Role of mitochondrial reactive oxygen species in homeostasis regulation

Zhang, Baoyi; Pan, Cunyao; Feng, Chong; Yan, Changqing; Yu, Yifan; Chen, Zhaoli; Guo, Changjiang; Wang, Xinxing

doi:10.1080/13510002.2022.2046423

Cited by 173 publications

(110 citation statements)

References 109 publications

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“…In the 20 μg/mL NH 2 -PS NPs-treated groups, the examined genes including cycs , mt-co-1 , cox7a2, and slc25a4 showed a significant downward tendency ( Figure 5 i,k,l,n), indicating the potential risks of NH 2 -PS NPs to mitochondria function of HUVEC. Mitochondria are vital subcellular organelles to eukaryotic cells, which play valuable roles in energy production, ROS generation, and cellular signaling [ 37 ]. Therefore, we assessed the effects of PS NPs on the ATP production capacity.…”

Section: Resultsmentioning

confidence: 99%

Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells

Fan

et al. 2022

Toxics

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As emerging contaminants, nano-plastics have become a major cause for concern for their adverse effects on the ecosystem and human health. The nano-sized properties of nano-plastics enable their exposure risks to humans through the food chain or other ways. However, the fate and adverse impact of nano-plastics on the human cardiovascular system are lacking. In this regard, the human umbilical vein endothelial cell line HUVEC was applied as a cell model to investigate the biological effects of noncharged polystyrene nano-plastics (PS NPs) and amino-functionalized nano-plastics (NH2-PS NPs). The positively charged PS NPs exhibited higher cytotoxicity to HUVEC, as evidenced by the decreased cell viability, enhanced ROS generation, and decreased mitochondria membrane potential triggered by NH2-PS NPs. Importantly, RT-PCR analysis revealed that NH2-PS NPs dysregulated the mitochondrial dynamics, replication, and function-related gene expression. This study demonstrated that NH2-PS NPs presented higher risks to endothelial cells than non-charged nano-plastics by interfering with mitochondria, which supported the direct evidence and expanded the potential risks of PS NPs.

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Section: Resultsmentioning

confidence: 99%

Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells

Fan

et al. 2022

Toxics

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“…It has been shown that resveratrol increased mitochondrial content in ECs. This was related with SIRT1 activation, further eNOS upregulation, and induction of mitochondrial biogenesis [ 54 ]. Resveratrol treatment also stimulated biogenesis of mitochondria in type 2 diabetic mice aortas [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

“…This was related with SIRT1 activation, further eNOS upregulation, and induction of mitochondrial biogenesis [ 54 ]. Resveratrol treatment also stimulated biogenesis of mitochondria in type 2 diabetic mice aortas [ 54 ]. However, manipulating the mitochondrial function may also be unfavorable in ECs, due to mitochondrial ROS (mROS) production [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

CoCl2-Mimicked Endothelial Cell Hypoxia Induces Nucleotide Depletion and Functional Impairment That Is Reversed by Nucleotide Precursors

et al. 2022

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Chronic hypoxia drives vascular dysfunction by various mechanisms, including changes in mitochondrial respiration. Although endothelial cells (ECs) rely predominantly on glycolysis, hypoxia is known to alter oxidative phosphorylation, promote oxidative stress and induce dysfunction in ECs. Our work aimed to analyze the effects of prolonged treatment with hypoxia-mimetic agent CoCl2 on intracellular nucleotide concentration, extracellular nucleotide breakdown, mitochondrial function, and nitric oxide (NO) production in microvascular ECs. Moreover, we investigated how nucleotide precursor supplementation and adenosine deaminase inhibition protected against CoCl2-mediated disturbances. Mouse (H5V) and human (HMEC-1) microvascular ECs were exposed to CoCl2-mimicked hypoxia for 24 h in the presence of nucleotide precursors: adenine and ribose, and adenosine deaminase inhibitor, 2′deoxycoformycin. CoCl2 treatment decreased NO production by ECs, depleted intracellular ATP concentration, and increased extracellular nucleotide and adenosine catabolism in both H5V and HMEC-1 cell lines. Diminished intracellular ATP level was the effect of disturbed mitochondrial phosphorylation, while nucleotide precursors effectively restored the ATP pool via the salvage pathway and improved endothelial function under CoCl2 treatment. Endothelial protective effects of adenine and ribose were further enhanced by adenosine deaminase inhibition, that increased adenosine concentration. This work points to a novel strategy for protection of hypoxic ECs by replenishing the adenine nucleotide pool and promoting adenosine signaling.

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“…Exposure to a sudden change of environmental conditions typically induces stress reactions in organisms to counteract and prevent irreversible damage of cells, tissues or organs. Stabilization of metabolism plays a central role in such stress response because it is preliminary to perceive and integrate environmental signals (Zhang et al, 2022). Stability properties of a biochemical reaction network can be quantified via an SKM approach (Steuer et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

The trade-off function of photorespiration in a changing environment

Hernandez

Nägele

2022

Preprint

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The photorespiratory pathway in plants comprises metabolic reactions distributed across several cellular compartments. It emerges from the dual catalytic function of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) which either carboxylates or oxygenates ribulose-1,5-bisphosphate (RuBP). Carboxylation reactions produce 3-phospho-glycerate (3PGA) molecules which are substrate for central carbohydrate metabolism while oxygenation forms 2-phosphoglycolate (2PG) molecules which are substrate for the multicompartmental recovery process of photorespiration. Further, 2PG is a strong inhibitor of several enzymes involved in the Calvin-Benson-Bassham cycle which challenges the experimental and theoretical study of carbon assimilation, photorespiration and metabolic regulation in vivo. Here, an approach of structural kinetic modeling (SKM) is presented to investigate the extend of stabilization of CBC and carbohydrate metabolism by photorespiration. Further, our approach highlights the importance of feedback regulation by 2-PG for alleviation of environmental perturbation. Our findings indicate that oxygenation of RuBP by Rubisco significantly stabilizes CBC activity and, thus, carbohydrate metabolism. Based on our findings, we suggest a trade-off function of photorespiration which reduces carbon assimilation rates but simultaneously stabilizes metabolism by increasing plasticity of metabolic regulation within the chloroplast. Furthermore, our analysis suggests a stabilizing effect of increasing the partition of newly assimilated carbon going towards sucrose biosynthesis. With this, our analysis sheds light on the role of a multicompartmental metabolic pathway in stabilizing plant metabolism within a changing environment.

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Role of mitochondrial reactive oxygen species in homeostasis regulation

Cited by 173 publications

References 109 publications

Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells

Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells

CoCl2-Mimicked Endothelial Cell Hypoxia Induces Nucleotide Depletion and Functional Impairment That Is Reversed by Nucleotide Precursors

The trade-off function of photorespiration in a changing environment

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