Overexpression of miR‑30c‑5p reduces cellular cytotoxicity and inhibits the formation of kidney stones through ATG5

Wang, Xin; Zhang, Yanan; Han, Shuai; Chen, Hongshen; Chen, Chen; Ji, Lü; Gao, Bihu

doi:10.3892/ijmm.2019.4440

Cited by 11 publications

(9 citation statements)

References 42 publications

(37 reference statements)

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“…In brief, mice received intraperitoneal injection with vehicle (saline) or glyoxylate (Gly; 75 mg/kg/d; 200 μl) on days 8 through 14. Mice in TF (MCE, HY-N0243) intervention groups were daily treated with TF by gavage at three different doses (20,50, and 100 mg/kg) on days 1 through 14. Theaflavin dosages were based on two previous studies [6,27].…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

“…Our published paper revealed that the interaction of lncRNA H19 with miR-216b contributed to the development of CaOx nephrocalcinosis-induced oxidative stress and tubular cell injury through the regulation of HMGB1/TLR4/NF-kB signaling pathway 5 . Several studies also identified some miRNAs exerting protective effects in the formation of kidney stones, such as miR‑30c‑5p 20 , miR-93-5p 17 , miR-34a 21 , and miR-142a 22 . All in all, miRNAs work in a variety of roles in kidney stone disease.…”

Section: Introductionmentioning

confidence: 99%

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Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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Renal tubular cell injury induced by calcium oxalate (CaOx) is a critical initial stage of kidney stone formation. Theaflavin (TF) has been known for its strong antioxidative capacity; however, the effect and molecular mechanism of TF against oxidative stress and injury caused by CaOx crystal exposure in kidneys remains unknown. To explore the potential function of TF on renal crystal deposition and its underlying mechanisms, experiments were conducted using a CaOx nephrocalcinosis mouse model established by glyoxylate intraperitoneal injection, and HK-2 cells were subjected to calcium oxalate monohydrate (COM) crystals, with or without the treatment of TF. We discovered that TF treatment remarkably protected against CaOx-induced kidney oxidative stress injury and reduced crystal deposition. Additionally, miR-128-3p expression was decreased and negatively correlated with SIRT1 level in mouse CaOx nephrocalcinosis model following TF treatment. Moreover, TF suppressed miR-128-3p expression and further abolished its inhibition on SIRT1 to attenuate oxidative stress in vitro. Mechanistically, TF interacted with miR-128-3p and suppressed its expression. In addition, miR-128-3p inhibited SIRT1 expression by directly binding its 3'-untranslated region (UTR). Furthermore, miR-128-3p activation partially reversed the acceerative effect of TF on SIRT1 expression. Taken together, TF exhibits a strong nephroprotective ability to suppress CaOx-induced kidney damage through the recovery of the antioxidant defense system regulated by miR-128-3p/SIRT1 axis. These findings provide novel insights for the prevention and treatment of renal calculus.

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Section: Animals and Experimental Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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“…Besides, miR-30c-1-3p and miR-30c-5p played a negative regulatory role in xenophagy induced by H. pylori infection in GES-1 cell lines. However, studies have reported that miR-30c-5p relieves kidney stones by targeting ATG5 in human renal tubular epithelial cells [32]. More researches are needed to confirm the regulatory roles of miR-30c-1-3p and miR-30c-5p in different cell lines, tissues, organs, and even different disease processes.…”

Section: Discussionmentioning

confidence: 99%

miR-30c Increases the Intracellular Survival of Helicobacter pylori by Inhibiting Autophagy

Deng

Zhong

et al. 2022

Cellular Microbiology

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Persistent Helicobacter pylori infection causes a variety of gastrointestinal diseases and even gastric cancer. H. pylori invades gastric epithelial cells to survive and proliferate, which is one of the key factors in persistent colonization. A Published study has confirmed that cells can eliminate intracellular H. pylori through xenophagy to maintain intracellular balance. However, a growing body of evidences indicate that H. pylori can inhibit xenophagy by miRNA through regulating the expression of key autophagy-related genes. Through western blot analysis, mRFP-GFP-LC3 transfection assay, and transmission electron microscopy, we found that H. pylori infection obstructed autophagy flux degradation stage in GES-1 cell lines. Gentamicin protection assay confirmed that inhibit xenophagy is benefit for intracellular H. pylori survive. miR-30c-1-3p and miR-30c-5p were upregulated in GES-1 cell lines after infecting with H. pylori, resulting in the negative regulation on xenophagy. Further studies through bioinformatics analysis and dual-luciferase reporter assays confirmed that ATG14 and ULK1 were the target genes of miR-30c-1-3p and that ATG12 was the target gene of miR-30c-5p. The overexpression of miR-30c-1-3p and miR-30c-5p reduces the expression of ATG14, ULK1, and ATG12 at mRNA level and also decreased intracellular H. pylori elimination in GES-1 cells. The above results suggested that the inhibition on xenophagy by miR-30c-1-3p and miR-30c-5p through ATG14, ULK1, and ATG12 targeting benefitted intracellular H. pylori in the evasion of xenophagy clearance.

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“…Interestingly, miR-103a-3p regulates the progression of both autophagy and apoptosis of cardiomyocytes through binding to ATG5 (Zhang et al, 2019b ). Previous research also showed that miR-30c-5p targets ATG5 to protect renal tubular epithelial cells against oxidative stress injury (Wang X. et al, 2020 ). Moreover, bioinformatics predicted that miR-30c-5p could target AGT5 in our preliminary study, indicating that miR-30c-5p has the potential of regulating autophagy.…”

Section: Introductionmentioning

confidence: 89%

MiR-30c-5p/ATG5 Axis Regulates the Progression of Parkinson’s Disease

Zhang

Chen

Chang

et al. 2021

Front. Cell. Neurosci.

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Serum miR-30c-5p correlates with Parkinson’s disease (PD), yet its role has not been illustrated. This research analyzed the function of miR-30c-5p in PD. The behavioral evaluation was performed on MPTP-treated PD mice transfected with miR-30c-5p agomiR, antagomiR, siATG5, or 3-MA (an autophagy inhibitor). Oxidative stress-related factors, miR-30c-5p, and apoptosis- and autophagy-associated proteins in brain tissues or cells were determined by molecular experiments. Tyrosine hydroxylase (TH) and dopamine metabolic markers were detected using immunofluorescence and Diode Array Detector (DAD), respectively. Effects of miR-30c-5p and its target gene Autophagy-related gene (ATG) 5 protein (ATG5) on MPP+-treated SH-SY5Y cells were determined through a series of molecular experiments. MiR-30c-5p was upregulated but ATG5 was downregulated in PD mice. MiR-30c-5p antagomiR attenuated the decrease of ATG5 in PD mice. MiR-30c-5p antagomiR partly alleviated the behavioral symptoms and inhibited the increases of malondialdehyde (MDA), catalase (CAT), and SOD in PD mice. The levels of Bcl-2, dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), TH, and LC3 II were downregulated in PD mice, while Bax, cleaved caspase-3, P62, and LC3 I were upregulated. However, miR-30c-5p antagomiR partly reversed the levels of these factors in PD mice. 3-MA could block the effects of miR-30c-5p antagomiR on PD mice. MiR-30c-5p antagomiR attenuated apoptosis and induced autophagy in brain tissues of MPTP-treated mice by targeting ATG5. In vitro assay results also showed that silence of ATG5 reduced the protective effect of miR-30c-5p downregulation on the cells. MiR-30c-5p regulates the progression of Parkinson’s disease through attenuating ATG5-inhibited apoptosis and -induced autophagy.

show abstract

Overexpression of miR‑30c‑5p reduces cellular cytotoxicity and inhibits the formation of kidney stones through ATG5

Cited by 11 publications

References 42 publications

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

miR-30c Increases the Intracellular Survival of Helicobacter pylori by Inhibiting Autophagy

MiR-30c-5p/ATG5 Axis Regulates the Progression of Parkinson’s Disease

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