Huang Hai-Tao, Sun Zhi-Gang, Liu Hua-Wei, Ma Jun-Tao, Hu Min
Department of Stomatology, Chinese PLA General Hospital, Beijing 100853, China.
Department of Maxillofacial Surgery, The 1st Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
Saudi J Biol Sci. 2017 Dec;24(8):1853-1858. doi: 10.1016/j.sjbs.2017.11.027. Epub 2017 Nov 28.
The in-vitro study indicated that ERK/MAPK and PI3K/AKT signal channels may play an important role in reparative regeneration process after peripheral nerve injury. But, relevant in-vivo study was infrequent. In particular, there has been no report on simultaneous activation of ERK/MAPK and PI3K/AKT signal channels in facial nerve cell and axon after facial nerve injury.
The expression of P-ERK enhanced in nerve cells at the injury side on the 1 d after the rat facial nerve was cut and kept on a higher level until 14 d, but decreased on 28 d. The expression of P-AKT enhanced in nerve cells at the injury side on 1 d after injury, and kept on a higher level until 28 d. The expression of P-ERK enhanced at the near and far sections of the injured axon on 1 d, then increased gradually and reached the maximum on 7 d, but decreased on 14 d, until down to the level before the injury on 28 d. The expression of P-AKT obviously enhanced in the injured axon on 1 d, especially in the axon of the rear section, but decreased in the axon of the rear section on 7 d, while the expression of axon in the far section increased to the maximum and kept on till 14 d. On 28 d, the expression of P-AKT decreased in both rear and far sections of the axon.
The facial nerve simultaneously activated ERK/MAPK and PI3K/AKT signal channels in facial nerve cells and axons after the cut injury, but the expression levels of P-ERK and P-AKT varied as the function of the time. In particular, they were quite different in axon of the far section. It has been speculated that two signal channels might have different functions after nerve injury. However, their specific regulating effects should still be testified by further studies in regenerative process of peripheral nerve injury.
体外研究表明,ERK/MAPK和PI3K/AKT信号通路可能在周围神经损伤后的修复性再生过程中发挥重要作用。但是,相关的体内研究较少。特别是,面神经损伤后面神经细胞和轴突中ERK/MAPK和PI3K/AKT信号通路同时激活的情况尚无报道。
大鼠面神经切断术后1天,损伤侧神经细胞中P-ERK表达增强,并持续维持在较高水平直至14天,但在28天时降低。损伤后1天,损伤侧神经细胞中P-AKT表达增强,并持续维持在较高水平直至28天。损伤轴突的近端和远端在术后1天P-ERK表达增强,随后逐渐升高并在7天时达到最大值,但在14天时降低,直至28天时降至损伤前水平。损伤后1天,损伤轴突中P-AKT表达明显增强,尤其是在后部轴突中,但在7天时后部轴突中P-AKT表达降低,而远端轴突中P-AKT表达升高至最大值并持续至14天。在28天时,轴突的后部和远端P-AKT表达均降低。
面神经切断损伤后,面神经细胞和轴突中ERK/MAPK和PI3K/AKT信号通路同时被激活,但P-ERK和P-AKT的表达水平随时间变化。特别是,它们在远端轴突中的变化差异较大。据推测,神经损伤后两条信号通路可能具有不同的功能。然而,它们在周围神经损伤再生过程中的具体调节作用仍需进一步研究证实。