miR-135b expression downregulates Ppm1e to activate AMPK signaling and protect osteoblastic cells from dexamethasone

Fan, Jiyang; Ruan, Jing; Liu, Wei; Zhu, Ling; Zhu, Xiao Feng; Yi, Hong; Cui, Shengyu; Zhao, Jianning; Cui, Zhiming

doi:10.18632/oncotarget.12138

Cited by 50 publications

(89 citation statements)

References 39 publications

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“…It belongs to the Ppm family [34,35]. Our previous study demonstrated that microRNA-135b downregulated Ppm1e expression to activate AMPK signaling, which in turn protected osteoblastic cells from Dex-induced injuries [4]. In the present study, our results suggest that Lnc-MALAT1 protects human osteoblasts from Dex-induced injury via activation of Ppm1e-AMPK signaling.…”

Section: Introductionsupporting

confidence: 68%

“…Quantitative real-time polymerase chain reaction assay As described previously [4,38], TRIzol reagent was used to extract total cellular RNA, which was then reverse-transcribed. cDNA was then amplified by quantitative real-time polymerase chain reaction (qPCR).…”

Section: Cell Culturementioning

confidence: 99%

“…The primer sequences used for theNrf2 genes, including heme oxygenase-1 (HO1), NAD(P)H quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine ligase catalytic subunit (GCLC) were described previously [39]. Ppm1e mRNA primer sequences were described early [4]. Lnc-MALAT1 primer sequences were as follows: forward: 5′-AAAGCAAGGTCTCCCCACAAG-3′, reverse: 5′-GGTCTGTGCTAGATCAAAAGGCA-3′, as described previously [40].…”

Section: Cell Culturementioning

confidence: 99%

“…Dex treatment has been shown to exert direct cytotoxic effects on cultured human osteoblasts in vitro [2,[4][5][6][7]. Studies focusing on the pathological mechanisms of Dex-induced injuries in osteoblasts have been previously conducted [8][9][10][11][12][13], and have been the main area of focus of our research group as well [4,9,11,14].…”

Section: Introductionmentioning

confidence: 99%

“…AMPK can attenuate oxidative stress via activation of nicotinamide adenine dinucleotide phosphate (NADPH) [27] and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling [28][29][30]. Recent studies have implied that AMPK activation can efficiently protect human osteoblasts from Dex-induced injuries [4,5,30,31].…”

Section: Introductionmentioning

confidence: 99%

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Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Fan¹,

Zhang²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Dexamethasone (Dex) induces injuries to human osteoblasts. In this study, we tested the potential role of the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (Lnc-MALAT1) in this process. Materials: Two established human osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts were treated with Dex. Lnc-MALAT1 expression was analyzed by quantitative real-time polymerase chain reaction assay. Cell viability, apoptosis, and death were tested by the MTT assay, histone-DNA assay, and trypan blue staining assay, respectively. AMP-activated protein kinase (AMPK) signaling was evaluated by western blotting and AMPK activity assay. Results: Lnc-MALAT1 expression was downregulated by Dex treatment in the established osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts. The level of Lnc-MALAT1 was decreased in the necrotic femoral head tissues of Dex-administered patients. In osteoblastic cells and primary human osteoblasts, forced overexpression of Lnc-MALAT1 using a lentiviral vector (LV-MALAT1) inhibited Dex-induced cell viability reduction, cell death, and apoptosis. Conversely, transfection with Lnc-MALAT1 small interfering RNA aggravated Dex-induced cytotoxicity. Transfection with LV-MALAT1 downregulated Ppm1e (protein phosphatase, Mg^2+/ Mn²⁺-dependent 1e) expression to activate AMPK signaling. Treatment of osteoblasts with AMPKα1 short hairpin RNA or dominant negative mutation (T172A) abolished LV-MALAT1-induced protection against Dex-induced cytotoxicity. Furthermore, LV-MALAT1 induced an increase in nicotinamide adenine dinucleotide phosphate activity and activation of Nrf2 signaling. Dex-induced reactive oxygen species production was significantly attenuated by LV-MALAT1 transfection in osteoblastic cells and primary osteoblasts. Conclusion: Lnc-MALAT1 protects human osteoblasts from Dex-induced injuries, possibly via activation of Ppm1e-AMPK signaling.

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Section: Introductionsupporting

confidence: 68%

Section: Cell Culturementioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Fan¹,

Zhang²,

Liu³

et al. 2018

Cell Physiol Biochem

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Inhibition of MAGL activates the Keap1/Nrf2 pathway to attenuate glucocorticoid‐induced osteonecrosis of the femoral head

Yang

Sun

Xue

et al. 2021

Clinical & Translational Med

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MiR‐320 promotes B cell proliferation and the production of aberrant glycosylated IgA1 in IgA nephropathy

Shi

Zhao

2018

J of Cellular Biochemistry

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IgA nephropathy (IgAN) is one of the most common primary glomerulonephritis. However, the etiology of this disease is complex and the pathogenesis of IgAN is still unknown. MicroRNAs (miRNAs) play important roles in a lot of pathological and physiological processes. In this study, we showed that the expression of miR-320 was significantly upregulated in renal tissues and urinary of IgAN patients. Moreover, the intra-renal expression level of miR-320 had significant correlation with miR-320 expression in the urinary of IgAN patients. Overexpression of miR-320 increased B cell proliferation and promoted cyclin D1 expression. Furthermore, we identified that PTEN was direct target gene of miR-320 in the B cell. Ectopic expression of miR-320 suppressed PTEN expression. Overexpression of miR-320 decreased Cosmc expression in the B cell. In addition, we demonstrated that Cosmc expression was significantly downregulated in the renal tissues and urinary of IgAN patients. The intra-renal expression level of Cosmc had significant correlation with Cosmc expression of urinary in IgAN patients. We proved that the expression level of Cosmc was negatively correlated with the expression of miR-320 in the renal tissues of IgAN patients. Overexpression of miR-320 promoted the B cell proliferation through suppressing PTEN expression. Taken together, these data suggested that miR-320 acted an important role in the development of IgAN.

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miR-135b expression downregulates Ppm1e to activate AMPK signaling and protect osteoblastic cells from dexamethasone

Cited by 50 publications

References 39 publications

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Inhibition of MAGL activates the Keap1/Nrf2 pathway to attenuate glucocorticoid‐induced osteonecrosis of the femoral head

MiR‐320 promotes B cell proliferation and the production of aberrant glycosylated IgA1 in IgA nephropathy

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