Zauli G, Marchisio M, Bertagnolo V, Celeghini C, Capitani S
Oncol Rep. 1994 Jul;1(4):773-7. doi: 10.3892/or.1.4.773.
In order to evaluate the effect of the regulatory human immunodeficiency virus-type 1 (HIV-1) Tat protein on the process of neuronal differentiation, two tat-transfected and mock-transfected PC12 cell lines were cultured in the absence or presence of 100-1000 ng/ml of nerve growth factor (NGF). As expected, NGF was able to induce a clearcut morphological differentiation of mock-transfected PC12 into sympathetic-like neurons, also reducing the percentage of cells in S phase. On the other hand, NGF was unable to reduce the percentage of PC12-tat cells in S phase and/or to induce their neuronal differentiation. Only the addition in culture of 5 mu g/ml neutralizing anti-Tat antibody plus 1000 ng/ml NGF was effective in decreasing the percentage of PC12-tat in S phase and inducing partial signs of neuronal differentiation in serum-free cultures. The ability of Tat protein to suppress the neuronal differentiation pathway controlled by NGF further contribute to the definition of its role in tumor promotion during the course of HTV-1 disease.
为了评估调节性人类免疫缺陷病毒1型（HIV-1）Tat蛋白对神经元分化过程的影响，将两个转染tat和mock转染的PC12细胞系在不存在或存在100 - 1000 ng/ml神经生长因子（NGF）的情况下进行培养。正如预期的那样，NGF能够诱导mock转染的PC12细胞向交感样神经元进行明显的形态学分化，同时也降低了处于S期的细胞百分比。另一方面，NGF无法降低PC12 - tat细胞处于S期的百分比和/或诱导其神经元分化。只有在培养基中添加5μg/ml中和抗Tat抗体加1000 ng/ml NGF才能有效降低PC12 - tat细胞处于S期的百分比，并在无血清培养中诱导出部分神经元分化迹象。Tat蛋白抑制由NGF控制的神经元分化途径的能力进一步有助于明确其在HTV-1疾病过程中促进肿瘤作用的定义。
