Role of rockfish (Sebastes schlegelii) glutaredoxin 1 in innate immunity, and alleviation of cellular oxidative stress: Insights into localization, molecular characteristics, transcription, and function

Maintaining mitochondrial health is essential for the survival and function of eukaryotic organisms. Misfunctioning mitochondria activate stress-responsive pathways to restore mitochondrial network homeostasis, remove damaged or toxic proteins, and eliminate damaged organelles via selective autophagy of mitochondria, a process termed mitophagy. Failure of these quality control pathways is implicated in the pathogenesis of Parkinson's disease and other neurodegenerative diseases. Impairment of mitochondrial quality control has been demonstrated to activate innate immune pathways, including inflammasome-mediated signaling and the antiviral cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING)–regulated interferon response. Immune system malfunction is a common hallmark in many neurodegenerative diseases; however, whether inflammation suppresses or exacerbates disease pathology is still unclear. The goal of this review is to provide a historical overview of the field, describe mechanisms of mitochondrial quality control, and highlight recent advances on the emerging role of mitochondria in innate immunity and inflammation.

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Roles of Autophagy in Oxidative Stress

International Journal of Molecular Sciences ◽

10.3390/ijms21093289 ◽

2020 ◽

Vol 21 (9) ◽

pp. 3289 ◽

Cited By ~ 4

Author(s):

Hyeong Rok Yun ◽

Yong Hwa Jo ◽

Jieun Kim ◽

Yoonhwa Shin ◽

Sung Soo Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Stress Responses ◽

Basic Mechanism ◽

Redox Signalling ◽

Mitochondrial Ros ◽

Related Stress ◽

And Function ◽

Catabolic Process

Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology.

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Structure and Function of the Plant Alternative Oxidase: Its Putative Role in the Oxygen Defence Mechanism

Bioscience Reports ◽

10.1023/a:1027388729586 ◽

1997 ◽

Vol 17 (3) ◽

pp. 319-333 ◽

Cited By ~ 108

Author(s):

Anneke M. Wagner ◽

Anthony L. Moore

Keyword(s):

Oxidative Stress ◽

Alternative Oxidase ◽

Structure And Function ◽

Current Understanding ◽

Defence Mechanism ◽

Putative Role ◽

And Function

Current understanding of the structure and function of the plant alternative oxidase is reviewed. In particular, the role of the oxidase in the protection of tissues against oxidative stress is developed.

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P-glycoprotein (ABCB1) and Oxidative Stress: Focus on Alzheimer’s Disease

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/7905486 ◽

2017 ◽

Vol 2017 ◽

pp. 1-13 ◽

Cited By ~ 16

Author(s):

Giulia Sita ◽

Patrizia Hrelia ◽

Andrea Tarozzi ◽

Fabiana Morroni

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Therapeutic Drug ◽

Amyloid A ◽

P Glycoprotein ◽

And Function ◽

The Brain ◽

Brain Homeostasis

ATP-binding cassette (ABC) transporters, in particular P-glycoprotein (encoded by ABCB1), are important and selective elements of the blood-brain barrier (BBB), and they actively contribute to brain homeostasis. Changes in ABCB1 expression and/or function at the BBB may not only alter the expression and function of other molecules at the BBB but also affect brain environment. Over the last decade, a number of reports have shown that ABCB1 actively mediates the transport of beta amyloid (Aβ) peptide. This finding has opened up an entirely new line of research in the field of Alzheimer’s disease (AD). Indeed, despite intense research efforts, AD remains an unsolved pathology and effective therapies are still unavailable. Here, we review the crucial role of ABCB1 in the Aβtransport and how oxidative stress may interfere with this process. A detailed understanding of ABCB1 regulation can provide the basis for improved neuroprotection in AD and also enhanced therapeutic drug delivery to the brain.

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17β-estradiol improves hepatic mitochondrial biogenesis and function through PGC1B

Journal of Endocrinology ◽

10.1530/joe-16-0350 ◽

2017 ◽

Vol 232 (2) ◽

pp. 297-308 ◽

Cited By ~ 14

Author(s):

Bel M Galmés-Pascual ◽

Antonia Nadal-Casellas ◽

Marco Bauza-Thorbrügge ◽

Miquel Sbert-Roig ◽

Francisco J García-Palmer ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Biogenesis ◽

Oxidative Capacity ◽

Protective Role ◽

Rat Tissues ◽

Peroxisome Proliferator ◽

Ovx Rats ◽

17Β Estradiol ◽

And Function

Sexual dimorphism in mitochondrial biogenesis and function has been described in many rat tissues, with females showing larger and more functional mitochondria. The family of the peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1) plays a central role in the regulatory network governing mitochondrial biogenesis and function, but little is known about the different contribution of hepatic PGC1A and PGC1B in these processes. The aim of this study was to elucidate the role of 17β-estradiol (E2) in mitochondrial biogenesis and function in liver and assess the contribution of both hepatic PGC1A and PGC1B as mediators of these effects. In ovariectomized (OVX) rats (half of which were treated with E2) estrogen deficiency led to impaired mitochondrial biogenesis and function, increased oxidative stress, and defective lipid metabolism, but was counteracted by E2 treatment. In HepG2 hepatocytes, the role of E2 in enhancing mitochondrial biogenesis and function was confirmed. These effects were unaffected by the knockdown of PGC1A, but were impaired when PGC1B expression was knocked down by specific siRNA. Our results reveal a widespread protective role of E2 in hepatocytes, which is explained by enhanced mitochondrial content and oxidative capacity, lower hepatic lipid accumulation, and a reduction of oxidative stress. We also suggest a novel hepatic protective role of PGC1B as a modulator of E2 effects on mitochondrial biogenesis and function supporting activation of PGC1B as a therapeutic target for hepatic mitochondrial disorders.

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The Role of Oxidative Stress-Altered Lipoprotein Structure and Function and Microinflammation on Cardiovascular Risk in Patients with Minor Renal Dysfunction

Journal of the American Society of Nephrology ◽

10.1097/01.asn.0000111744.00916.e6 ◽

2004 ◽

Vol 15 (3) ◽

pp. 538-548 ◽

Cited By ~ 116

Author(s):

G. A. Kaysen

Keyword(s):

Oxidative Stress ◽

Cardiovascular Risk ◽

Renal Dysfunction ◽

Structure And Function ◽

And Function

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Non-Coding RNAs in Response to Drought Stress

International Journal of Molecular Sciences ◽

10.3390/ijms222212519 ◽

2021 ◽

Vol 22 (22) ◽

pp. 12519

Author(s):

Temesgen Assefa Gelaw ◽

Neeti Sanan-Mishra

Keyword(s):

Drought Stress ◽

Abiotic Stresses ◽

Regulatory Networks ◽

Molecular Characteristics ◽

Plant Responses ◽

Overall Response ◽

Multiple Genes ◽

Non Coding Rnas ◽

And Function

Drought stress causes changes in the morphological, physiological, biochemical and molecular characteristics of plants. The response to drought in different plants may vary from avoidance, tolerance and escape to recovery from stress. This response is genetically programmed and regulated in a very complex yet synchronized manner. The crucial genetic regulations mediated by non-coding RNAs (ncRNAs) have emerged as game-changers in modulating the plant responses to drought and other abiotic stresses. The ncRNAs interact with their targets to form potentially subtle regulatory networks that control multiple genes to determine the overall response of plants. Many long and small drought-responsive ncRNAs have been identified and characterized in different plant varieties. The miRNA-based research is better documented, while lncRNA and transposon-derived RNAs are relatively new, and their cellular role is beginning to be understood. In this review, we have compiled the information on the categorization of non-coding RNAs based on their biogenesis and function. We also discuss the available literature on the role of long and small non-coding RNAs in mitigating drought stress in plants.

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Macrophages in bacterial lung diseases: phenotype and functions (review)

Bulletin of Siberian Medicine ◽

10.20538/1682-0363-2019-1-142-154 ◽

2019 ◽

Vol 18 (1) ◽

pp. 142-154

Author(s):

E. G. Churina ◽

A. V. Sitnikova ◽

O. I. Urazova ◽

S. P. Chumakova ◽

M. V. Vins ◽

...

Keyword(s):

Innate Immunity ◽

Literature Review ◽

Lung Diseases ◽

Functional Heterogeneity ◽

Protective Function ◽

Immunoregulatory Cells ◽

Macrophage Plasticity ◽

And Function ◽

Disease Understanding

This literature review is devoted to the analysis of the role of macrophages in the immunopathogenesis of infectious lung diseases of bacterial etiology. The article summarizes information about the origin of macrophages, their phenotypic and functional heterogeneity. The mechanisms of impaired protective function of innate immunity are associated with the polarization of the program of maturation and activation of macrophages in the direction to tolerogenic or immunoregulatory cells with phenotype of M2. Alveolar macrophages perform a variety of functions (from pro-inflammatory to regenerative) in the development of inflammation in the respiratory organs. Their inherent plasticity suggests that the same macrophages can change their phenotype and function depending on the microenvironment in the inflammatory focus at different stages of the disease. Understanding the mechanisms that regulate macrophage plasticity will be an important step towards realizing the potential of personalized immunomodulatory therapy.

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It Is All about (U)biquitin: Role of Altered Ubiquitin-Proteasome System and UCHL1 in Alzheimer Disease

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/2756068 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 43

Author(s):

Antonella Tramutola ◽

Fabio Di Domenico ◽

Eugenio Barone ◽

Marzia Perluigi ◽

D. Allan Butterfield

Keyword(s):

Oxidative Stress ◽

Alzheimer Disease ◽

Ubiquitin Proteasome System ◽

Oxidative Modification ◽

Age Related ◽

Ubiquitin Proteasome ◽

Proteasome Pathway ◽

And Function ◽

Cellular Components

Free radical-mediated damage to macromolecules and the resulting oxidative modification of different cellular components are a common feature of aging, and this process becomes much more pronounced in age-associated pathologies, including Alzheimer disease (AD). In particular, proteins are particularly sensitive to oxidative stress-induced damage and these irreversible modifications lead to the alteration of protein structure and function. In order to maintain cell homeostasis, these oxidized/damaged proteins have to be removed in order to prevent their toxic accumulation. It is generally accepted that the age-related accumulation of “aberrant” proteins results from both the increased occurrence of damage and the decreased efficiency of degradative systems. One of the most important cellular proteolytic systems responsible for the removal of oxidized proteins in the cytosol and in the nucleus is the proteasomal system. Several studies have demonstrated the impairment of the proteasome in AD thus suggesting a direct link between accumulation of oxidized/misfolded proteins and reduction of this clearance system. In this review we discuss the impairment of the proteasome system as a consequence of oxidative stress and how this contributes to AD neuropathology. Further, we focus the attention on the oxidative modifications of a key component of the ubiquitin-proteasome pathway, UCHL1, which lead to the impairment of its activity.

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