Li Ruifeng, Wu Yimin, Jiang Dianming
Department of Orthopedic, The First Affiliated Hospital of Chongqing Medical University, Yuzhong District Yueyuan Road No1, Chongqing, China.
Department of Cervical Surgery, The Second Affiliated Hospital of Inner Mongolia Medical University, Muslims camp Square Road No 1, Hohhot, China.
Cytotechnology. 2016 Aug;68(4):659-64. doi: 10.1007/s10616-014-9813-1. Epub 2014 Dec 11.
Spinal cord injury is a devastating health problem that affects thousands of individuals each year. The neurons were destroyed. NT-3 is a recently discovered neurotrophin. This study sought to understand the potential involvement of MAPKs in NT-3-mediated growth inhibition of human neurons. We applied different concentrations of NT-3 and observed the growth rate of the cells and the changes in the phosphorylation state of the MAPKs ERK1/2, JNK and p38. This study discovered that NT-3-induced HNC growth was promoted primarily by phosphorylated ERK1/2, and that this phosphorylation, as well p90(rsk)phosphorylation, was mediated by TrkC. The ERK1/2 pathway is known to play an essential role in the NT-3-mediated growth of human neurons. In conclusion, our study suggests that NT-3 promotes the growth of human neurons cells primarily through the TrkC/ERK pathway.
脊髓损伤是一个严重的健康问题，每年影响着成千上万的人。神经元遭到了破坏。神经营养因子-3（NT-3）是最近发现的一种神经营养蛋白。本研究旨在了解丝裂原活化蛋白激酶（MAPKs）在NT-3介导的人类神经元生长抑制中的潜在作用。我们应用不同浓度的NT-3，并观察细胞的生长速率以及MAPKs细胞外信号调节激酶1/2（ERK1/2）、应激活化蛋白激酶（JNK）和p38磷酸化状态的变化。本研究发现，NT-3诱导的人神经嵴细胞（HNC）生长主要由磷酸化的ERK1/2促进，并且这种磷酸化以及p90核糖体S6激酶（p90(rsk)）的磷酸化是由酪氨酸激酶C（TrkC）介导的。已知ERK1/2通路在NT-3介导的人类神经元生长中起重要作用。总之，我们的研究表明，NT-3主要通过TrkC/ERK通路促进人类神经元细胞的生长。
