MicroRNA profiling in the dentate gyrus in epileptic rats

Zhang, Suya; Kou, Yubin; Hu, Chunmei; Yan, Han

doi:10.1097/md.0000000000006744

Cited by 11 publications

(9 citation statements)

References 47 publications

(64 reference statements)

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“…There appears marked global disparity in the treatment for epilepsy between high-and low-income countries; and between rural and urban regions (Meyer, Dua, Ma, Saxena, & Birbeck, 2010). Recently, several studies have reported that microRNAs (miRNAs) are emerging as a critical new layer of gene expression control with implications for the cause and treatment of epilepsy, such as miR-146a, miR-187-3p, and miR-129-5p (Aronica et al, 2010;Jimenez-Mateos and Henshall, 2013;Liu, Wu, & Wang, 2017;Zhang, Kou, Hu, & Han, 2017).…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐421 suppresses the apoptosis and autophagy of hippocampal neurons in epilepsy mice model by inhibition of the TLR/MYD88 pathway

Wen

Han

Wang

et al. 2018

Journal Cellular Physiology

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Epilepsy is a group of neurological disorders characterized by epileptic seizures. In this study, we aim to explore the role of microRNA-421 (miR-421) in hippocampal neurons of epilepsy mice via the TLR/MYD88 pathway. Forty mice were randomly served as the normal and model (established as epilepsy model) groups. Hippocampal neurons were assigned into seven groups with different transfections. The RT-qPCR and western blotting were conducted to examine the expression of miR-421 TLR2, TLR4, MYD88, Bax, Bcl-2, p53, Beclin-1, and LC3II/LC3I. Cell proliferation and apoptosis were detected by MTT and flow cytometry.MYD88 is a target gene of miR-421. Model mice showed elevated expression of TLR2, TLR4, MYD88, Bax, p53, Beclin-1, and LC3II/LC3I but reduced expression of miR-421 and Bcl-2. In vitro experiments reveals that overexpression of miR-421 inhibited the TLR/MYD88 pathway. Besides, overexpressed miR-421 declined cell apoptosis but increased cell proliferation. It reveals that miR-421 targeting MYD88 could inhibit the apoptosis and autophagy of hippocampal neurons in epilepsy mice by down-regulating the TLR/MYD88 pathway.

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Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐421 suppresses the apoptosis and autophagy of hippocampal neurons in epilepsy mice model by inhibition of the TLR/MYD88 pathway

Wen

Han

Wang

et al. 2018

Journal Cellular Physiology

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“…Four of these genes were differentially methylated in the opposite direction: Babam1 has been linked to schizophrenia 65 , Cacnb1 to autism 66 and depression 67 , Coro2b , a candidate gene for ciliopathies to intellectual disability 68 and Gmppa to intellectual disability and autonomic dysfunction 69 . Two genes that are differentially methylated in the same direction in males and females are Rusc1 whose gene product serves as neuronal adaptor protein 70 and Paqr4 which was recently associated with the development of epilepsy 71 .…”

Section: Discussionmentioning

confidence: 99%

Fetal glucocorticoid receptor (Nr3c1) deficiency alters the landscape of DNA methylation of murine placenta in a sex-dependent manner and is associated to anxiety-like behavior in adulthood

et al. 2019

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Prenatal stress defines long-term phenotypes through epigenetic programming of the offspring. These effects are potentially mediated by glucocorticoid release and by sex. We hypothesized that the glucocorticoid receptor (Gr, Nr3c1) fashions the DNA methylation profile of offspring. Consistent with this hypothesis, fetal Nr3c1 heterozygosity leads to altered DNA methylation landscape in fetal placenta in a sex-specific manner. There was a significant overlap of differentially methylated genes in fetal placenta and adult frontal cortex in Nr3c1 heterozygotes. Phenotypically, Nr3c1 heterozygotes show significantly more anxiety-like behavior than wildtype. DNA methylation status of fetal placental tissue is significantly correlated with anxiety-like behavior of the same animals in adulthood. Thus, placental DNA methylation might predict behavioral phenotypes in adulthood. Our data supports the hypothesis that Nr3c1 influences DNA methylation at birth and that DNA methylation in placenta correlates with adult frontal cortex DNA methylation and anxiety-like phenotypes.

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“…Target genes of miR-187-3p were involved in the regulation of signaling pathways, including phosphatidylinositol 3-kinase-AKT and hypoxia-inducible factor 1 signaling pathways in epileptic rats ( 44 ). Hendrix et al ( 45 ) revealed that FGF9 was a downstream target of the Wnt signaling pathway, which may be an indirect transcription target of β-catenin in ovarian endometrioid adenocarcinomas.…”

Section: Discussionmentioning

confidence: 99%

miR‑187‑3p increases gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression

Ying-qi

Liang

et al. 2020

Exp Ther Med

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Breast cancer is the most common type of malignancy in women, which remains a significant health concern worldwide. Gemcitabine is a frequently applied anticancer pharmacological agent. However, the efficacy of gemcitabine is limited by chemoresistance. In the present study, a combination of reverse transcription quantitative-PCR, cell viability, flow cytometry, luciferase reporter assay and western blot analysis were performed to elucidate the potential effects of miR-187-3p on gemcitabine sensitivity in the breast cancer cell line, MDA-MB-231. The results revealed that miR-187-3p was significantly decreased in the breast cancer tumor tissues. Moreover, the overexpression of miR-187-3p significantly inhibited cell viability and promoted apoptosis in MDA-MB-231 cells. In addition, miR-187-3p overexpression enhanced the anti-proliferative and pro-apoptotic effects of gemcitabine, indicating that miR-187-3p regulated gemcitabine sensitivity in breast cancer cells. Mechanistically, miR-187-3p negatively regulated the expression of fibroblast growth factor 9 (FGF9) by binding to its 3'-untranslated region. Overexpression of FGF9 reversed the aforementioned effects of miR-187-3p overexpression on cell viability and apoptosis in the presence of gemcitabine. In conclusion, the present study indicated that miR-187-3p increased gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression.

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MicroRNA profiling in the dentate gyrus in epileptic rats

Abstract: Supplemental Digital Content is available in the text

Cited by 11 publications

References 47 publications

Retracted: MicroRNA‐421 suppresses the apoptosis and autophagy of hippocampal neurons in epilepsy mice model by inhibition of the TLR/MYD88 pathway

Retracted: MicroRNA‐421 suppresses the apoptosis and autophagy of hippocampal neurons in epilepsy mice model by inhibition of the TLR/MYD88 pathway

Fetal glucocorticoid receptor (Nr3c1) deficiency alters the landscape of DNA methylation of murine placenta in a sex-dependent manner and is associated to anxiety-like behavior in adulthood

miR‑187‑3p increases gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression

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