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#29055786   2017/10/22 Save this To Up

Carbon monoxide releasing molecule improves structural and functional cardiac recovery after myocardial injury.

Carbon monoxide (CO), produced by heme oxygenase-1 (HO-1), is an endogenous paracrine factor involved in the regulation of cardiovascular structure and function. We studied the effects of a synthetic CO releasing molecule (CORM-3) on cardiac recovery and myocardial microRNA expression after myocardial infarction (MI). Male Wistar rats with MI (n=75) or sham-operated controls (n=75) were treated from day 4 to day 14 after MI either with synthetic CORM-3 or with inactive iCORM and killed 2, 4 or 8 weeks post-MI. Infarct size, vascular and capillary densities, the amount of cardiomyocytes in the infarct area, and cardiomyocyte proliferation and apoptosis were determined. PCR was used for microRNA and mRNA quantification, western blotting to evaluate protein expression and echocardiography to assess cardiac structure and function. CORM-3 treatment increased vascular density (P<0.05 vs. iCORM) and the proportion of cardiomyocytes (P<0.05 vs. iCORM) in the infarct area. Ejection fraction improved (P<0.05) and left ventricular volumes decreased (P<0.05) in CORM-3 treated MI groups compared to iCORM treatment. CORM-3 treatment decreased the amount of proliferating Ki67 positive cardiomyocytes in the infarct/border area at week 2 after MI compared to iCORM treatment, whereas the amount of apoptotic cardiomyocytes did not differ between CORM-3 and iCORM groups. Compared to iCORM treatment, CORM-3 decreased expression on miR-206 in the remote area at week 2 after MI. The CO releasing molecule CORM-3 improved structural and functional cardiac recovery after MI. Modulation of HO-1-CO axis may prove novel drug targets to facilitate cardiac recovery after myocardial injury.

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#29055114   2017/10/21 Save this To Up

Sorafenib Response in Hepatocellular Carcinoma: MicroRNAs as Tuning Forks miRNAs as regulators of sorafenib response in HCC.

Hepatocellular carcinoma (HCC), the primary liver malignancy attributes towards the second foremost cause of cancer related mortality. The targeted chemotherapeutic agent, sorafenib is known to exhibit a statistically significant but limited overall survival advantage in advanced HCC. However, the individual patient response towards sorafenib varies drastically with most of them demonstrating stable disease (SD), few with partial response (PR) and very rare complete response (CR). Progressive disease (PD) despite the treatment has also been demonstrated in many patients indicating drug resistance. These varied responses have been linked with the modulation of several signaling pathways, intracellularly. Notably, the regulation of these pathways through diverse operating biomolecules including microRNAs (miRNAs) is studied recently. miRNAs are tiny, non-coding RNA molecules that regulate the expression of several target genes. Besides, miRNAs are known to have an evident role in HCC carcinogenesis to progression. Interestingly, miRNAs have also been identified to play differential roles in terms of sorafenib response in HCC such as biomarkers, functional modulation of cellular response to sorafenib, hence, they are also being therapeutically evaluated. This review outlines the role of the reported miRNAs in different aspects of sorafenib response in HCC.

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#29054970   2017/10/21 Save this To Up

miR-19a protects cardiomyocytes from hypoxia/reoxygenation-induced apoptosis via PTEN/PI3K/p-Akt pathway.

MicroRNAs have been implicated in processing of cardiac hypoxia/reoxygenation (H/R)-induced injury. Recent studies demonstrated that miR-19a might provide a potential cardioprotective effect on myocardial disease. However, the effect of miR-19a in regulating myocardial ischemic injury has not been previously addressed. This study was to investigate the function of miR-19a on myocardial ischemic injury and identified the potential molecular mechanisms involved. Using the hypoxia/reoxygenation (H/R) model of rat cardiomyocytes H9C2 in vitro, we found that miR-19a was low expression in H9C2 cells after H/R treatment and hypoxia/reoxygenation (H/R) dramatically decreased cardiomyocyte viability, increased LDH release and cardiomyocyte apoptosis, which were attenuated by co-transfection with miR-19a mimic. Dual-luciferase reporter assay and western blotting assay revealed that PTEN was a direct target gene of miR-19a, and miR-19a suppressed the expression of PTEN via binding to its 3'-UTR. We further identified that overexpression of miR-19a inhibited the expression of PTEN at the mRNA and protein levels. Moreover, PTEN was highly expressed in H/R H9C2 cells and the apoptosis induced by H/R was associated with the increase in PTEN expression. Importantly, miR-19a mimic significantly increased p-Akt levels under H/R. In conclusion, our findings indicates that miR-19a could protect against H/R-induced cardiomyocyte apoptosis by inhibiting PTEN /PI3K/p-Akt signaling pathway.

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#29054965   2017/10/21 Save this To Up

Adenovirus-mediated artificial microRNA targeting fibrinogen-like protein 2 attenuates the severity of acute pancreatitis in mice.

Severe acute pancreatitis (SAP) remains to be challenging for its unpredictable inflammatory progression from acute pancreatitis to SAP. Apoptosis is an important pathology of SAP. Fibrinogen-like protein 2 (FGL2) has been reported to be involved in apoptosis. The present study aimed to explore the therapeutic effect of an adenovirus-mediated artificial microRNA targeting FGL2 (Ad-FGL2-miRNA) in taurocholate-induced murine pancreatitis models. Sodium taurocholate was retrogradely injected into the biliopancreatic ducts of the C57/BL mice to induce SAP. FGL2 expression was measured with reverse transcription-PCR, western blotting and immunohistochemical staining. ELISA was used to detect the activity of amylase and the concentrations of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). In addition, the mRNA levels of TNF-α and IL-1β were also detected. Finally, apoptosis was assessed by TUNEL method and western blotting. Ad-FGL2-miRNA significantly suppressed FGL2 expression and alleviated pancreatic injury. Also, Ad-FGL2-miRNA markedly inhibited a post-SAP increase in the activation of TNF-α and IL-1β. Finally, pretreatment with Ad-FGL2-miRNA ameliorated apoptosis at the early stage of SAP by modulating cleaved caspase-3 and therefore played a protective role. These results indicated that FGL2 might be a promising target for attenuating the severity of SAP and adenovirus-mediated artificial miRNAs targeting FGL2 represented a potential therapeutic approach for the treatment of SAP.

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#29054858   2017/10/21 Save this To Up

MiRNA directed cancer therapies: Implications in melanoma intervention.

Acquired tumor resistance to cancer therapies pose major challenges in the treatment of cancers including melanoma. Among several signaling pathways or factors that affect neocarcinogenesis, cancer progression and therapies, altered microRNAs (miRNAs) expression has been identified as crucial players in modulating the key pathways governing these events. While studies on miRNA field has grown exponentially in the last decade, much remains to be discovered, particularly with respect to their roles in cancer therapies. As immune and non-immune signaling cascades prevail in cancers, identification and evaluation of miRNAs, their molecular mechanisms and cellular targets involved in underlying development of cancers as well as acquired therapeutic resistance would help in devising new strategies for the prognosis, treatment and an early detection of recurrence. Importantly, an in-depth validation of miRNAs-targeted molecular events could lead to the development of an accurate progression-risk biomarkers, improved effectiveness as well as patient's responses to standard therapies. The current review focuses on the roles of miRNAs with recent updates including on its regulated cell cycle and proliferation, immune responses, oncogenic/epigenetic signaling pathways, invasion, metastasis and apoptosis with broader attention on melanomagenesis and melanoma therapies.

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#29054825   2017/10/21 Save this To Up

Integrative mRNA-miRNA interaction analysis associate with immune response of sea cucumber Apostichopus japonicus based on transcriptome database.

MicroRNAs (miRNAs) constitute a family of endogenous non-coding small RNAs that have been demonstrated to be the key effectors in mediating host-pathogen interactions. Additionally, high-throughput sequencing provides unexampled opportunities to identify the pathogenic mechanism underlying miRNAs. In the present study, the target genes of immune-related miRNAs (miR-31, miR-2008, miR-92a, miR-210 and miR-7) and specific miRNAs (miR-2004) in Echinodermata were predicted in silico and validated. Gene ontology (GO) analysis of the target genes of these six miRNAs were conducted to further understand the regulatory function in thehost immunity of Apostichopus japonicus (A. japonicus). Among the putative target genes of the six miRNAs, various immune-related targets were annotated, such as Nephl, SEC14Ll, p105, GL2, LYS, FNIAL, mTOR, LITAF, SLC44, TLR3, Apaf-1, andCNTN4. This work will provide valuable genetic resources to understand the interaction of multiple mRNA-miRNAs and the regulation mechanism in the anti-bacterial process in the sea cucumber.

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#29054762   2017/10/21 Save this To Up

MiR-34a, as a suppressor, enhance the susceptibility of gastric cancer cell to luteolin by directly targeting HK1.

Luteolin is a flavonoid compound derived from Lonicera japonica Thunb, which has been reported to exert anticancer effects on different types of tumors. miRNAs are a kind of endogenous non-coding small RNAs, which involved in occurrence and development of multi cancer, including miR-34a. However, the relationship between miR-34a and luteolin's susceptibility to cancer cells still remains unclear. In this study, we explored the roles of miR-34a and the effects of luteolin on GC cells as well as the underlying mechanism of miR-34a in mediating the susceptibility of GC cell to luteolin. Retrospectively study revealed that miR-34a expression was downregulated in human primary GC tissues compared with non-tumor tissues and low miR-34a expression was associated with a significantly shorter overall survival and disease-free survival. MiR-34a overexpression could inhibit GC cells and induce G1 phase arrest via p53/p21 and MAPK /ERK pathways. Luteolin decreased viability of GC cells in a dose-dependent manner. Meanwhile, miR-34a was found to be markedly upregulated in GC cells induced by luteolin and decreased miR-34a level was found in the artificial luteolin-resistant GC cells. Upregulation of miR-34a in luteolin-resistant GC cell could enhance the sensibility of GC cells to luteolin. On the other hand, miR-34a inhibitor could partly counter the anticancer effect of luteolin. In a further assay, we also found that targeting miR-34a could mediate the susceptibility of mouse xenografts to luteolin. Subsequent study found that HK1 was a direct target of miR-34a and downregulated HK1 mRNA or protein levels were presented after miRNA-34a overexpression in GC cells. Moreover, HK1 protein levels was decreased after luteolin treatment and partly restored when co-treated with luteolin and miR-34a inhibitor. Downregulation of HK1 in luteolin-resistant GC cell could increase the cell's sensitivity to luteolin. Therefore, our findings firstly suggested that miR-34a could modulate the susceptibility of gastric cancer cell to luteolin via targeting HK1, potentially benefiting GC patients' treatment in the future.

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#29054761   2017/10/21 Save this To Up

Differential expression levels of plasma microRNA in Hashimoto's disease.

The altered expression of circulating miRNAs has been discovered in many autoimmune diseases (ADs). With rare existing research, it is still unclear in Hashimoto's thyroiditis (HT). We detected plasma miRNA expression of HT patients in this three-stage designed study.

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#29054757   2017/10/21 Save this To Up

MiR-767 promoted cell proliferation in human melanoma by suppressing CYLD expression.

MicroRNAs (miRNAs) have emerged as critical regulators for cancer development and progression of human melanoma. However, the potential molecular mechanism of miR-767 in human melanoma has not been intensively investigated. In this present study, we confirmed that miR-767 was frequently up-regulated in human melanoma tissues and cell lines. Ectopic expression of miR-767 promoted cell proliferation in human melanoma cell lines A375 and WM35, whereas miR-767-in reversed the function. Bioinformatics analysis revealed that cylindromatosis (CYLD) was hypothesized to be a possible target gene of miR-767, and this was confirmed by luciferase activity assay. Knockdown of CYLD counteracted the proliferation arrest by miR-767-in in melanoma cells A375 and WM35. In conclusion, our study indicated that miR-767 acted as a role of tumor promoter by targeting CYLD in human melanoma, and might serve as a prognostic or therapeutic target for human melanoma.

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#29054152   2017/10/21 Save this To Up

Target-initiated labeling for the dual-amplified detection of multiple microRNAs.

Herein we exploited a novel target-initiated labeling strategy for the multiplex detection of microRNAs (miRNAs) by coupling duplex-specific nuclease (DSN) with terminal deoxynucleotidyl transferase (TdT). In the presence of target miRNA, the immobilized and 3'-blocked capture probes hybridized with target and thus the formed DNA-RNA hybrid was recognized by DSN. DSN mediated the digestion of 3'-phosphated capture probes (CPs) in the hybrids and synchronously target was released and recycled for another round of hybridization and cleavage. The cleaved CP fragments with a free 3'-OH were then elongated and labeled with multiple biotin-dUTP nucleotides by TdT. Fluorescence reporter streptavidin-phycoerythin was finally added to react with the immobilized biotins and render fluorescence signals. This dual-amplification labeling strategy was successfully demonstrated to sensitively detect multiple miRNAs, taking advantage of DSN-mediated target recycling and TdT-catalyzed multiple signal modification with analysis by a commercial Luminex xMAP array platform. Our experimental results showed the simultaneous quantitative measurement of three sequence-specific miRNAs at concentrations from 1 pM to 2.5 nM. Attempts were also made to directly detect miRNAs in total RNA extracted from cancer cells. The dual-amplification labeling strategy reported here shows a great potential for the development of a method for the multiplexed, sensitive, selective, and simple analysis of multiple miRNAs in tissues or cells for biomedical research and clinical early diagnosis.

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