Protein chip and bioinformatic analyses of differentially expressed proteins involved in the effect of hydrogen-rich water on myocardial ischemia-reperfusion injury

Li, Liangtong; Liu, Tongtong; Li, Xiangzi; Liu, Xuanchen; Liu, Li; Li, Shaochun; Li, Zhilin; Zhou, Yujuan; Liu, Fulin

doi:10.7150/ijms.35984

Cited by 5 publications

(4 citation statements)

References 28 publications

(26 reference statements)

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“…The InnoScan 300 microarray scanner was used to scan the signal using the Cy3 channel (532 nm excitation frequency) to detect fluorescence. GSR‐CAA‐67 software was used to analyse the data (Li et al, 2019).…”

Section: Methodsmentioning

confidence: 99%

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Jiang

Chen

et al. 2023

Int Endodontic J

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Aim To investigate the regulatory role of miR‐155 and Kinesin Superfamily Proteins‐5C (KIF‐5C) in the progression of pulpitis based on bioinformatic analysis. Methodology Normal pulp tissues and pulpitis pulp tissues were collected and subjected to high‐throughput sequencing and the differentially expressed miRNAs were determined. An in vitro and in vivo pulpitis model was established. HE, IHC staining and histological evaluation were used to verify the inflammatory state of human and mouse pulp tissues. The mRNA expression of IL‐1β and TGF‐β1 were determined by RT‐qPCR and protein expression of IL‐1α, IL‐4, IL‐8, IL‐13, IFN‐γ, IL‐6, IL‐10 and MCP‐1 were determined by protein chip. The target genes of miR‐155 were predicted by miRanda database and verified by Dual‐luciferase reporter assay, RT‐qPCR and western blotting. MiR‐155 lentivirus were used to upregulate or downregulate miR‐155 and the siRNA of KIF‐5C was used to downregulate KIF‐5C. The expression of miR‐155 or KIF‐5C was determined by RT‐qPCR. All statistics were analysed using GraphPad prism 8.2. Results The high‐throughput sequencing results showed that 6 miRNAs (miR‐155, miR‐21, miR‐142, miR‐223, miR‐486, miR‐675) were significantly upregulated in diseased human pulp tissues, and miR‐155 was significantly elevated among the six miRNAs. RT‐qPCR results demonstrated that miR‐155 expression was upregulated in human pulpitic tissue, mice pulpitic tissue and LPS‐HDPCs. IL‐1β was increased while TGF‐β1 was decreased in lenti‐miR‐155 transfected LPS‐HDPCs. Analysis of protein chip results indicated that lenti‐miR‐155 transfected LPS‐HDPCs produced higher levels of IL‐8, IL‐6, MCP‐1. The opposite results were obtained when miR‐155 was inhibited. Through miRanda database screen and Dual‐luciferase reporter assay, the target gene (KIF‐5C) of miR‐155 was identified. In lenti‐miR‐155 transfected LPS‐HDPCs, the expression of KIF‐5C was downregulated. However, when shRNA‐miR‐155 was transfected to LPS‐HDPCs, the opposite result was obtained. Silent RNA was used to knock down KIF‐5C, the results showed that when both KIF‐5C and miR‐155 were knocked down simultaneously, the downregulated expression of inflammatory factors observed in LPS‐HDPCs following miR‐155 knockdown was rescued. Conclusion MiR‐155 plays an important role in promoting pulpitis through targeting KIF‐5C and may serve as a potential therapeutic target.

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Section: Methodsmentioning

confidence: 99%

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Jiang

Chen

et al. 2023

Int Endodontic J

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“…In a recent study using an isolated heart model with I/R injury, perfusion with HRW resulted in a decrease in apoptosis by up-regulating the JAK-STAT and PI3K-AKT signaling pathways (Fig. 2 ) [ 44 ]. All of these ex vivo reports are comprehensively summarized in Table 4 .…”

Section: Effects Of Hydrogen Treatment On the Heart: Reports From Ex ...mentioning

confidence: 99%

Hydrogen therapy as a potential therapeutic intervention in heart disease: from the past evidence to future application

Saengsin

Sittiwangkul

Chattipakorn

2023

Cell. Mol. Life Sci.

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Cardiovascular disease is the leading cause of mortality worldwide. Excessive oxidative stress and inflammation play an important role in the development and progression of cardiovascular disease. Molecular hydrogen, a small colorless and odorless molecule, is considered harmless in daily life when its concentration is below 4% at room temperature. Owing to the small size of the hydrogen molecule, it can easily penetrate the cell membrane and can be metabolized without residue. Molecular hydrogen can be administered through inhalation, the drinking of hydrogen-rich water, injection with hydrogen-rich-saline, and bathing of an organ in a preservative solution. The utilization of molecular hydrogen has shown many benefits and can be effective for a wide range of purposes, from prevention to the treatment of diseases. It has been demonstrated that molecular hydrogen exerts antioxidant, anti-inflammatory, and antiapoptotic effects, leading to cardioprotective benefits. Nevertheless, the exact intracellular mechanisms of its action are still unclear. In this review, evidence of the potential benefits of hydrogen molecules obtained from in vitro, in vivo , and clinical investigations are comprehensively summarized and discussed with a focus on the cardiovascular aspects. The potential mechanisms involved in the protective effects of molecular hydrogen are also presented. These findings suggest that molecular hydrogen could be used as a novel treatment in various cardiovascular pathologies, including ischemic–reperfusion injury, cardiac injury from radiation, atherosclerosis, chemotherapy-induced cardiotoxicity, and cardiac hypertrophy.

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“…A multicenter, open-label clinical trial showed that hydrogen/oxygen mixed gas inhalation improved disease severity and dyspnea in patients with Coronavirus disease 2019 (COVID-19) ( Guan et al, 2020 ). In addition, H 2 has an excellent therapeutic effect on inflammation, ischemia-reperfusion injury, diabetes, cancer, atherosclerosis, and other diseases ( Li et al, 2013 ; Lee et al, 2015 ; Shimada et al, 2016 ; Li et al, 2019 ). It can reduce the levels of serum Low-Density Lipoprotein Cholesterol (LDL-C) and apolipoprotein- B (Apo-B), improve the high-density lipoprotein (HDL) functions damaged by dyslipidemia ( Song et al, 2013 ), reduce the formation of neointima after vein transplantation in rats ( Sun et al, 2012 ), and decrease hypertension, angiogenesis imbalance and oxidative stress caused by placental ischemia ( Ushida et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells Injury via PI3K/AKT/eNOS Pathway

et al. 2022

Front. Pharmacol.

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Endotoxins and other harmful substances may cause an increase in permeability in endothelial cells (ECs) monolayers, as well as ECs shrinkage and death to induce lung damage. Lipopolysaccharide (LPS) can impair endothelial progenitor cells (EPCs) functions, including proliferation, migration, and tube formation. EPCs can migrate to the damaged area, differentiate into ECs, and participate in vascular repair, which improves pulmonary capillary endothelial dysfunction and maintains the integrity of the endothelial barrier. Hydrogen (H2) contributes to the repairment of lung injury and the damage of ECs. We therefore speculate that H2 protects the EPCs against LPS-induced damage, and it’s mechanism will be explored. The bone marrow-derived EPCs from ICR Mice were treated with LPS to establish a damaged model. Then EPCs were incubated with H2, and treated with PI3K inhibitor LY294002 and endothelial nitric oxide synthase (eNOS) inhibitor L-NAME. MTT assay, transwell assay and tube formation assay were used to detect the proliferation, migration and angiogenesis of EPCs. The expression levels of target proteins were detected by Western blot. Results found that H2 repaired EPCs proliferation, migration and tube formation functions damaged by LPS. LY294002 and L-NAME significantly inhibited the repaired effect of H2 on LPS-induced dysfunctions of EPCs. H2 also restored levels of phosphor-AKT (p-AKT), eNOS and phosphor-eNOS (p-eNOS) suppressed by LPS. LY294002 significantly inhibited the increase of p-AKT and eNOS and p-eNOS expression exposed by H2. L-NAME significantly inhibited the increase of eNOS and p-eNOS expression induced by H2. H2 repairs the dysfunctions of EPCs induced by LPS, which is mediated by PI3K/AKT/eNOS signaling pathway.

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Protein chip and bioinformatic analyses of differentially expressed proteins involved in the effect of hydrogen-rich water on myocardial ischemia-reperfusion injury

Cited by 5 publications

References 28 publications

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Hydrogen therapy as a potential therapeutic intervention in heart disease: from the past evidence to future application

Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells Injury via PI3K/AKT/eNOS Pathway

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