MicroRNA-184 attenuates hypoxia and oxidative stress-related injury via suppressing apoptosis, DNA damage and angiogenesis in an in vitro age-related macular degeneration model

Aykutlu, Merve Şambel; Güçlü, Hande; Doğanlar, Zeynep Banu; Kurtdere, Ayşe Kardelen; Doğanlar, Oğuzhan

doi:10.1016/j.tiv.2022.105413

Cited by 10 publications

(3 citation statements)

References 46 publications

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“…miR-21, upregulated in the mouse renal calcinosis model triggered by glyoxylic acid, has been validated to target PPARA to dampen HK2 cell proliferation and facilitate apoptosis and lipid accumulation [ 26 ]. Notably, miR-184 plays a vital role in mediating inflammation and oxidative stress [ 9 , 27 ]. For example, there are enhanced levels of miR-184 and miR-150 in aging glomerular mesangial cells (GMCs) compared with them in young GMCs.…”

Section: Discussionmentioning

confidence: 99%

Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway

Han,

Zhang,

et al. 2023

Aging

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Background: Renal calculi are a very prevalent disease with a high incidence. Calcium oxalate (CaOx) is a primary constituent of kidney stones. Our paper probes the regulatory function and mechanism of miR-184 in CaOx-mediated renal cell damage. Methods: CaOx was used to treat HK2 cells and human podocytes (HPCs) to simulate kidney cell damage. The qRT-PCR technique checked the profiles of miR-184 and IGF1R. The examination of cell proliferation was conducted employing CCK8. TUNEL staining was used to monitor cell apoptosis. Western blot analysis was used to determine the protein profiles of apoptosis-concerned related proteins (including Mcl1, Bcl-XL, and Caspase-3), the NF-κB, Nrf2/HO-1, and Rap1 signaling pathways. ELISA confirmed the levels of the inflammatory factors IL-6, TNF-α, MCP1, and ICAM1. The targeting relationship between miR-184 and IGF1R was validated by dual luciferase assay and RNA immunoprecipitation assay. Results: Glyoxylate-induced rat kidney stones model and HK2 and HPC cells treated with CaOx demonstrated an increase in the miR-184 profile. Inhibiting miR-184 relieved CaOx-mediated renal cell inflammation, apoptosis and oxidative stress and activated the Rap1 pathway. IGF1R was targeted by miR-184. IGF1R activation by IGF1 attenuated the effects of miR-184 on renal cell damage, and Hippo pathway suppression reversed the inhibitory effect of miR-184 knockdown on renal cell impairment. Conclusions: miR-184 downregulation activates the Rap1 signaling pathway to ameliorate renal cell damage mediated by CaOx.

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Section: Discussionmentioning

confidence: 99%

Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway

Han,

Zhang,

et al. 2023

Aging

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“…miR‐184 was reduced in RPE cells from AMD patients and could regulate phagocytic activities by modulating the expression of ezrin and LAMP‐1 in ARPE‐19 cells 21 . A recent study indicated that miR‐184 could attenuate oxidative stress and DNA damage in an in vitro AMD model using ARPE‐19 cells 22 . miR‐184 is also the top miRNA detected in human aqueous humor and aqueous humor exosomes 23–25 .…”

Section: Introductionmentioning

confidence: 99%

“…21 A recent study indicated that miR-184 could attenuate oxidative stress and DNA damage in an in vitro AMD model using ARPE-19 cells. 22 miR-184 is also the top miRNA detected in human aqueous humor and aqueous humor exosomes. [23][24][25] However, the function of miR-184 during eye development is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Knockout of miR‐184 in zebrafish leads to ocular abnormalities by elevating p21 levels

Zhang

Sun

et al. 2023

The FASEB Journal

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miR‐184 is one of the most abundant miRNAs expressed in the lens and corneal tissue. Mutations in the seed region of miR‐184 are responsible for inherited anterior segment dysgenesis. Animal models recapitulating miR‐184‐related anterior segment dysgenesis are still lacking, and the molecular basis of ocular abnormalities caused by miR‐184 dysfunction has not been well elucidated in vivo. In the present study, we constructed a miR‐184−/− zebrafish line by destroying both two dre‐mir‐184 paralogs with CRISPR‐Cas9 technology. Although there were no gross developmental defects, the miR‐184−/− zebrafish displayed microphthalmia and cataract phenotypes. Cytoskeletal abnormalities, aggregation of γ‐crystallin, and lens fibrosis were induced in miR‐184−/− lenses. However, no obvious corneal abnormalities were observed in miR‐184−/− zebrafish. Instead of apoptosis, deficiency of miR‐184 led to aberrant cell proliferation and a robust increase in p21 levels in zebrafish eyes. Inhibition of p21 by UC2288 compromised the elevation of lens fibrosis markers in miR‐184−/− lenses. RNA‐seq demonstrated that levels of four transcriptional factors HSF4, Sox9a, CTCF, and Smad6a, all of which could suppress p21 expression, were reduced in miR‐184−/− eyes. The predicted zebrafish miR‐184 direct target genes (e.g., atp1a3a and nck2a) were identified and verified in miR‐184−/− eye tissues. The miR‐184−/− zebrafish is the first animal model mimicking miR‐184‐related anterior segment dysgenesis and could broaden our understanding of the roles of miR‐184 in eye development.

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Vitamin D alleviation of oxidative stress in human retinal pigment epithelial cells

Yang,

Qi,

Zuo

et al. 2024

Int Ophthalmol

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MicroRNA-184 attenuates hypoxia and oxidative stress-related injury via suppressing apoptosis, DNA damage and angiogenesis in an in vitro age-related macular degeneration model

Cited by 10 publications

References 46 publications

Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway

Downregulating miR-184 relieves calcium oxalate crystal-mediated renal cell damage via activating the Rap1 signaling pathway

Knockout of miR‐184 in zebrafish leads to ocular abnormalities by elevating p21 levels

Vitamin D alleviation of oxidative stress in human retinal pigment epithelial cells

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