IngentaConnect Nerve Growth Factor Prevents the Apoptosis-associated Increase in...

Authors: JIANG, Hua; ZHANG, Jingya; ZHU, Hui; LI, Hong¹; ZHANG, Xuejun

Source: Acta Biochimica et Biophysica Sinica, Volume 39, Number 1, January 2007 , pp. 46-56(11)

Abstract:

Acetylcholinesterase (AChE) is thought to play an important role during apoptosis. Our results showed that H₂O₂ induced AChE activity, a functional marker in apoptosis, increases in neuronal-like PC12 cells. Glutathione, which is involved in cellular redox homeostasis, inhibited the increase of AChE activity, suggesting that reactive oxygen species (ROS) play a key role in this process. Further investigation showed that the elevation of AChE was observed after the degradation of Akt, release of cytochrome c from mitochondria into the cytosol, and activation of caspase family members. When nerve growth factor (NGF) was present, with the maintenance of Akt level, the elevation of AChE, the cytochrome c diffusion, as well as apoptosis were markedly attenuated in H₂O₂-treated PC12 cells. However, wortmannin, an inhibitor of the PI3K/Akt pathway, accelerated the apoptosis and increased the AChE activity. The overexpression of constitutively activated Akt, which is a downstream signalling element of the NGF receptor TrkA, delayed mitochondrial collapse and inhibited elevation of AChE activity. Thus, NGF prevented apoptosis and elevation of AChE activity by activating the Akt pathway and stabilizing the function of mitochondria.

Edited by Young YOO

Keywords: acetylcholinesterase (AChE); reactive oxygen species (ROS); Akt; apoptosis

Document Type: Research article

DOI: 10.1111/j.1745-7270.2007.00247.x

Affiliations: 1: DEFEMA, Faculté de Medecine et de Pharmacie, University of Rouen, Rouen 76821, France

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Nerve Growth Factor Prevents the Apoptosis-associated Increase in Acetylcholinesterase Activity after Hydrogen Peroxide Treatment by Activating Akt