Crosstalk between Oxidative Stress and Exosomes

Zhang, Wenjun; Liu, Rong; Chen, Yuhua; Wang, Minghua; Du, Juan

doi:10.1155/2022/3553617

Cited by 31 publications

(25 citation statements)

References 71 publications

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“…Our study showed the antioxidant e cacy of ADSC exosomes in recipient keratinocytes, consistent with previous ndings. The antioxidant effects of MSC-derived exosomes are thought to involve the transfer of antioxidative enzyme mRNA, proteins, or miRNAs into recipient cells [39]. MSC-derived exosome therapy offers several advantages over stem cell transplantation itself [40].…”

Section: Discussionmentioning

confidence: 99%

Exosomes from adipose-derived stem cells alleviate inflammation and oxidative stress induced by psoriasis serum exosomes via autophagy regulation in keratinocytes

Kim,

Lee,

You

et al. 2023

Preprint

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Exosomes play a key role in cell communication and are involved in both pathological and physiological processes. Autophagy dysfunction and oxidative stress are linked to immune-mediated inflammatory diseases such as psoriasis. Stem cell-derived exosomes exhibit immunomodulatory and antioxidant efficacy. We aimed to investigate the impact of psoriasis serum-derived exosomes on inflammation, oxidative stress, and autophagy in keratinocytes. Additionally, we explored the therapeutic potential of adipose-derived stem cell (ADSC) exosomes against inflammation induced by psoriasis serum exosomes. To validate psoriasis patient serum-derived exosomes and ADSC exosomes, we used nanoparticle tracking analysis, western blotting, flow cytometry, and immunofluorescence. qPCR was used to study changes in the gene expression of proinflammatory cytokines and oxidative stress markers in HaCaT cells treated with psoriasis serum-derived exosomes or ADSC exosomes. The effects of these exosomes on autophagy in HaCaT cells were evaluated by western blotting and immunofluorescence. The treatment of HaCaT cells with psoriasis serum-derived exosomes increased proinflammatory cytokine production and oxidative stress-related factor (Nox2 and Nox4) expression and decreased Nrf2 expression via P65/NF-κB and P38/MAPK activation. Compared with healthy control serum-derived exosomes, psoriasis serum-derived exosomes decreased ATG5, P62, Beclin1, and LC3 expression and autophagosome production in HaCaT cells. Conversely, ADSC exosomes suppressed proinflammatory cytokine and oxidative stress production, and restored autophagy in HaCaT cells treated with psoriasis serum-derived exosomes. These findings suggest that ADSC exosomes exhibit a suppressive effect on psoriasis serum exosome-induced inflammation and oxidative stress by regulating autophagy in keratinocytes.

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Section: Discussionmentioning

confidence: 99%

Exosomes from adipose-derived stem cells alleviate inflammation and oxidative stress induced by psoriasis serum exosomes via autophagy regulation in keratinocytes

Kim,

Lee,

You

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Therefore, IL-1β may induce hyperglycolysis in multiple cells [ 33 ]. It must be noted that IL-1β can induce elevated superoxide formation via activation of NADPH oxidases, since ROS can be produced not only via the mitochondrial electron transport chain but also via NADPH oxidases [ 34 ]. Moreover, a drop in the ΔΨm is a distinguishing mark of apoptotic cell death [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent

et al. 2022

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Recent studies have related mitochondrial impairment with peritoneal membrane damage during peritoneal dialysis (PD) therapy. Here, we assessed the involvement of mitochondrial dysfunction in the inflammatory response in human mesothelial cells, a hallmark in the pathogenesis of PD-related peritoneal membrane damage. Our ex vivo studies showed that IL-1β causes a drop in the mitochondrial membrane potential in cells from peritoneal effluent. Moreover, when mitochondrial damage was induced by inhibitors of mitochondrial function, a low-grade inflammatory response was generated. Interestingly, mitochondrial damage sensitized mesothelial cells, causing a significant increase in the inflammatory response induced by cytokines, in which ROS generation and NF-κB activation appear to be involved, since inflammation was counteracted by both mitoTEMPO (mitochondrial ROS scavenger) and BAY-117085 (NF-κB inhibitor). Furthermore, the natural anti-inflammatory antioxidant resveratrol significantly attenuated the inflammatory response, by reversing the decline in mitochondrial membrane potential and decreasing the expression of IL-8, COX-2 and PGE2 caused by IL-1β. These findings suggest that IL-1β regulates mitochondrial function in mesothelial cells and that mitochondrial dysfunction could induce an inflammatory scenario that sensitizes these cells, causing significant amplification of the inflammatory response induced by cytokines. Resveratrol may represent a promising strategy in controlling the mesothelial inflammatory response to PD.

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“…In contrast, OS can notably affect the number of exosomes by regulating the degradation of multivesicular bodies. High levels of OS promote the degradation of intracellular multivesicular bodies by activating autophagy, lessening the amount of exosomes, thereby influencing exosome function, reducing the antioxidant effect of exosomes, and exacerbating the damage of OS on oocytes (201). Qu et al determined that human umbilical cord MSC-derived exosomes carrying miR-126-3p promoted angiogenesis in POI rats and attenuated apoptosis of ovarian GCs, highlighting the potential of miR-126-3p-containing exosomes as an effective therapeutic strategy for POI treatment (202).…”

Section: Os-mediated Exosomes In Poimentioning

confidence: 99%

Premature ovarian insufficiency: a review on the role of oxidative stress and the application of antioxidants

Shi,

Zhu,

Zhang

et al. 2023

Front. Endocrinol.

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Normal levels of reactive oxygen species (ROS) play an important role in regulating follicular growth, angiogenesis and sex hormone synthesis in ovarian tissue. When the balance between ROS and antioxidants is disrupted, however, it can cause serious consequences of oxidative stress (OS), and the quantity and quality of oocytes will decline. Therefore, this review discusses the interrelationship between OS and premature ovarian insufficiency (POI), the potential mechanisms and the methods by which antioxidants can improve POI through controlling the level of OS. We found that OS can mediate changes in genetic materials, signal pathways, transcription factors and ovarian microenvironment, resulting in abnormal apoptosis of ovarian granulosa cells (GCs) and abnormal meiosis as well as decreased mitochondrial Deoxyribonucleic Acid(mtDNA) and other changes, thus accelerating the process of ovarian aging. However, antioxidants, mesenchymal stem cells (MSCs), biological enzymes and other antioxidants can delay the disease process of POI by reducing the ROS level in vivo.

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Crosstalk between Oxidative Stress and Exosomes

Cited by 31 publications

References 71 publications

Exosomes from adipose-derived stem cells alleviate inflammation and oxidative stress induced by psoriasis serum exosomes via autophagy regulation in keratinocytes

Exosomes from adipose-derived stem cells alleviate inflammation and oxidative stress induced by psoriasis serum exosomes via autophagy regulation in keratinocytes

Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent

Premature ovarian insufficiency: a review on the role of oxidative stress and the application of antioxidants

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