Screening and validation of differentially expressed extracellular miRNAs in acute pancreatitis

Meng, Shishuai; Wang, Hao; Xue, Dongbo; Zhang, Weihui

doi:10.3892/mmr.2017.7374

Cited by 12 publications

(11 citation statements)

References 38 publications

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“…These previous studies provided the first conclusive evidence indicating that inhibition of trypsinogen activation can reduce the extent of AP. Previous in vitro cell experiments used different treatments (TLC-S, cerulein and TNF-α) to induce trypsinogen activation or AR42J cell apoptosis in order to elucidate the underlying mechanisms of AP development and to determine the genes or pathways of interest (14,16,30,31). Studies using AP animal models will be performed.…”

Section: Discussionmentioning

confidence: 99%

miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells

et al. 2019

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acute pancreatitis (aP) exhibits high morbidity and mortality rates. The onset of aP is characterized by early trypsinogen activation.The present study aimed to investigate the expression of microrna (mir)-92a-3p and early growth response protein 1 (egr1), and the effect of mir-92a-3p on trypsinogen activation in the pancreatic exocrine cell line ar42J. mrna and mirna microarrays were used to identify differentially expressed mrnas and mirnas in ar42J cells. a mirna-mrna network was constructed using bioinformatics software, and egr1 and its regulated mirna subnetworks were identified by reviewing previous literature. The results suggested that mir-92a-3p could bind to egr1 3'untranslated region sequence. Subsequently, mir-92a-3p mimic and inhibitor were used to transfect ar42J cells. Following transfection, reverse transcription-quantitative Pcr and western blotting were performed to detect egr1 expression. Furthermore, ar42J cells were cotransfected with mir-92a-3p inhibitor and small interfering (si)-egr1. The trypsinogen activation rate of ar42J cells was measured by flow cytometry. Microarrays and bioinformatics results indicated that egr1 may be a target gene of mir-92a-3p. in addition, the present study suggested that mir-92a-3p downregulated egr1 in vitro and that mir-92a-3p and egr1 expression was associated with trypsinogen activation. Furthermore, mir-92a-3p inhibitor reversed the effect of si-egr1 on trypsinogen activation. in conclusion, mir-92a-3p may negatively regulate the activation of trypsinogen in ar42J cells via egr1.

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Section: Discussionmentioning

confidence: 99%

miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells

et al. 2019

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“…In the miRanda algorithm, target genes with Max-Energy >-10 were excluded. The overlapping prediction results were selected as the candidate target genes of miR-22 (30,31).…”

Section: B I O I N F O R M a T I C S A N A L Y S I Smentioning

confidence: 99%

Sodium hydrosulfide alleviates dexamethasone‑induced cell senescence and dysfunction through targeting the miR‑22/sirt1 pathway in osteoblastic MC3T3‑E1 cells

Mao

Zhang

et al. 2021

Exp Ther Med

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Glucocorticoid-induced osteoporosis is characterized by osteoblastic cell and microarchitecture dysfunction, as well as a loss of bone mass. Cell senescence contributes to the pathological process of osteoporosis and sodium hydrosulfide (NaHS) regulates the potent protective effects through delaying cell senescence. The aim of the present study was to investigate whether senescence could contribute to dexamethasone (Dex)-induced osteoblast impairment and to examine the effect of NaHS on Dex-induced cell senescence and damage. It was found that the levels of the senescence-associated markers, p53 and p21, were markedly increased in osteoblasts exposed to Dex. A p53 inhibitor reversed Dex-induced osteoblast injury, a process that was mitigated by NaHS administration through alleviating osteoblastic cell senescence. MicroRNA (miR)-22 blocked the impact of NaHS on Dex-induced osteoblast damage and senescence through targeting the regulation of Sirtuin 1 (sirt1) expression, as shown by the decreased cell viability and alkaline phosphatase activity, as well as an increased expression of p53 and p21. It was revealed that the sirt1 gene was the target of miR-22 in osteoblastic MC3T3-E1 cells through combining the results of dual luciferase reporter assays and reverse transcription-quantitative PCR, as well as western blot analyses. Silencing of sirt1 abolished the protective effect of NaHS against Dex-associated osteoblast senescence and injury. Taken together, the present study showed that NaHS prevents Dex-induced cell senescence and damage through targeting the miR-22/sirt1 pathway in osteoblastic MC3T3-E1 cells.

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“…In the miRanda algorithm, target genes with Max-Energy >-10 were excluded. The overlapping prediction results were selected as the candidate target genes of miR-22 (24,25).…”

Section: Reverse Transcription-quantitative Pcr (Rt-qpcr)mentioning

confidence: 99%

MicroRNA‑22 contributes to dexamethasone‑induced osteoblast differentiation inhibition and dysfunction through targeting caveolin‑3 expression in osteoblastic cells

Mao

Zhang

et al. 2021

Exp Ther Med

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Osteoporosis is a common complication of long-term use of glucocorticoids (GCs) characterized by the loss of bone mass and damage of the microarchitecture as well as osteoblast dysfunction. Previous studies have demonstrated that microRNA-22 (miR-22) is the negative modulator of osteogenesis that may target caveolin-3 (CAV3), which has been reported to enhance bone formation and inhibit the progression of osteoporosis as well as apoptosis. The present study aimed to investigate whether miR-22 may be involved in dexamethasone (DEX)-induced inhibition of osteoblast differentiation and dysfunction by regulating CAV3 expression. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure the expression of miR-22 and western blotting was performed to determine protein levels. The results demonstrated that miR-22 expression was upregulated in DEX-treated osteoblastic cells compared with the control group. In addition, miR-22 mimic aggravated, whereas miR-22 inhibitor mitigated DEX-induced damage in osteoblastic cells compared with the control groups. Additionally, CAV3 was identified as the target of miR-22 in osteoblasts using RT-qPCR, western blotting and dual-luciferase reporter gene assay analysis. The results also demonstrated that silencing of CAV3 blocked the beneficial effects of miR-22 inhibitor against DEX-induced cell damage and apoptosis in osteoblasts, as evidenced by the increased expression levels of cleaved caspase-3, Bax and alkaline phosphatase activity as well as decreased cell viability and Bcl-2 levels. Collectively, these results indicate a novel molecular mechanism by which miR-22 contributes to DEX-induced osteoblast dysfunction and apoptosis via the miR-22/CAV3 pathway.

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Screening and validation of differentially expressed extracellular miRNAs in acute pancreatitis

Cited by 12 publications

References 38 publications

miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells

miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells

Sodium hydrosulfide alleviates dexamethasone‑induced cell senescence and dysfunction through targeting the miR‑22/sirt1 pathway in osteoblastic MC3T3‑E1 cells

MicroRNA‑22 contributes to dexamethasone‑induced osteoblast differentiation inhibition and dysfunction through targeting caveolin‑3 expression in osteoblastic cells

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