Multifaceted promotion of apoptosis by acetylcholinesterase

Abstract

Elevated expression of acetylcholinesterase (AChE) is a common characteristic of apoptotic cells in both invertebrate and vertebrate species. While increased levels of acetylcholinesterase sensitize cells to apoptogenic stimuli, its absence or pharmacological inactivation interferes with apoptotic cell death. acetylcholinesterase may exert its pro-apoptotic function directly as an integral component of the apoptotic molecular machinery or indirectly by limiting the availability of receptor ligands and structural binding partners that promote cell survival under non-apoptogenic conditions. acetylcholinesterase promotes formation of the apoptosome and degrades DNA after nuclear accumulation. Its esterase activity limits the availability of acetylcholine as ligand for cell membrane-located nicotinic and muscarinic ACh-receptors and mitochondrial nicotinic ACh-receptors that normally support vital physiological states. Studies on insects suggest, that cytokine-activated cell-protective pathways may suppress acetylcholinesterase overexpression under apoptogenic conditions to prevent apoptotic cell death. We provide an overview of studies on various organisms and cell types that summarizes the contribution of acetylcholinesterase to the progress of apoptosis via multiple mechanisms.

Possible Prophylactic Effects of Sulforaphane on LPS-Induced Recognition Memory Impairment Mediated by Regulating Oxidative Stress and Neuroinflammatory Proteins in the Prefrontal Cortex Region of the Brain

“…AChE is considered to be a key regulatory enzyme in the cholinergic nervous system [70]. Increased AChE activity makes the cell more susceptible to apoptosis and serves as an intrinsic regulator of inflammation [71,72]. In the present investigation, LPS administration resulted in the enhancement of AChE activity, which correlates with several previous studies [73,74].…”

The Role of Life Stages in the Sensitivity of Hediste diversicolor to Nanoplastics: A Case Study with Poly(Methyl)Methacrylate (PMMA)

“…Another possible explanation for the AChE activity increase appointed in the literature is cell apoptosis, a form of programmed cell death with important roles in development, tissue homeostasis, and various diseases [83]. Studies have been investigating the relation between AChE and apoptosis and have demonstrated that AChE also plays an important role as a regulator of apoptosis (caused by oxidative stress) and that apoptogenic stimuli may increase AChE levels in organisms, including invertebrates [84]. Moreover, at higher concentrations, higher NPs aggregation may have occurred, which could have prevented the action of PMMA NPs at higher concentrations, since larger particles cannot penetrate cell membranes; therefore, organisms exposed to lower concentrations were more affected.…”