Expression of tyrosine kinase receptors in cultured dorsal root ganglion neurons in the presence of monosialoganglioside and skeletal muscle cells

被引:2
作者
Li, Hao [1 ,2 ]
Zhang, Weiwei [1 ]
Liu, Guixiang [3 ]
Li, Jianmin [2 ]
Liu, Huaxiang [4 ]
Li, Zhenzhong [1 ]
机构
[1] Shandong Univ, Sch Med, Dept Anat, Jinan 250012, Peoples R China
[2] Shandong Univ, Qilu Hosp, Dept Orthopaed, Jinan 250012, Peoples R China
[3] Binzhou Med Coll, Dept Histol & Embryol, Binzhou 256603, Peoples R China
[4] Shandong Univ, Dept Rheumatol, Qilu Hosp, Jinan 250012, Peoples R China
基金
中国国家自然科学基金;
关键词
Monosialoganglioside; Tyrosine kinase receptor; Dorsal root ganglion; Neuron; Skeletal muscle cell; NERVE GROWTH-FACTOR; ENDOGENOUS GM1 GANGLIOSIDE; SPINAL-CORD; MOTOR-NEURONS; FACTOR NGF; RAT; NEUROTROPHINS; INVOLVEMENT; PREVENTION; COCULTURES;
D O I
10.1007/s10974-012-9322-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The neurotrophic factor-like activity of monosialoganglioside (GM1) has been shown to activate tyrosine kinase receptors (Trk). Targets of neuronal innervation play a vital role in regulating the survival and differentiation of innervating neurotrophin-responsive neurons. Both GM1 and target skeletal muscle (SKM) cells are essential for the maintenance of the function of neurons. However, much less is known about the effects of GM1 or/and target SKM cells on the expression of Trk receptors in dorsal root ganglion (DRG) neurons. Here we have tested what extent to the expression of TrkA, TrkB, and TrkC receptors in primary cultured of DRG neurons in absence or presence of GM1 or/and SKM cells. In this experiment, we found that: (1) GM1 promoted expression of TrkA and TrkB but not TrkC in primary cultured DRG neurons; (2) target SKM cells promoted expression of TrkC but not TrkA and TrkB in neuromuscular cocultures without GM1 treatment; and (3) GM1 and target SKM cells had additional effects on expression of these three Trk receptors. The results of the present study offered new clues for a better understanding of the association of GM1 and target SKM on the expression of Trk receptors.
引用
收藏
页码:341 / 350
页数:10
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