Resolvin D1 reduces mitochondrial damage to photoreceptors of primary retinal cells exposed to high glucose

Trotta, Maria Consiglia; Pieretti, Gorizio; Petrillo, Francesco; Alessio, Nicola; Maisto, Rosa; D’Amico, Michele

doi:10.1002/jcp.29303

Cited by 16 publications

(14 citation statements)

References 43 publications

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“…It is reported that these differential genes play an important role in the process of mitochondrial damage. [34][35][36][37][38][39] For example, the expression of ndufb6 and ndufs3 increased after AF-HF001 treatment, which increased myocardial contractility and improved oxidative damage. 38 Overexpression of Uqcrh can improve mitochondrial function.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of agrimonolide on hypoxia‐induced H9c2 cell injury by maintaining mitochondrial homeostasis

Wang

Liu

et al. 2021

J of Cellular Biochemistry

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Cardiomyocyte death caused by hypoxia is one of the main causes of myocardial infarction or heart failure, and mitochondria play an important role in this process. Agrimonolide (AM) is a monomeric component extracted from Agrimonia pilosa L. and has antioxidant, antitumor, and anti-inflammatory effects. This study aimed to investigate the role and mechanism of AM in improving hypoxia-induced H9c2 cell damage. The results showed that low AM concentrations promote H9c2 cell proliferation and increase cellular ATP content. Transcriptome sequencing showed that AM induces differential expression of genes in H9c2 cells. Gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that these genes were concentrated in mitochondrial function. Subsequent experiments confirmed that AM regulates hypoxia-induced cell cycle arrest. AM inhibited the rate of apoptosis by regulating the expression of apoptosis-related proteins, reducing the level of cleaved Caspase 3 and Bax, and increasing the level of Bcl2, thereby protecting H9c2 cells from hypoxiainduced apoptosis. AM restored the mitochondrial membrane potential, inhibited the generation of ROS, maintained the normal shape of the mitochondria, improved the level of the mitochondrial functional proteins OPA1, MFN1, MFN2, Tom20, and increased the level of ATP. In conclusion, AM protects H9c2 cells from hypoxia-induced cell damage.

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Section: Discussionmentioning

confidence: 99%

Protective effects of agrimonolide on hypoxia‐induced H9c2 cell injury by maintaining mitochondrial homeostasis

Wang

Liu

et al. 2021

J of Cellular Biochemistry

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“…Therefore, mitochondrial damage determines myocardial damage during IR and subsequent remodeling [34][35][36]. RvD1 has already been proven to reduce reactive oxygen species levels, improve mitochondrial morphology and function, promote mitochondrial DNA repair in primary retinal cells with diabetic retinopathy [37]. In diabetes, high blood glucose and free fatty acids induce ECs mitochondrial ssion, with high levels of reactive oxygen species (ROS), leading to blunted cell growth and altered cell-adhesion molecule expression on the cell surface [38].…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 Inhibits Endothelial Permeability and Mitochondrial Damage Following Cardiac Ischemia–Reperfusion in Diabetic Mice

Zhang¹,

Huang²,

Chen³

et al. 2021

Preprint

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Purpose Resolvin D1(RvD1), a metabolite derived from docosahexaenoic acid, plays important therapeutic roles in inflammatory diseases. However, the role of RvD1 in diabetic myocardial ischemia/reperfusion (IR) is still unknown. Methods Diabetic mice was established by high-fat diet and streptozotocin, RvD1 was pretreated by intraperitoneal injection for 3 days, followed by myocardial IR. To evaluate the effects of RvD1 on chronic cardiac remodeling, RvD1 was administered for another 2 weeks after IR. The effects of RvD1 following myocardial IR injury were measured, including severity of infarct size, regional inflammation, cardiac function, as well as permeability of cultured endothelial monolayer. Mitochondrial reactive oxygen species (mito-ROS) and mitochondrial membrane potential (MMP) were determined by MitoSOX and JC-1. Results RvD1 pretreatment significantly reduced infarct size and the content of Evans blue in injured heart, which was associated with decreased endothelial damage. RvD1 also reduced leukocyte density, gene expression of inflammatory cytokines, cardiomyocytes death, and mitochondrial damage compared to control group. At 2 weeks after myocardial IR, RvD1 treatment partially improved cardiac performance, and reduced cardiac fibrosis in diabetic IR. In vitro, RvD1 attenuated endothelial leakage induced by hypoxia-reoxygenation, H2O2, and Lipopolysaccharide (LPS), meanwhile, RvD1 also remarkably protected endothelial cells from H2O2-induced mitochondrial damage as evident from the decreased MMP and increased mito-ROS, which were associated with the preservation of VE-cadherin Conclusion RvD1 protects the heart against diabetic IR-induced injuries by attenuating endothelial permeability and mitochondrial damage. Our study also provide insight into a novel underlying mechanism and a new strategy for treating diabetic IR.

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“…Dietary supplementation with sh oil for MCMV infection promoted mitochondrial biosynthesis in the liver cells of male C57BL/6 mice [38]. Both RvD1 and MCTR1 have been reported to improve mitochondrial biogenesis and function induced by multiple adverse factors, such as in ammation or high sugar [39][40][41].…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic Acid Supplementation Represses the Early Immune Response Against Murine Cytomegalovirus but Enhances NK Cell Effector Function

Wu¹,

Wang²,

Peng³

et al. 2021

Preprint

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Background Docosahexaenoic acid (DHA) supplementation is beneficial for several chronic diseases; however, its effect on immune regulation is still debated. Given the prevalence of cytomegalovirus (CMV) infection and because natural killer (NK) cells are the component of innate immunity critical for controlling CMV infection, the current study explored the effect of a DHA-enriched diet on susceptibility and the NK cell effector response to murine (M) CMV infection. Results Male C57BL/6 mice fed a control or DHA-enriched diet for 3 weeks were infected with MCMV and sacrificed at the indicated time points postinfection. Compared with control mice, DHA-fed mice had higher liver and spleen viral loads on day 7 postinfection, but final MCMV clearance was not affected. The ratio and total numbers of NK cells and their terminal mature cell subset (KLRG1+ and Ly49H+ NK cells) were reduced compared with those in control mice on day 7 but not day 21 postinfection. DHA feeding resulted in higher IFN-γ and granzyme B expression in splenic NK cells on day 7 postinfection. A mechanistic analysis showed that the splenic NK cells of DHA-fed mice showed enhanced glucose uptake, increased CD71 and CD98 expression, and higher mitochondrial mass and activity than those of control mice. In addition, DHA-fed mice showed reductions in the total numbers and activation of CD4+ and CD8+ T cells. Conclusions These results suggest that DHA supplementation represses the early response to CMV infection but preserves NK cell effector functions by improving mitochondrial activity, which may play critical roles in subsequent MCMV clearance.

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Resolvin D1 reduces mitochondrial damage to photoreceptors of primary retinal cells exposed to high glucose

Cited by 16 publications

References 43 publications

Protective effects of agrimonolide on hypoxia‐induced H9c2 cell injury by maintaining mitochondrial homeostasis

Protective effects of agrimonolide on hypoxia‐induced H9c2 cell injury by maintaining mitochondrial homeostasis

Resolvin D1 Inhibits Endothelial Permeability and Mitochondrial Damage Following Cardiac Ischemia–Reperfusion in Diabetic Mice

Docosahexaenoic Acid Supplementation Represses the Early Immune Response Against Murine Cytomegalovirus but Enhances NK Cell Effector Function

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