MiR-410 exerts neuroprotective effects in a cellular model of Parkinson's disease induced by 6-hydroxydopamine via inhibiting the PTEN/AKT/mTOR signaling pathway

Ge, Hanming; Yan, Zhengcun; Zhu, Haochun; Zhao, Hang

doi:10.1016/j.yexmp.2019.05.002

Cited by 28 publications

(20 citation statements)

References 35 publications

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“…Furhtermore, SNHG1 activated PTEN/AKT/ mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p. Consistently, PTEN was previously found to participate in PD process via affecting Akt/mTOR signaling pathway [45,46].…”

Section: Discussionsupporting

confidence: 54%

SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p

et al. 2020

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Background: Long non-coding RNA small molecule RNA host gene 1 (SNHG1) was previously identified to be relevant with Parkinson's disease (PD) pathogenesis. This work aims to further elucidate the regulatory networks of SNHG1 involved in PD. Methods: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-hydrochloride (MPTP)-induced mice and 1-methyl-4-phenylpyridinium (MPP +)-treated SH-SY5Y cells were respectively constructed as the in vivo and in vitro PD models. Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCR. Protein expression levels of phosphate and tension homology deleted on chromosome ten (PTEN) were measured by western blotting assay. Cell viability and apoptosis were determined by MTT and flow cytometry assays. The interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis. Results: Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP +-treated SH-SY5Y cells. Overexpression of SNHG1 lowered viability and enhanced apoptosis in MPP +-treated SH-SY5Y cells. Moreover, SNHG1 acted as a molecular sponge to inhibit the expression of miR-153-3p. Furthermore, miR-153-3p-mediated suppression of MPP +-induced cytotoxicity was abated following SNHG1 up-regulation. Additionally, PTEN was identified as a direct target of miR-153-3p, and SNHG1 could serve as a competing endogenous RNA (ceRNA) of miR-153-3p to improve the expression of PTEN. Besides, enforced expression of PTEN displayed the similar functions as SNHG1 overexpression in regulating the viability and apoptosis of MPP +-treated SH-SY5Y cells. Finally, SNHG1 was found to activate PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p. Conclusion: SNHG1 aggravates MPP +-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.

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Section: Discussionsupporting

confidence: 54%

SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p

et al. 2020

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“…A study has reported that miR-410 has been found to be abnormally expressed in several human pernicious cancer types and can be used as a tumor inhibitor in endometrial, lung cancer, myeloma, and breast cancer [7–10]. Another study revealed that there is a neuroprotective effect of miR-410 on Parkinson’s disease cell model induced by 6-hydroxydopamine by suppressing PTEN/AKT/mTOR signaling pathway [11]. Moreover, miR-410 has been revealed to modulate malignant biological behaviors of children with acute lymphoblastic leukemia via targeting FKBP5 and AKT signaling pathways [12].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Upregulating MicroRNA-410 or Downregulating Wnt-11 Increases Osteoblasts and Reduces Osteoclasts to Alleviate Osteonecrosis of the Femoral Head

et al. 2019

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Background: Little is known regarding the functional role of microRNA-410 (miR-410) in osteonecrosis of the femoral head (ONFH); hence, the aim of the present study was to investigate miR-410 targeting Wnt-11 to modulate the osteogenic and osteoclastic mechanism in the prevention of ONFH. Methods: Fifteen ONFH samples and 15 normal samples were gathered. The pathological changes of the femoral head, osteoblasts, and osteoclasts in the clinical samples were observed. The rat model of ONFH was injected with agomir-miR-410, Wnt-11-siRNA, or oe-Wnt-11. MiR-410; Wnt-11; osteoblast-related factors alkaline phosphatase (ALP), bone gamma-carboxyglutamate protein (BGLAP), and Collα1 expression; and osteoclast-related factors acid phosphatase 5 (ACP5), cathepsin K (CTSK), and MMP9, as well as Bcl-2 and Bax expression, were tested by RT-qPCR and western blot analysis. The osteogenic function index ALP and OCN together with osteoclast function index NTX-1 and CTX-1 in serum was tested by ELISA. Results: MiR-410, ALP, BGLAP, and Collα1 degraded as well as Wnt-11, ACP5, CTSK, and MMP9 enhanced in ONFH tissues of the clinical samples. Upregulated miR-410 and downregulated Wnt-11 enhanced bone mineral density (BMD) and BV/TV of rats, heightened the BMD level of the femoral shaft, femoral head, and spinal column, and also raised the serum calcium and phosphorus levels of rats, while restrained apoptosis of osteocytes, elevated OCN, ALP, BGLAP, and Collα1 expression and declined ACP5, CTSK, NTX-1, CTX-1, and MMP9 expression in rats. Conclusion: This study suggested that upregulating miR-410 or downregulating Wnt-11 increases osteoblasts and reduces osteoclasts to alleviate the occurrence of ONFH. Thus, miR-410 may serve as a potential target for the treatment of ONFH.

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“…Furthermore, the decreased miR-433 and miR-133b expression levels are potential biomarkers for Pd (13). A previous study also demonstrated that miR-410 exerts neuroprotective effects in an in vitro model of 6-hydroxydopamine-induced Pd (14). Recently, in another previous study, in an in vitro model of rotenone-induced Pd, an increased miR-384-5p level was observed, and the downregulation of this miRNA exerted a neuroprotective effect against rotenone by targeting GRP78 (15).…”

Section: Introductionmentioning

confidence: 81%

“…instance, miRNA-155-5p and miRNA-146a-5p (12), miR-433 and miR-133b (13) and miR-410 (14). In a recent study, in an in vitro model of Pd induced by rotenone, miR-384-5p expression was increased, and the downregulation of this miRNA exerted a neuroprotective effect against rotenone by targeting GRP78 (15).…”

Section: Discussionmentioning

confidence: 99%

miRNA‑384‑5p regulates the progression of Parkinson's�disease by targeting SIRT1 in mice and SH‑SY5Y cell

2019

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Parkinson's disease (Pd) is the second most common neurodegenerative disorder. miR-384-5p expression has been shown to be increased in an in vitro model of Pd; however, it remains unknown whether there are other molecules that can be regulated by miR-384-5p in in vivo and in vitro models of Pd; thus, the present study aimed to elucidate this matter. Rotenone was applied for the establishment of in vitro and in vivo models of Pd in the present study. Motor disability and equilibrium were determined by a swimming test and traction test, respectively. mRNA and protein levels were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPcR) and western blot analysis, respectively. The association between miR-384-5p and Sirtuin 1 (SIRT1) expression was verified by dual luciferase reporter assay. The α-synuclein aggregation was evaluated by immunofluorescence. The results from the in vitro model of Pd demonstrated that, the mice in the Pd group exhibited decreased scores in the swimming test and traction test, which were accompanied by increased α-synuclein aggregation. In addition, the expression of miR-384-5p, which targeted the 3'untranslated region (3'UTR) of SIRT1, was verified to be increased in mice and SH-SY5Y cells in the Pd group, whereas SIRT1 exhibited the opposite changes. Moreover, increased mRNA and protein levels of p53 and FOXO1 were observed in mice and SH-SY5Y cells in the Pd group. In addition, the SH-SY5Y cells in the Pd group exhibited a higher cell apoptotic rate. On the whole, the findings of this study demonstrate that miRNA-384-5p promotes the progression of Pd by targeting SIRT1.

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MiR-410 exerts neuroprotective effects in a cellular model of Parkinson's disease induced by 6-hydroxydopamine via inhibiting the PTEN/AKT/mTOR signaling pathway

Cited by 28 publications

References 35 publications

SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p

SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p

RETRACTED ARTICLE: Upregulating MicroRNA-410 or Downregulating Wnt-11 Increases Osteoblasts and Reduces Osteoclasts to Alleviate Osteonecrosis of the Femoral Head

miRNA‑384‑5p regulates the progression of Parkinson's�disease by targeting SIRT1 in mice and SH‑SY5Y cell

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