Sirt3 overexpression alleviates hyperglycemia-induced vascular inflammation through regulating redox balance, cell survival, and AMPK-mediated mitochondrial homeostasis

2019 ◽  
Vol 39 (4) ◽  
pp. 341-349
Author(s):  
Yunfei Wang ◽  
Xue Zhang ◽  
Peng Wang ◽  
Yiting Shen ◽  
Kai Yuan ◽  
...  
Keyword(s):  
Cell Survival ◽  
Vascular Inflammation ◽  
Redox Balance ◽  
Mitochondrial Homeostasis

BNIP3 Mediates the Different Adaptive Responses of Fibroblast-like Synovial Cells to Hypoxia in Patients With Osteoarthritis and Rheumatoid Arthritis

2021 ◽  
Author(s):  
Deng Ran ◽  
Wang Yan ◽  
Bu Yanhong ◽  
Hong Wu
Keyword(s):  
Rheumatoid Arthritis ◽  
Flow Cytometry ◽  
Western Blot ◽  
Cell Survival ◽  
Redox Balance ◽  
Adaptation To Hypoxia ◽  
Synovial Cells ◽  
Adaptive Responses ◽  
Promote Cell Survival ◽  
The Difference

Abstract Background: Hypoxia is one of the important characteristics of synovial microenvironment in rheumatoid arthritis (RA), and it is very important in the process of synovial hyperplasia. Fibroblast-like synovial cells (FLSs) are relatively affected by hypoxia injury in cell survival, while FLSs from patients with RA (RA-FLSs) are particularly resistant to hypoxia-induced cell death. The purpose of this study was to evaluate whether FLSs in patients with osteoarthritis (OA) and RA-FLSs have the same adaptation to hypoxia. Methods: CCK-8, flow cytometry and BrdU were used to detect the proliferation of OA-FLSs and RA-FLSs under different oxygen concentrations. Apoptosis was detected by AV/PI, TUNEL and Western blot, mitophagy was observed by electron microscope and Western blot, mitochondrial state was detected by reactive oxygen species (ROS) and mitochondrial membrane potential by flow cytometry, BNIP3 and HIF-1α were detected by Western blot and RT-qPCR. The silencing of BNIP3 is achieved by stealth RNA system technology. Results: After hypoxia, the survival rate of OA-FLSs was reduced, and the proliferation activity of RA-FLSs was further increased. Hypoxia induced increased apoptosis and inhibited autophagy of OA-FLSs, but not in RA-FLSs. Hypoxia treatment led to a more lasting adaptive response. RA-FLSs showed a more significant increase in gene expression regulated by HIF-1α transcription. Interestingly, they showed higher BNIP3 expression than OA-FLSs, and showed stronger mitophagy and proliferation activities. The BNIP3 siRNA experiment in RA-FLSs confirmed the potential role of BNIP3 in the survival of FLSs. The inhibition of BNIP3 resulted in the decrease of cell proliferation and the decrease of mitophagy and the increase of apoptosis. Conclusion: In summary, RA-FLSs maintained redox balance through mitophagy to promote cell survival under hypoxia. The mitophagy of OA-FLSs was too little to maintain the redox balance of mitochondria, leading to apoptosis. The difference of mitophagy between OA-FLSs and RA-FLSs under hypoxia is mediated by the expression of BNIP3.

scholarly journals Bmi1 regulates auditory hair cell survival by maintaining redox balance

2015 ◽  
Vol 6 (1) ◽  
pp. e1605-e1605 ◽  
Author(s):  
Y Chen ◽  
L Li ◽  
W Ni ◽  
Y Zhang ◽  
S Sun ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Survival ◽  
Redox Balance

scholarly journals Antioxidant intervention promotes cell survival and redox balance within the ovary and subsequent oocyte resulting in improved IVF outcomes

2018 ◽  
Vol 110 (4) ◽  
pp. e320
Author(s):  
J. Parks ◽  
B. McCallie ◽  
A. Patton ◽  
N.I. McCubbin ◽  
W.B. Schoolcraft ◽  
...  
Keyword(s):  
Cell Survival ◽  
Redox Balance ◽  
Ivf Outcomes

scholarly journals A co-opted endogenous retroviral envelope promotes cell survival by controlling SLC31A1/CTR1-mediated copper transport and homeostasis

2021 ◽  
Author(s):  
Sandrine Tury ◽  
Lise Chauveau ◽  
Valerie Courgnaud ◽  
Jean-Luc Battini
Keyword(s):  
Cell Survival ◽  
Redox Balance ◽  
Copper Accumulation ◽  
Cell Physiology ◽  
Critical Element ◽  
Cellular Functions ◽  
Copper Transporter ◽  
Metabolic Functions ◽  
Copper Excess ◽  
Unique Mechanism

Copper is a critical element for eukaryotic life, involved in numerous cellular functions and in redox balance but it can be toxic in excess. Therefore, tight regulation of copper acquisition and homeostasis is essential for cell physiology and survival. Here, we identified a unique mechanism for cell survival involving the regulation of copper homeostasis by an endogenous retroviral (ERV) envelope glycoprotein called Refrex1. We show that extracellular copper sensing by cells increased Refrex1 expression, which in turn regulated copper acquisition through interaction with the main copper transporter SLC31A1/CTR1. Downmodulation of Refrex1 resulted in intracellular copper accumulation leading to ROS production and subsequent apoptosis, which could be reverted by copper chelator treatment. Our results demonstrate that Refrex1 has been co-opted for its ability to regulate copper entry through CTR1 interaction in order to limit copper excess for a proper redox balance, and suggests that other ERV may have similar metabolic functions among vertebrates.

scholarly journals PRDX4 and Its Roles in Various Cancers

2019 ◽  
Vol 18 ◽  
pp. 153303381986431
Author(s):  
Wenqiao Jia ◽  
Pengxiang Chen ◽  
Yufeng Cheng
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Stem Cells ◽  
Cell Survival ◽  
Redox Regulation ◽  
Redox Balance ◽  
Vital Role ◽  
Research Progress ◽  
A Cell ◽  
Novel Target

Reactive oxygen species play a vital role in cell survival by regulating physiological metabolism and signal transduction of cells. The imbalance of oxidant and antioxidant states induces oxidative stress within a cell. Redox regulation and oxidative stress are closely related to survival and proliferation of stem cells, cancer cells, and cancer stem cells. Peroxiredoxin 4, a typical endoplasmic reticulum-resident 2-Cys antioxidant of peroxiredoxins, can fine-tune hydrogen peroxide catabolism which affects cell survival by affecting redox balance, oxidative protein folding, and regulation of hydrogen peroxide signaling. Recent studies revealed the overexpression of peroxiredoxin 4 in several kinds of cancers, such as breast cancer, prostate cancer, ovarian cancer, colorectal cancer, and lung cancer. And it has been demonstrated that peroxiredoxin 4 causally contributes to tumorigenesis, therapeutic resistance, metastasis, and recurrence of tumors. In this article, the characteristics of peroxiredoxin 4 in physiological functions and the cancer-related research progress of mammalian peroxiredoxin 4 is reviewed. We believe that peroxiredoxin 4 has the potential of serving as a novel target for multiple cancers.

Effect of mitophagy in oocytes and granulosa cells on oocyte quality†

2020 ◽  
Author(s):  
Qiuzi Shen ◽  
Yu Liu ◽  
Honggang Li ◽  
Ling Zhang
Keyword(s):  
Cell Survival ◽  
Granulosa Cells ◽  
Mitochondrial Function ◽  
Oocyte Quality ◽  
Reproductive Technology ◽  
Developmental Competence ◽  
Mitochondrial Homeostasis ◽  
New Directions ◽  
Developmental Capacity ◽  
Assisted Reproductive Technology Treatment

Abstract Mitophagy is the process by which cells selectively remove supernumerary or damaged mitochondria through autophagy, and is crucial for mitochondrial homeostasis and cell survival. Mitochondria play vital roles in determining the developmental competence of oocytes. During the early stages of oogenesis, aberrant mitochondria can be removed by mitophagy. After oocyte formation, mitophagy is not actively initiated to clear damaged mitochondria despite the presence of mitophagy regulators in oocytes, which leads to the transmission of dysfunctional mitochondria from the oocyte to the embryo. However, granulosa cells around oocytes can improve mitochondrial function through mitophagy, thereby improving oocyte developmental capacity. Furthermore, this review discusses recent work on the substances and environmental conditions that affect mitophagy in oocytes and granulosa cells, thus providing new directions for improving oocyte quality during assisted reproductive technology treatment.

Mitochondrial Proteases: Multifaceted Regulators of Mitochondrial Plasticity

2020 ◽  
Vol 89 (1) ◽  
pp. 501-528 ◽  
Author(s):  
Soni Deshwal ◽  
Kai Uwe Fiedler ◽  
Thomas Langer
Keyword(s):  
Quality Control ◽  
Cell Survival ◽  
Protein Processing ◽  
Regulatory Proteins ◽  
Mitochondrial Proteins ◽  
Signaling Cascades ◽  
Dual Function ◽  
Mitochondrial Homeostasis ◽  
Physiological Demands

Mitochondria are essential metabolic hubs that dynamically adapt to physiological demands. More than 40 proteases residing in different compartments of mitochondria, termed mitoproteases, preserve mitochondrial proteostasis and are emerging as central regulators of mitochondrial plasticity. These multifaceted enzymes limit the accumulation of short-lived, regulatory proteins within mitochondria, modulate the activity of mitochondrial proteins by protein processing, and mediate the degradation of damaged proteins. Various signaling cascades coordinate the activity of mitoproteases to preserve mitochondrial homeostasis and ensure cell survival. Loss of mitoproteases severely impairs the functional integrity of mitochondria, is associated with aging, and causes pleiotropic diseases. Understanding the dual function of mitoproteases as regulatory and quality control enzymes will help unravel the role of mitochondrial plasticity in aging and disease.

scholarly journals Pro- and Antioxidant Functions of the Peroxisome-Mitochondria Connection and Its Impact on Aging and Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Amparo Pascual-Ahuir ◽  
Sara Manzanares-Estreder ◽  
Markus Proft
Keyword(s):  
Protein Complexes ◽  
Accelerated Aging ◽  
Redox Balance ◽  
Specific Protein ◽  
Environmental Cues ◽  
Dynamic Feature ◽  
Dynamic Nature ◽  
Functional Connection ◽  
Mitochondrial Homeostasis ◽  
The Impact

Peroxisomes and mitochondria are the main intracellular sources for reactive oxygen species. At the same time, both organelles are critical for the maintenance of a healthy redox balance in the cell. Consequently, failure in the function of both organelles is causally linked to oxidative stress and accelerated aging. However, it has become clear that peroxisomes and mitochondria are much more intimately connected both physiologically and structurally. Both organelles share common fission components to dynamically respond to environmental cues, and the autophagic turnover of both peroxisomes and mitochondria is decisive for cellular homeostasis. Moreover, peroxisomes can physically associate with mitochondria via specific protein complexes. Therefore, the structural and functional connection of both organelles is a critical and dynamic feature in the regulation of oxidative metabolism, whose dynamic nature will be revealed in the future. In this review, we will focus on fundamental aspects of the peroxisome-mitochondria interplay derived from simple models such as yeast and move onto discussing the impact of an impaired peroxisomal and mitochondrial homeostasis on ROS production, aging, and disease in humans.

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