Specific microRNAs Regulate Heat Stress Responses in Caenorhabditis elegans

Nehammer, Camilla; Podolska, Agnieszka; Mackowiak, Sebastian D.; Kagias, Konstantinos; Pocock, Roger

doi:10.1038/srep08866

Cited by 54 publications

(58 citation statements)

References 41 publications

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“…LBP's concentrationdependent immunologic function and structural integrity must require precise genetic regulation of gene transcription, suggesting that genetic variation in the elements controlling LBP production or structure may affect an individual's immune response to LPS and gram-negative bacteria. This idea is supported by a previous detailed study of truncation mutation experiments of the LBP promoter region, which indicate that a region of the LBP promoter is responsible for regulating the efficiency of gene transcription (Nehammer et al 2015). Genetic variation in the promoter region of the LBP gene is associated with the blood level of LBP and with the risk of developing gram-negative bacteremia and gram-negative bacteremia-related death after hematopoietic cell transplantation (HCT) .…”

Section: Discussionsupporting

confidence: 61%

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

Sun

et al. 2016

Cell Stress and Chaperones

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Lipopolysaccharide (LPS)-binding protein (LBP) plays a crucial role in the recognition of bacterial components, such as LPS that causes an immune response. The aim of this study was to compare the different effects of recombinant bovine wild LBP and mutant LBP (67 Ala → Thr) on the LPSinduced inflammatory response of bovine mammary epithelial cells (BMECs). When BMECs were treated with various concentrations of recombinant bovine lipopolysaccharide-binding protein (RBLBP) (1, 5, 10, and 15 μg/mL) for 12 h, RBLBP of 5 μg/mL increased the apoptosis of BMECs induced by LPS without cytotoxicity, and mutant LBP resulted in a higher cell apoptosis than wild LBP did. By gene-chip microarray and bioinformatics, the data identified 2306 differentially expressed genes that were changed significantly between the LPSinduced inflamed BMECs treated with 5 μg/mL of mutant LBP and the BMECs only treated with 10 μg/mL of LPS (fold change ≥2). Meanwhile, 1585 genes were differently expressed between the inflamed BMECs treated with 5 μg/mL of wild LBP and 10 μg/mL of LPS-treated BMECs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that these differentially expressed genes were involved in different pathways that regulate the inflammation response. It predicted that carriers of this mutation increase the risk for a more severe inflammatory response. Our study provides an overview of the gene expression profile between wild LBP and mutant LBP on the LPS-induced inflammatory response of BMECs, which will lead to further understanding of the potential effects of LBP mutations on bovine mammary glands.

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Section: Discussionsupporting

confidence: 61%

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

Sun

et al. 2016

Cell Stress and Chaperones

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“…MicroRNAs (miRNAs) are composed of a group of endogenous and non-coding small RNAs that operate as key posttranscriptional regulators of eukaryotic gene expression through imperfect base-pairing with sites harbored in the 3′UTR regions of their mRNA targets (Bartel 2004(Bartel , 2009Nehammer et al 2015). MiRNAs are involved in almost every biological process, including cell growth and differentiation, pathogenesis, and disease prevention (McKenna et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen

Shi

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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Heat stress can weaken the immune system and even increase livestock's susceptibility to disease. MicroRNA (miR) is short non-coding RNA that functions in post-transcriptional regulation of gene expression and some phenotypes. Our recent study found that miR-181a is highly expressed in the serum of heat-stressed Holstein cows, but the potential function of miR-181a is still not clarified. In this study, peripheral blood mononuclear cells (PBMCs), isolated from Holstein cows' peripheral blood, were used to investigate the effects of miR-181a inhibitor on heat stress damage. Our results showed that significant apoptosis and oxidative damage were induced by heat stress in PBMCs. However, with apoptosis, the levels of reactive oxygen species (ROS) and content of malondialdehyde (MDA) were reduced, while the content of glutathione (GSH) and the activity of superoxide dismutase (SOD) were increased even under heat stress conditions after transfecting miR-181a inhibitors to PBMCs. Meanwhile, mRNA expression of bax and caspase-3 was significantly decreased, but mRNA expression of bcl-2 was increased in transfected PBMCs. In conclusion, our results demonstrated that down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows.

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“…MicroRNAs (miRNAs) are pivotal regulators for gene expression in metazoa14. In animals, miRNAs normally target several mRNAs through base pairing with 3′-untranslated region (3′-UTR) of the corresponding target mRNAs15.…”

mentioning

confidence: 99%

microRNAs Involved in the Control of Innate Immunity in Candida Infected Caenorhabditis elegans

Sun

Zhi

Shakoor

et al. 2016

Sci Rep

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The role of microRNAs (miRNAs) in regulating innate immune response to Candida albicans infection in Caenorhabditis elegans is still largely unclear. Using small RNA SOLiD deep sequencing technique, we profiled the miRNAs that were dysregulated by C. albicans infection. We identified 16 miRNAs that were up-regulated and 4 miRNAs that were down-regulated in nematodes infected with C. albicans. Bioinformatics analysis implied that these dysregulated miRNAs may be involved in the control of many important biological processes. Using available mutants, we observed that mir-251 and mir-252 loss-of-function mutants were resistant to C. albicans infection, whereas mir-360 mutants were hypersensitive to C. albicans infection. The expression pattern of antimicrobial genes suggested that mir-251, mir-252, and mir-360 played crucial roles in regulating the innate immune response to C. albicans infection. Fungal burden might be closely associated with altered lifespan and innate immune response in mir-251, mir-252, and mir-360 mutants. Moreover, mir-251 and mir-252 might function downstream of p38 mitogen activated protein kinase (MAPK) or IGF-1/insulin-like pathway to regulate the innate immune response to C. albicans infection. Our results provide an important molecular basis for further elucidating how miRNA-mRNA networks may control the innate immune response to C. albicans infection.

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Specific microRNAs Regulate Heat Stress Responses in Caenorhabditis elegans

Cited by 54 publications

References 41 publications

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

Comparison of the effect of recombinant bovine wild and mutant lipopolysaccharide-binding protein in lipopolysaccharide-challenged bovine mammary epithelial cells

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

microRNAs Involved in the Control of Innate Immunity in Candida Infected Caenorhabditis elegans

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