ABSTRACT
The article "Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal", by K. Zhao, J.-Y. Tan, Q.-D. Mao, K.-Y. Ren, B.-G. He, C.-P. Zhang, L.-Z. Wei published in Eur Rev Med Pharmacol Sci 2019; 23 (1): 312-320-DOI: 10.26355/eurrev_201901_16778-PMID: 30657572 has been retracted by the authors for the following reasons: We are still conducting research in the effect of long non-codingRNA TUG1 in interstitial cells of Cajal recently. It turned out that some of the current experimental results are inconsistent with the previous results. Some data cannot be repeated by further research. We need to further confirm the effect of long non-coding RNA TUG1 on alleviating TNF-α-induced inflammatory injury in interstitial cells of Cajal and for this reason, the authors all agreed to withdraw the manuscript. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16778.
ABSTRACT
OBJECTIVE: Irritable bowel syndrome (IBS) is a common functional disorder in the gastrointestinal tract. Inflammatory response has been found to participate in the pathogenesis of IBS. This study aimed to explore the effects of long non-coding RNA taurine upregulated gene 1 (TUG1) on tumor necrosis factor alpha (TNF-α)-induced interstitial cells of Cajal (ICC) inflammatory injury, which was relevant to the pathogenesis of IBS. PATIENTS AND METHODS: The expression levels of TUG1 and microRNA-127 (miR-127) were analyzed by qRT-PCR. Viability, apoptosis and the expression of apoptosis-associated factors were analyzed by CCK-8 assay, flow cytometry and Western blot, respectively. The mRNA and protein levels of pro-inflammatory cytokines were detected by qRT-PCR and Western blot, respectively. Finally, activations of nuclear factor kappa-B (NF-κB) and Notch pathways were evaluated by Western blot. RESULTS: TNF-α treatment inhibited ICC viability, induced ICC apoptosis and promoted an inflammatory response in ICC. TUG1 was downregulated in TNF-α-treated ICC. TUG1 overexpression protected ICC from TNF-α-induced apoptosis and pro-inflammatory cytokines expression. TUG1 suppression showed opposite effects. MiR-127 was negatively regulated by TUG1 and implicated in the action of TUG1 in ICC. MiR-127 up-regulation largely reversed the effects of TUG1 on TNF-α-treated ICC. Mechanistically, TUG1 inhibited TNF-α-induced activation of NF-κB and Notch pathways in ICC by down-regulating miR-127. CONCLUSIONS: TUG1 attenuated TNF-α-caused apoptosis and inflammatory response in ICC by down-regulating miR-127 and then inactivating NF-κB and Notch pathways.
Subject(s)
Interstitial Cells of Cajal/immunology , Irritable Bowel Syndrome/genetics , MicroRNAs/genetics , RNA, Long Noncoding/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Apoptosis/genetics , Apoptosis/immunology , Cell Survival/genetics , Cell Survival/immunology , Cells, Cultured , Female , Gene Expression Profiling , Humans , Interstitial Cells of Cajal/pathology , Irritable Bowel Syndrome/immunology , Irritable Bowel Syndrome/pathology , Mice , MicroRNAs/metabolism , Primary Cell Culture , RNA, Long Noncoding/agonists , RNA, Long Noncoding/antagonists & inhibitors , RNA, Long Noncoding/genetics , RNA, Small Interfering/metabolism , Receptors, Notch/immunology , Receptors, Notch/metabolism , Signal Transduction/genetics , Signal Transduction/immunology , Tumor Necrosis Factor-alpha/immunology , Up-RegulationABSTRACT
Mycoplasmas were effectively eliminated from contaminated LTK and CHO cell lines by means of the antibiotic Tiamutin (10 micrograms/ml), while Kanamycin and Gentamycin were less potential. An elimination procedure which involved the consecutive treatment of the cell cloning over a periods of 21-28 days was adopted. This procedure was effective when applied to cell lines contaminated with unidentified and partially non-cultivable strains of mycoplasmas which could be detected by electronic microscope.
Subject(s)
Anti-Bacterial Agents/pharmacology , Mycoplasma/drug effects , Animals , Cell Line , Cells, Cultured , Cricetinae , Diterpenes/pharmacology , Female , Mycoplasma/isolation & purification , Ovary/cytologyABSTRACT
Hepatitis B virus surface antigen (HBsAg) mRNA has been enriched from a hepatoma cell line (PLC/PRF/5) by specific polysome immunoprecipitation and used for cDNA cloning. A HBsAg cDNA clone was identified by in situ hybridization with a cloned viral probe. It was characterized by restriction endonuclease mapping and DNA sequence analysis. Molecular hybridization of PLC/PRF/5 cellular DNA and RNA to [32P]-labeled HBsAg cDNA revealed the integration of at least six copies of the hepatitis B virus (HBV) DNA into the host genome and expression of three DNA species containing HBsAg-specific sequences. The possible role of HBV in the oncogenesis of primary hepatocellular carcinoma is discussed.
