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Roles of Mitochondria Regulating Physiological and Pathological Process in the...
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Roles of Mitochondria Regulating Physiological and Pathological Process in the Brain

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 3167

Special Issue Editors

Dr. Han-A Park

E-Mail Website
Guest Editor
Department of Human Nutrition and Hospitality Management, University of Alabama, P.O. Box 870311, Tuscaloosa, AL 35487, USA
Interests: apoptosis; neurodegeneration; mitochondria; Bcl2; antioxidant; nutrition; oxidative stress
Dr. Elizabeth A. Jonas

E-Mail Website
Guest Editor
Internal Medicine (Endocrinology) and Neuroscience, Yale School of Medicine, New Haven, CT, USA
Interests: mitochondrial ion channel; regulation of apoptosis; control of the strength of synaptic transmission in the nervous system; permeability transition pore
Dr. Kim A. Caldwell

E-Mail Website
Guest Editor
Department of Biological Sciences, University of Alabama, Tuscaloosa, AL, USA
Interests: C. elegans; mitochondria; genetics; Parkinson disease
Dr. Guy A. Caldwell

E-Mail Website1 Website2
Guest Editor
Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA
Interests: C. elegans; neurodegeneration; movement disorders; epilepsy; proteostasis; endolysosomal trafficking; functional annotation of genomic variation; epigenetic regulation of neuronal resilience

Special Issue Information

Dear Colleagues,

The brain is one of the most metabolically demanding organs accounting for >20% of basal energy expenditure. The mitochondrion is the central organelle of ATP production via oxidative phosphorylation. Maintaining a healthy mitochondrial population is critical to support brain function, whereas mitochondrial dysfunction is highly associated with brain cell loss, as occurs during neurodegeneration and brain injury. In addition to regulating neuronal energy metabolism, mitochondria regulate intracellular redox status. Improperly processed oxygen during oxidative phosphorylation generates reactive oxygen species (ROS), and ROS can activate redox-sensitive cell signaling pathways. Lastly, mitochondria play a key role in regulating cell death. Opening of mitochondrial permeability transition pore (mPTP) is an important event that causes abnormal mitochondrial channel activity leading to neuronal death. Oligomerization of pro-apoptotic Bcl2 proteins Bax and Bak in the mitochondrial membrane increases cytochrome c release, activates caspases, and causes apoptotic death. In summary, mitochondria are a major governor of physiological and pathological processes in brain cells.

In this Special Issue entitled “Roles of Mitochondria Regulating Physiological and Pathological Process in the Brain”, we invite submission of original research articles, reviews, short communications and perspectives. We also welcome submissions from diverse disciplines—basic to translational research including, but not limited to, biology, biochemistry, genetics, medicine, pharmacology, nutrition, and clinical sciences.

Dr. Han-A Park
Dr. Elizabeth A. Jonas
Dr. Kim A. Caldwell
Dr. Guy A. Caldwell
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Mitochondria
  • ATP
  • Oxidative stress
  • Antioxidant
  • Apoptosis
  • Neurodegeneration
  • Mitochondrial permeability transition pore

Published Papers (1 paper)

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Research

14 pages, 2777 KiB  
Article
Bcl-xL Is Required by Primary Hippocampal Neurons during Development to Support Local Energy Metabolism at Neurites
by Joseph Jansen, Madison Scott, Emma Amjad, Allison Stumpf, Kimberly H. Lackey, Kim A. Caldwell and Han-A Park
Biology 2021, 10(8), 772; https://doi.org/10.3390/biology10080772 - 13 Aug 2021
Cited by 1 | Viewed by 2536
Abstract
B-cell lymphoma-extra large (Bcl-xL) is a mitochondrial protein known to inhibit mitochondria-dependent intrinsic apoptotic pathways. An increasing number of studies have demonstrated that Bcl-xL is critical in regulating neuronal energy metabolism and has a protective role in pathologies associated with an energy deficit. [...] Read more.
B-cell lymphoma-extra large (Bcl-xL) is a mitochondrial protein known to inhibit mitochondria-dependent intrinsic apoptotic pathways. An increasing number of studies have demonstrated that Bcl-xL is critical in regulating neuronal energy metabolism and has a protective role in pathologies associated with an energy deficit. However, it is less known how Bcl-xL regulates physiological processes of the brain. In this study, we hypothesize that Bcl-xL is required for neurite branching and maturation during neuronal development by improving local energy metabolism. We found that the absence of Bcl-xL in rat primary hippocampal neurons resulted in mitochondrial dysfunction. Specifically, the ATP/ADP ratio was significantly decreased in the neurites of Bcl-xL depleted neurons. We further found that neurons transduced with Bcl-xL shRNA or neurons treated with ABT-263, a pharmacological inhibitor of Bcl-xL, showed impaired mitochondrial motility. Neurons lacking Bcl-xL had significantly decreased anterograde and retrograde movement of mitochondria and an increased stationary mitochondrial population when Bcl-xL was depleted by either means. These mitochondrial defects, including loss of ATP, impaired normal neurite development. Neurons lacking Bcl-xL showed significantly decreased neurite arborization, growth and complexity. Bcl-xL depleted neurons also showed impaired synapse formation. These neurons showed increased intracellular calcium concentration and were more susceptible to excitotoxic challenge. Bcl-xL may support positioning of mitochondria at metabolically demanding regions of neurites like branching points. Our findings suggest a role for Bcl-xL in physiological regulation of neuronal growth and development. Full article
(This article belongs to the Special Issue Roles of Mitochondria Regulating Physiological and Pathological Process in the Brain)
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