对应的核蛋白与NGFRp75启动子结合，这表明Zif268与NGFR基因的直接相互作用是其在施万细胞中表达所必需的。
