miR-214 Protects Against Uric Acid-Induced Endothelial Cell Apoptosis

Yang, Bingyu; Li, Shuzhen; Zhu, Jun; Huang, Songming; Zhang, Aihua; Ding, Guofu; Zhang, Yue

doi:10.3389/fmed.2020.00411

Cited by 12 publications

(8 citation statements)

References 40 publications

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“…Uric acid is mainly excreted in the kidney [ 36 ]. Some in vitro studies have found that PGE2 release of cells increases under the stimulation of uric acid [ 37 , 38 ]. However, these experiments were not confirmed in vivo.…”

Section: Discussionmentioning

confidence: 99%

The association of urinary prostaglandins with uric acid in hyperuricemia patients

Lin

Zheng

et al. 2022

BMC Nephrol

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Purpose To explore the association between uric acid and urinary prostaglandins in male patients with hyperuricemia. Methods A total of 38 male patients with hyperuricemia in outpatients of Huadong Hospital from July 2018 to January 2020 were recruited. Serum uric acid (SUA), 24 h urinary uric acid excretion and other indicators were detected respectively. 10 ml urine was taken to determine prostaglandin prostaglandin D (PGD), prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), 6-keto-PGF1α, thromboxane A2 (TXA2) and thromboxane B2 (TXB2). Fraction of uric acid excretion (FEua) and uric acid clearance rate (Cua) were calculated. According to the mean value of FEua and Cua, patients were divided into two groups, respectively. The independent-samples t test and the Mann–Whitney U test were applied for normally and non-normally distributed data, respectively. Results After adjusting confounding factors (age, BMI, eGFR, TG, TC, HDL and LDL), SUA was negatively correlated with urinary PGE1(r = -0.615, P = 0.009) and PGE2(r = -0.824, P < 0.001). Compared with SUA1 group (SUA < 482.6 mg/dl), SUA2 (SUA $$\ge$$ ≥ 482.6 mg/dl) had lower urinary PGE1(P = 0.022) and PGE2(P = 0.019) levels. Cua was positively correlated with PGE2 (r = 0.436, P = 0.01). The correlation persisted after adjustment for age, BMI, eGFR, TG, TC, HDL and LDL by multiple linear regression analysis. In the Cua1 group (Cua < 4.869 mL /min/1.73 m2), PGE2 were lower than that in Cua2 (Cua $$\ge$$ ≥ 4.869 mL /min/1.73 m2) group (P = 0.011). Conclusions In male patients with hyperuricemia, SUA was negatively correlated with urinary PGE2, Cua was positively correlated with urinary PGE2. Urinary PGE2 were significantly different between different SUA and Cua groups.

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Section: Discussionmentioning

confidence: 99%

The association of urinary prostaglandins with uric acid in hyperuricemia patients

Lin

Zheng

et al. 2022

BMC Nephrol

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“…miRNAs are non-coding RNAs, 18-22 nucleotides in length, that regulate the expression of their target genes by specific binding to their 3'-UTR (10). Emerging evidence has suggested that miRNAs are involved in several cellular processes, including cell proliferation, apoptosis, differentiation and invasion (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑25 protects nucleus pulposus cells against apoptosis via targeting SUMO2 in intervertebral disc degeneration

Lei

Tang

et al. 2021

Mol Med Rep

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It has been repor ted that m icroR NA (miRNA/miR)-25 is downregulated in patients with intervertebral disc degeneration (IVDD). However, the potential role of miR-25 in IVDD remains unclear. Therefore, the present study aimed to investigate the effects of miR-25 on human intervertebral disc nucleus pulposus cells (NPCs). The expression levels of miR-25 and those of small ubiquitin-related modifier 2 (SUMO2) were determined in human nucleus pulposus (NP) tissues by reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses. Subsequently, the potential interaction between miR-25 and SUMO2 was validated via dual-luciferase reporter assay and RNA pull-down assay with biotinylated miRNA. The effects of miR-25 on NPC proliferation and apoptosis were evaluated using Cell Counting Kit-8 assay, 5-ethynyl-2'-deoxyuridine incorporation assay, and flow cytometry. The results showed that miR-25 was downregulated in patients with IVDD. In addition, miR-25 increased the proliferation of NPCs and inhibited their apoptosis. Furthermore, the current study verified that miR-25 could directly target SUMO2 and regulate its expression via the p53 signaling pathway. Additionally, the effects of miR-25 on NPCs were abrogated following SUMO2 overexpression. Overall, the results of the present study demonstrated that miR-25 could promote the proliferation and inhibit the apoptosis of NPCs via targeting SUMO2, suggesting that miR-25 may be a potential target in the treatment of IVDD.

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“…Hyperuricemia is considered a risk factor for a number of disorders, including diabetes mellitus, cardiovascular diseases and metabolic syndrome ( 21 ). Accumulating evidence suggests that UA can cause endothelial injury and dysfunction, though the mechanism remain unclear ( 22 , 23 ). Apoptosis induced by ox-LDL in vascular endothelial cells is an important process in the progression of atherosclerosis ( 11 ).…”

Section: Discussionmentioning

confidence: 99%

FGF21 attenuates high uric acid‑induced endoplasmic reticulum stress, inflammation and vascular endothelial cell dysfunction by activating Sirt1

et al. 2021

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Uric acid (UA) is the final oxidation product of purine metabolism. Hyperuricemia has been previously reported to contribute to vascular endothelial dysfunction and the development of cardiovascular diseases, metabolic syndrome and chronic kidney diseases. In addition, it has been reported that fibroblast growth factor 21 (FGF21) can exert regulatory effects on UA-induced lipid accumulation. Therefore, the present study aimed to investigate the possible role of FGF21 in HUVEC cell injury induced by UA. The study used UA to induce HUVEC cell injury, inhibited sirtuin 1 (Sirt1) expression using EX527 and overexpressed FGF21 by transfection. Subsequently, reverse transcription-quantitative PCR was performed to measure the mRNA expression levels of FGF21, Sirt1 and inflammatory cytokines TNF-α, IL-1β and IL-6, whereas western blotting was performed to measure their corresponding protein expression levels including FGF21, Sirt1, NLR family pyrin domain containing 3, pro-caspase1, apoptosis-associated speck-like protein containing a CARD, activating transcription factor 4, C/EBP homologous protein and eukaryotic initiation factor 2. Furthermore, dichloro-dihydro-fluorescein diacetate staining was performed to measure intracellular reactive oxygen species (ROS) generation in HUVECs. The levels of ROS and nitric oxide were also quantified using commercial assay kits. The results demonstrated that overexpression of FGF21 significantly inhibited UA treatment-induced endoplasmic reticulum (ER) stress, inflammation and oxidative stress in HUVECs. Furthermore, overexpression of FGF21 significantly activated Sirt1. The sirt1 inhibitor, EX527, significantly abrogated the suppressive effects of FGF21 overexpression on ER stress, inflammation and oxidative stress in UA-stimulated HUVECs. To conclude, results of the present study suggested that FGF21 may attenuate UA-induced ER stress, inflammation and vascular endothelial cell dysfunction by activating Sirt1. Therefore, FGF21 may be a potential effective target for the future treatment of vascular endothelial cell dysfunction.

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miR-214 Protects Against Uric Acid-Induced Endothelial Cell Apoptosis

Cited by 12 publications

References 40 publications

The association of urinary prostaglandins with uric acid in hyperuricemia patients

The association of urinary prostaglandins with uric acid in hyperuricemia patients

MicroRNA‑25 protects nucleus pulposus cells against apoptosis via targeting SUMO2 in intervertebral disc degeneration

FGF21 attenuates high uric acid‑induced endoplasmic reticulum stress, inflammation and vascular endothelial cell dysfunction by activating Sirt1

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