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Front Physiol. 2014 Sep 17;5:355. doi: 10.3389/fphys.2014.00355. eCollection 2014.

Bcl-xL in neuroprotection and plasticity.

Author information

1
Section of Endocrinology, Department of Internal Medicine, Yale University New Haven, CT, USA ; Department of Neurobiology, Yale University New Haven, CT, USA.
2
Departments of Pediatrics (Cardiology), University of Rochester Medical Center Rochester, NY, USA ; Internal Medicine (Aab Cardiovascular Research Institute), University of Rochester Medical Center Rochester, NY, USA ; Department of Pharmacology and Physiology, University of Rochester Medical Center Rochester, NY, USA.
3
Division of Brain Sciences, Department of Medicine, Imperial College London London, UK.

Abstract

Accepted features of neurodegenerative disease include mitochondrial and protein folding dysfunction and activation of pro-death factors. Neurons that experience high metabolic demand or those found in organisms with genetic mutations in proteins that control cell stress may be more susceptible to aging and neurodegenerative disease. In neurons, events that normally promote growth, synapse formation, and plasticity are also often deployed to control neurotoxicity. Such protective strategies are coordinated by master stress-fighting proteins. One such specialized protein is the anti-cell death Bcl-2 family member Bcl-xL, whose myriad death-protecting functions include enhancement of bioenergetic efficiency, prevention of mitochondrial permeability transition channel activity, protection from mitochondrial outer membrane permeabilization (MOMP) to pro-apoptotic factors, and improvement in the rate of vesicular trafficking. Synapse formation and normal neuronal activity provide protection from neuronal death. Therefore, Bcl-xL brings about synapse formation as a neuroprotective strategy. In this review we will consider how this multi-functional master regulator protein uses many strategies to enhance synaptic and neuronal function and thus counteracts neurodegenerative stimuli.

KEYWORDS:

apoptosis; calcium; mitochondria; permeability transition pore; synaptic plasticity

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