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IJMS
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ER Stress, Mitochondrial Dysfunction, and Neuroinflammation in Neurodegenerative Diseases
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ER Stress, Mitochondrial Dysfunction, and Neuroinflammation in Neurodegenerative Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 July 2024) | Viewed by 3864

Special Issue Editors

Dr. Muhammad Hossain

E-Mail Website
Guest Editor
Department of Environmental Health Sciences, Robert Stempel College of Public Health and Social Work, Florida International University, Miami, FL 33199, USA
Interests: neurotoxicology; pesticides; ER stress; neuroinflammation; neurodegeneration; adult neurogenesis; learning and memory
Prof. Dr. Jason Cannon

E-Mail Website
Guest Editor
School of Health Sciences, Purdue University, West Lafayette, IN 47907, USA
Interests: neurobiology of disease; neurodegeneration; neurotoxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

However, the precise mechanism(s) for neurodegeneration in neurological diseases is unknown, there is extensive evidence which indicates that endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and neuroinflammation are involved in the pathogenesis of many neurodegenerative diseases and disorders. Both ER and mitochondria are essential cellular organels that play a crucial role in the maintenance of cellular homeostasis for neuronal health and proper functioning of neurons. Perturbations in their normal functions lead to dysregulation of cellular homeostasis and initiate oxidative stress and neuroinflammation, which can contribute to neurodegeneration. Human post-mortem brains and animal models of neurological disorders, including Parkinson’s , Alzheimer’s, and Huntington’s diseases, consistently display the evidence of ER stress, mitochondrial dysfunction, and neuroinflammation, including glial cells activation and the increased expression of pro-inflammatory cytokines and other neurotoxic factors. Thus, this Special Issue of the International Journal of Molecular Sciences welcomes both original research articles and reviews to further advance the understanding of molecular and cellular mechanisms of neuroinflammation in patophysiology of neurodegeneration for targeting therapeautic intervention to halt these neurological disorders. Since IJMS is a journal of molecular science, pure clinical studies will not be suitable; however, clinical submissions including biomolecular experiments focusing on the above-mentioned topics are welcomed.

Dr. Muhammad Hossain
Prof. Dr. Jason Cannon
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • ER stress 
  • mitochondrial dysfunction 
  • neuroinflammation 
  • microglia 
  • astrocytes 
  • apotosis 
  • neurodegeneration 
  • neurodegenerative diseases

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Published Papers (2 papers)

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Research

13 pages, 5369 KiB  
Article
Endoplasmic Reticulum Stress Differently Modulates the Release of IL-6 and IL-8 Cytokines in Human Glial Cells
by Paulina Sokołowska, Anna Wiktorowska-Owczarek, Jakub Tambor, Sebastian Gawlak-Socka, Edward Kowalczyk and Marta Jóźwiak-Bębenista
Int. J. Mol. Sci. 2024, 25(16), 8687; https://doi.org/10.3390/ijms25168687 - 9 Aug 2024
Cited by 3 | Viewed by 1674
Abstract
Endoplasmic reticulum (ER) stress is a significant player in the pathophysiology of various neurodegenerative and neuropsychiatric disorders. Despite the established link between ER stress and inflammatory pathways, there remains a need for deeper exploration of the specific cellular mechanisms underlying ER stress-mediated neuroinflammation. [...] Read more.
Endoplasmic reticulum (ER) stress is a significant player in the pathophysiology of various neurodegenerative and neuropsychiatric disorders. Despite the established link between ER stress and inflammatory pathways, there remains a need for deeper exploration of the specific cellular mechanisms underlying ER stress-mediated neuroinflammation. This study aimed to investigate how the severity of ER stress (triggered by different concentrations of tunicamycin) can impact the release of proinflammatory cytokines IL-6 and IL-8 from astrocytes and microglia, comparing the effects with those induced by well-known immunostimulants—tumor necrosis factor alpha (TNF-α) or lipopolysaccharide (LPS). Mild ER stress has a distinct effect on the cytokine release compared to more intense stress levels, i.e., diminished IL-6 production was accompanied by an increase in IL-8 level, which was significantly more pronounced in astrocytes than in microglia. On the contrary, prolonged or more severe ER stress induced inflammation in glial cells, leading to a time- and concentration-dependent buildup of proinflammatory IL-6, but unlike inflammatory agents, an ER stress inducer diminished IL-8 secretions by glial cells. The differences could hold importance in identifying ER stress markers as potential drug targets for the treatment of neurodegenerative diseases or mood disorders, yet this requires confirmation in more complex animal studies. Full article
(This article belongs to the Special Issue ER Stress, Mitochondrial Dysfunction, and Neuroinflammation in Neurodegenerative Diseases)
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20 pages, 7780 KiB  
Article
The Preventive Effects of Salubrinal against Pyrethroid-Induced Disruption of Adult Hippocampal Neurogenesis in Mice
by Abigail C. Toltin, Abdelmadjid Belkadi, Laura M. Gamba and Muhammad M. Hossain
Int. J. Mol. Sci. 2023, 24(21), 15614; https://doi.org/10.3390/ijms242115614 - 26 Oct 2023
Cited by 1 | Viewed by 1634
Abstract
Environmental factors, including pesticide exposure, have been identified as substantial contributors to neurodegeneration and cognitive impairments. Previously, we demonstrated that repeated exposure to deltamethrin induces endoplasmic reticulum (ER) stress, reduces hippocampal neurogenesis, and impairs cognition in adult mice. Here, we investigated the potential [...] Read more.
Environmental factors, including pesticide exposure, have been identified as substantial contributors to neurodegeneration and cognitive impairments. Previously, we demonstrated that repeated exposure to deltamethrin induces endoplasmic reticulum (ER) stress, reduces hippocampal neurogenesis, and impairs cognition in adult mice. Here, we investigated the potential relationship between ER stress and hippocampal neurogenesis following exposure to deltamethrin, utilizing both pharmacological and genetic approaches. To investigate whether ER stress is associated with inhibition of neurogenesis, mice were given two intraperitoneal injections of eIf2α inhibitor salubrinal (1 mg/kg) at 24 h and 30 min prior to the oral administration of deltamethrin (3 mg/kg). Salubrinal prevented hippocampal ER stress, as indicated by decreased levels of C/EBP-homologous protein (CHOP) and transcription factor 4 (ATF4) and attenuated deltamethrin-induced reductions in BrdU-, Ki-67-, and DCX-positive cells in the dentate gyrus (DG) of the hippocampus. To further explore the relationship between ER stress and adult neurogenesis, we used caspase-12 knockout (KO) mice. The caspase-12 KO mice exhibited significant protection against deltamethrin-induced reduction of BrdU-, Ki-67-, and DCX-positive cells in the hippocampus. In addition, deltamethrin exposure led to a notable upregulation of CHOP and caspase-12 expression in a significant portion of BrdU- and Ki-67-positive cells in WT mice. Conversely, both salubrinal-treated mice and caspase-12 KO mice exhibited a considerably lower number of CHOP-positive cells in the hippocampus. Together, these findings suggest that exposure to the insecticide deltamethrin triggers ER stress-mediated suppression of adult hippocampal neurogenesis, which may subsequently contribute to learning and memory deficits in mice. Full article
(This article belongs to the Special Issue ER Stress, Mitochondrial Dysfunction, and Neuroinflammation in Neurodegenerative Diseases)
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