Yamamoto M, Mitsuma N, Ito Y, Hattori N, Nagamatsu M, Li M, Mitsuma T, Sobue G
Department of Neurology, Nagoya University School of Medicine, Japan.
Brain Res. 1998 Nov 2;809(2):175-81. doi: 10.1016/s0006-8993(98)00858-0.
The steady-state mRNA levels of glial cell line-derived neurotrophic factor (GDNF), GDNFR-alpha and RET were examined in various human peripheral neuropathies to determine the relationship with myelinated fiber pathology, and T cell and macrophage invasions in the diseased nerves. GDNF and GDNFR-alpha mRNA levels were elevated to variable extent in the diseased nerves, although they were not specific to the type of diseases. The increase of GDNFR-alpha mRNA levels was correlated with the extent of the nerves with axonal pathology, and was proportional to the extent of invasion of the nerves by T cells and macrophages. The GDNF mRNA levels were not related to axonal, demyelinating pathology, or inflammatory cell invasions. RET mRNA expression was not detected in normal nor diseased nerves. The GDNF and GDNFR-alpha expression in the diseased human nerves is regulated by an underlying pathology-related process, and could play a role in peripheral nerve repair.
在各种人类周围神经病变中检测了胶质细胞源性神经营养因子(GDNF)、GDNFR-α和RET的稳态mRNA水平,以确定它们与有髓纤维病理以及患病神经中T细胞和巨噬细胞浸润的关系。尽管GDNF和GDNFR-α mRNA水平在患病神经中并非特定于疾病类型,但在不同程度上有所升高。GDNFR-α mRNA水平的升高与有轴突病理的神经范围相关,并且与T细胞和巨噬细胞对神经的浸润程度成正比。GDNF mRNA水平与轴突、脱髓鞘病理或炎性细胞浸润无关。在正常神经和患病神经中均未检测到RET mRNA表达。患病人类神经中的GDNF和GDNFR-α表达受潜在的病理相关过程调节,并可能在周围神经修复中发挥作用。