Autophagy-Inhibition potentiates cell death and its Activation by trehalose does not protect hippocampal HT22 neurons against cell death induced by ER-Stress.

Autophagy-Inhibition potentiates cell death and its Activation by trehalose does not protect hippocampal HT22 neurons against cell death induced by ER-Stress.
Curr Neurovasc Res. 2019 Jan 31;:
Authors: Halbe L, Rami A
Abstract
ER stress leads to the activation of two protein degradation pathways, the ubiquitin-proteasome via ER-associated degradation and lysosome-mediated protein degradation via autophagy. ER-associated degradation involves translocation of unfolded ER proteins to the cytosol where they are ubiquitinated and degraded by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to degrade accumulated proteins and thus attenuate ER stress. Autophagy is the process by which cellular macromolecules and organelles components are sequestered within double membrane vesicles and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Initially, autophagy in response to ER stress acts as a survival response, functioning to degrade misfolded and aggregated proteins, as well as damaged organelles. However, like the ER stress response, while a limited amount of stress will induce a protective response, when the stress is more pronounced the response will trigger cell death. Because autophagy could exert both anti- and pro-apoptotic activities depending on the conditions, we examined the effects autophagy modulation on ER stress-ind...

Source: Current Neurovascular Research - January 31, 2019 Category: Neurology Authors: Halbe L, Rami A Tags: Curr Neurovasc Res Source Type: research