scholarly journals Dual Oxidase Mutant Retards Mauthner-Cell Axon Regeneration at an Early Stage via Modulating Mitochondrial Dynamics in Zebrafish

2020 ◽  
Vol 36 (12) ◽  
pp. 1500-1512
Author(s):  
Lei-Qing Yang ◽  
Min Chen ◽  
Da-Long Ren ◽  
Bing Hu
Keyword(s):  
Axon Regeneration ◽  
Early Stage ◽  
Mitochondrial Dynamics ◽  
Mauthner Cell ◽  
Cell Axon ◽  
Dual Oxidase

scholarly journals MicroRNA-133b Negatively Regulates Zebrafish Single Mauthner-Cell Axon Regeneration through Targeting tppp3 in Vivo

2017 ◽  
Vol 10 ◽  
Author(s):  
Rongchen Huang ◽  
Min Chen ◽  
Leiqing Yang ◽  
Mahendra Wagle ◽  
Su Guo ◽  
...  
Keyword(s):  
Axon Regeneration ◽  
Mauthner Cell ◽  
Cell Axon

scholarly journals Mitochondrial Behavior in Axon Degeneration and Regeneration

2021 ◽  
Vol 13 ◽  
Author(s):  
Biyao Wang ◽  
Minghao Huang ◽  
Dehao Shang ◽  
Xu Yan ◽  
Baohong Zhao ◽  
...  
Keyword(s):  
Axon Regeneration ◽  
Early Stage ◽  
Mitochondrial Dynamics ◽  
Neurological Diseases ◽  
Signal Transmission ◽  
High Energy ◽  
Biological Behavior ◽  
Axon Degeneration ◽  
Mitochondrial Transport ◽  
Cord Injury

Mitochondria are organelles responsible for bioenergetic metabolism, calcium homeostasis, and signal transmission essential for neurons due to their high energy consumption. Accumulating evidence has demonstrated that mitochondria play a key role in axon degeneration and regeneration under physiological and pathological conditions. Mitochondrial dysfunction occurs at an early stage of axon degeneration and involves oxidative stress, energy deficiency, imbalance of mitochondrial dynamics, defects in mitochondrial transport, and mitophagy dysregulation. The restoration of these defective mitochondria by enhancing mitochondrial transport, clearance of reactive oxidative species (ROS), and improving bioenergetic can greatly contribute to axon regeneration. In this paper, we focus on the biological behavior of axonal mitochondria in aging, injury (e.g., traumatic brain and spinal cord injury), and neurodegenerative diseases (Alzheimer's disease, AD; Parkinson's disease, PD; Amyotrophic lateral sclerosis, ALS) and consider the role of mitochondria in axon regeneration. We also compare the behavior of mitochondria in different diseases and outline novel therapeutic strategies for addressing abnormal mitochondrial biological behavior to promote axonal regeneration in neurological diseases and injuries.

scholarly journals 5-Azacytidine and Resveratrol Enhance Chondrogenic Differentiation of Metabolic Syndrome-Derived Mesenchymal Stem Cells by Modulating Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-20 ◽  
Author(s):  
K. Marycz ◽  
J. M. Irwin Houston ◽  
C. Weiss ◽  
M. Röcken ◽  
K. Kornicka
Keyword(s):  
Metabolic Syndrome ◽  
Stem Cells ◽  
Chondrogenic Differentiation ◽  
Therapeutic Potential ◽  
Early Stage ◽  
Mitochondrial Dynamics ◽  
The Body ◽  
Stem Cell Population ◽  
Wide Range

Recently, metabolic syndrome (MS) has gained attention in human and animal metabolic medicine. Insulin resistance, inflammation, hyperleptinemia, and hyperinsulinemia are critical to its definition. MS is a complex cluster of metabolic risk factors that together exert a wide range of effects on multiple organs, tissues, and cells in the body. Adipose stem cells (ASCs) are multipotent stem cell population residing within the adipose tissue that is inflamed during MS. Studies have indicated that these cells lose their stemness and multipotency during MS, which strongly reduces their therapeutic potential. They suffer from oxidative stress, apoptosis, and mitochondrial deterioration. Thus, the aim of this study was to rejuvenate these cells in vitro in order to improve their chondrogenic differentiation effectiveness. Pharmacotherapy of ASCs was based on resveratrol and 5-azacytidine pretreatment. We evaluated whether those substances are able to reverse aged phenotype of metabolic syndrome-derived ASCs and improve their chondrogenic differentiation at its early stage using immunofluorescence, transmission and scanning electron microscopy, real-time PCR, and flow cytometry. Obtained results indicated that 5-azacytidine and resveratrol modulated mitochondrial dynamics, autophagy, and ER stress, leading to the enhancement of chondrogenesis in metabolically impaired ASCs. Therefore, pretreatment of these cells with 5-azacytidine and resveratrol may become a necessary intervention before clinical application of these cells in order to strengthen their multipotency and therapeutic potential.

scholarly journals Mitochondrial Deficits With Neural and Social Damage in Early-Stage Alzheimer’s Disease Model Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Afzal Misrani ◽  
Sidra Tabassum ◽  
Qingwei Huo ◽  
Sumaiya Tabassum ◽  
Jinxiang Jiang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Early Stage ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Neuronal Morphology ◽  
Therapeutic Interventions ◽  
Early Event ◽  
Mitochondrial Morphology

Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide. Mitochondrial dysfunction is thought to be an early event in the onset and progression of AD; however, the precise underlying mechanisms remain unclear. In this study, we investigated mitochondrial proteins involved in organelle dynamics, morphology and energy production in the medial prefrontal cortex (mPFC) and hippocampus (HIPP) of young (1∼2 months), adult (4∼5 months) and aged (9∼10, 12∼18 months) APP/PS1 mice. We observed increased levels of mitochondrial fission protein, Drp1, and decreased levels of ATP synthase subunit, ATP5A, leading to abnormal mitochondrial morphology, increased oxidative stress, glial activation, apoptosis, and altered neuronal morphology as early as 4∼5 months of age in APP/PS1 mice. Electrophysiological recordings revealed abnormal miniature excitatory postsynaptic current in the mPFC together with a minor connectivity change between the mPFC and HIPP, correlating with social deficits. These results suggest that abnormal mitochondrial dynamics, which worsen with disease progression, could be a biomarker of early-stage AD. Therapeutic interventions that improve mitochondrial function thus represent a promising approach for slowing the progression or delaying the onset of AD.

scholarly journals Mitochondrial OPA1 deficiency causes reversible defects in adult neurogenesis-associated spatial memory in mice

2021 ◽  
Author(s):  
Trinovita Andraini ◽  
Lionel Mouledous ◽  
Petnoi Petsophonsakul ◽  
Cedrick Florian ◽  
Sebastien Lopez ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Neurodegenerative Diseases ◽  
Adult Neurogenesis ◽  
Mitochondrial Function ◽  
Optic Atrophy ◽  
Late Onset ◽  
Early Stage ◽  
Mitochondrial Dynamics ◽  
Voluntary Exercise ◽  
Mitochondrial Functions

Mitochondria are integrative hubs central to cellular adaptive pathways. Such pathways are critical in highly differentiated post-mitotic neurons, the plasticity of which sustains brain function. Consequently, defects in mitochondrial dynamics and quality control appear instrumental in neurodegenerative diseases and may also participate in cognitive impairments. To directly test this hypothesis, we analyzed cognitive performances in a mouse mitochondria-based disease model, due to haploinsufficiency in the mitochondrial optic-atrophy-type-1 (OPA1) protein. While in Dominant Optic Atrophy (DOA) models, the known main symptoms are late onset visual deficits, we discovered early impairments in hippocampus-dependent spatial memory attributable to defects in adult neurogenesis. Moreover, less connected hippocampal adult-born neurons showed a decrease in mitochondrial content. Remarkably, modulating mitochondrial function through voluntary exercise or pharmacological treatment restored spatial memory. Altogether, our study identifies a crucial role for OPA1-dependent mitochondrial functions in adult neurogenesis, and thus in hippocampal-dependent cognitive functions. More generally, our findings show that adult neurogenesis is highly sensitive to mild mitochondrial defects, generating impairments in spatial memory that can be detected at an early stage and counterbalanced by physical exercise and pharmacological targeting of mitochondrial dynamics. Thus, early amplification of mitochondrial function appears beneficial for late-onset neurodegenerative diseases.

Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve

2021 ◽  
pp. JN-RM-0555-21
Author(s):  
Sheri L. Peterson ◽  
Yiqing Li ◽  
Christina J. Sun ◽  
Kimberly A. Wong ◽  
Kylie S. Leung ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Axon Regeneration ◽  
Cell Activity ◽  
Myeloid Cell ◽  
Retinal Ganglion ◽  
Retinal Ganglion Cell Axon ◽  
Cell Axon ◽  
Ganglion Cell Axon
Sign in / Sign up

Export Citation Format

Share Document