大鼠嗜铬细胞瘤中酪氨酸激酶A介导的细胞死亡诱导方法。
Induction method of tyrosine kinase A-mediated cell death in rat pheochromocytoma.
作者信息
Ahn Jin-Young, Kang Lami, Kim Hyun-Jeong, Kang Hyejin, Kim Sung-Hoon, Kim Je-Yong, Kim Seung Ki, Wang Kyu-Chang, Cho Byung Kyu, Lee Kwang-Woo, Roh Jae-Kyu, Kim Manho
机构信息
Department of Neurology, Kangnam General Hospital Public Crop, Seoul, Korea.
出版信息
Biotechnol Lett. 2005 Apr;27(8):583-7. doi: 10.1007/s10529-005-2884-5.
Nerve Growth Factor (NGF) is a neurotrophic factor that prevents apoptosis in neuronal progenitor cells. In rat pheochromocytoma (PC12) cells, tyrosine kinase A receptor (TrkA) mediates neurotrophic or protective effects, while p75 neurotrophin receptor (p75NTR) functions as a death receptor. We have determined whether TrkA mediates any cytotoxic effect. Following serum deprivation, TrkA expression increased 2.2-fold and apoptosis began with expression of Bax proapoptotic protein. Application of NGF halved cell viability but this was reversed by K252a, the TrkA inhibitor. These results confirmed the paradoxical cytotoxic effect of neurotrophic NGF via TrkA in PC12 cells following serum deprivation.
神经生长因子（NGF）是一种神经营养因子，可防止神经祖细胞凋亡。在大鼠嗜铬细胞瘤（PC12）细胞中，酪氨酸激酶A受体（TrkA）介导神经营养或保护作用，而p75神经营养因子受体（p75NTR）则作为死亡受体发挥作用。我们已经确定TrkA是否介导任何细胞毒性作用。血清剥夺后，TrkA表达增加了2.2倍，细胞凋亡随着促凋亡蛋白Bax的表达而开始。应用NGF使细胞活力减半，但TrkA抑制剂K252a可逆转这种情况。这些结果证实了血清剥夺后神经营养性NGF通过TrkA在PC12细胞中产生的矛盾细胞毒性作用。
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