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  • 1.
    Das, Jyotirmoy
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology, Infection and Inflammation. Linköping University, Faculty of Medicine and Health Sciences.
    Verma, Deepti
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Gustafsson, Mika
    Linköping University, Department of Physics, Chemistry and Biology, Bioinformatics. Linköping University, Faculty of Science & Engineering.
    Lerm, Maria
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology, Infection and Inflammation. Linköping University, Faculty of Medicine and Health Sciences.
    Identification of DNA methylation patterns predisposing for an efficient response to BCG vaccination in healthy BCG-naive subjects2019In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 14, no 6, p. 589-601Article in journal (Refereed)
    Abstract [en]

    The protection against tuberculosis induced by the Bacille Calmette Guerin (BCG) vaccine is unpredictable. In our previous study, altered DNA methylation pattern in peripheral blood mononuclear cells (PBMCs) in response to BCG was observed in a subgroup of individuals, whose macrophages killed mycobacteria effectively (responders). These macrophages also showed production of Interleukin-1 beta (IL-1 beta) in response to mycobacterial stimuli before vaccination. Here, we hypothesized that the propensity to respond to the BCG vaccine is reflected in the DNA methylome. We mapped the differentially methylated genes (DMGs) in PBMCs isolated from responders/non-responders at the time point before vaccination aiming to identify possible predictors of BCG responsiveness. We identified 43 DMGs and subsequent bioinformatic analyses showed that these were enriched for actin-modulating pathways, predicting differences in phagocytosis. This could be validated by experiments showing that phagocytosis of mycobacteria, which is an event preceding mycobacteria-induced IL-1 beta production, was strongly correlated with the DMG pattern.

  • 2.
    Dmitriev, Alexey A
    et al.
    Karolinska Institute.
    Kashuba, Vladimir I
    Karolinska Institute.
    Haraldson, Klas
    Karolinska Institute.
    Senchenko, Vera N
    Engelhardt Institute Molecular Biology.
    Pavlova, Tatiana V
    Karolinska Institute.
    Kudryavtseva, Anna V
    Engelhardt Institute Molecular Biology.
    Anedchenko, Ekaterina A
    Engelhardt Institute Molecular Biology.
    Krasnov, George S
    Engelhardt Institute Molecular Biology.
    Pronina, Irina V
    Russian State Genet Centre GosNIIgenetika.
    Loginov, Vitalij I
    Russian State Genet Centre GosNIIgenetika.
    Kondratieva, Tatiana T
    RAMS, Blokhin Cancer Research Centre.
    Kazubskaya, Tatiana P
    RAMS, Blokhin Cancer Research Centre.
    Braga, Eleonora A
    Russian State Genet Centre GosNIIgenetika.
    Yenamandra, Surya P
    Karolinska Institute.
    Ignatjev, Ilya
    Karolinska Institute.
    Ernberg, Ingemar
    Karolinska Institute.
    Klein, George
    Karolinska Institute.
    Lerman, Michael I
    NHLBI.
    Zabarovsky, Eugene R
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Genetic and epigenetic analysis of non-small cell lung cancer with NotI-microarrays2012In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 7, no 5, p. 502-513Article in journal (Refereed)
    Abstract [en]

    This study aimed to clarify genetic and epigenetic alterations that occur during lung carcinogenesis and to design perspective sets of newly identified biomarkers. The original method includes chromosome 3 specific NotI-microarrays containing 180 NotI clones associated with genes for hybridization with 40 paired normal/tumor DNA samples of primary lung tumors: 28 squamous cell carcinomas (SCC) and 12 adenocarcinomas (ADC). The NotI-microarray data were confirmed by qPCR and bisulfite sequencing analyses. Forty-four genes showed methylation and/or deletions in more than 15% of non-small cell lung cancer (NSCLC) samples. In general, SCC samples were more frequently methylated/deleted than ADC. Moreover, the SCC alterations were observed already at stage I of tumor development, whereas in ADC many genes showed tumor progression specific methylation/deletions. Among genes frequently methylated/deleted in NSCLC, only a few were already known tumor suppressor genes: RBSP3 (CTDSPL), VHL and THRB. The RPL32, LOC285205, FGD5 and other genes were previously not shown to be involved in lung carcinogenesis. Ten methylated genes, i.e., IQSEC1, RBSP3, ITGA9, FOXP1, LRRN1, GNAI2, VHL, FGD5, ALDH1L1 and BCL6 were tested for expression by qPCR and were found downregulated in the majority of cases. Three genes (RBSP3, FBLN2 and ITGA9) demonstrated strong cell growth inhibition activity. A comprehensive statistical analysis suggested the set of 19 gene markers, ANKRD28, BHLHE40, CGGBP1, RBSP3, EPHB1, FGD5, FOXP1, GORASP1/TTC21, IQSEC1, ITGA9, LOC285375, LRRC3B, LRRN1, MITF, NKIRAS1/RPL15, TRH, UBE2E2, VHL, WNT7A, to allow early detection, tumor progression, metastases and to discriminate between SCC and ADC with sensitivity and specificity of 80-100%.

  • 3.
    Mostovich, Luydmila A
    et al.
    Institute Molecular Biol and Biophys SB RAMS, Russia .
    Prudnikova, Tatiana Y
    Institute Molecular Biol and Biophys SB RAMS, Russia .
    Kondratov, Aleksandr G
    Ukrainian Academic Science, Ukraine .
    Gubanova, Natalya V
    Institute Cytol and Genet SD RAS, Russia .
    Kharchenko, Olga A
    Karolinska Institute, Sweden .
    Kutsenko, Olesya S
    Institute Molecular Biol and Biophys SB RAMS, Russia .
    Vavilov, Pavel V
    Institute Molecular Biol and Biophys SB RAMS, Russia .
    Haraldson, Klas
    Karolinska Institute, Sweden .
    Kashuba, Vladimir I
    Ukrainian Academic Science, Ukraine .
    Ernberg, Ingemar
    Karolinska Institute, Sweden .
    Zabarovsky, Eugene R
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Grigorieva, Elvira V
    Institute Molecular Biol and Biophys SB RAMS, Russia Karolinska Institute, Sweden .
    The TCF4/beta-catenin pathway and chromatin structure cooperate to regulate D-glucuronyl C5-epimerase expression in breast cancer2012In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 7, no 8, p. 930-939Article in journal (Refereed)
    Abstract [en]

    D-glucuronyl C5-epimerase (GLCE) is a potential tumor-suppressor gene involved in heparan sulfate biosynthesis. GLCE expression is significantly decreased in breast tumors; however, the underlying molecular mechanisms remain unclear. This study examined the possible epigenetic mechanisms for GLCE inactivation in breast cancer. Very little methylation of the GLCE promoter region was detected in breast tumors in vivo and in breast cancer cells (MCF7 and T47D) in vitro and GLCE expression in breast cancer cells was not altered by 5-deoxyazacytidine (5-aza-dC) treatment, suggesting that promoter methylation is not involved in regulating GLCE expression. Chromatin activation by Trichostatin A (TSA) or 5-aza-dC/TSA treatment increased GLCE expression by two to 3-fold due to an increased interaction between the GLCE promoter and the TCF4/beta-catenin transactivation complex, or H3K9ac and H3K4Me3 histone modifications. However, ectopic expression of TCF4/beta-catenin was not sufficient to activate GLCE expression in MCF7 cells, suggesting that chromatin structure plays a key role in GLCE regulation. Although TSA treatment significantly repressed canonical WNT signaling in MCF7 cells, it did not influence endogenous TCF4/beta-catenin mRNA levels and activated TCF4/beta-catenin-driven transcription from the GLCE promoter, indicating GLCE as a novel target for TCF4/beta-catenin complex in breast cancer cells. A correlation was observed between GLCE, TCF4 and beta-catenin expression in breast cancer cells and primary tumors, suggesting an important role for TCF4/beta-catenin in regulating GLCE expression both in vitro and in vivo. Taken together, the results indicate that GLCE expression in breast cancer is regulated by a combination of chromatin structure and TCF4/beta-catenin complex activity.

  • 4.
    Prudnikova, Tatiana Y
    et al.
    Russian Academy of Medical Science, Russia .
    Mostovich, Luydmila A
    Russian Academy of Medical Science, Russia.
    Kashuba, Vladimir I
    Ukrainian National Academy of Science, Ukraine .
    Ernberg, Ingemar
    Karolinska Institute, Sweden .
    Zabarovsky, Eugene R
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Grigorieva, Elvira V
    Russian Academy of Medical Science, Russia.
    miRNA-218 contributes to the regulation of D-glucuronyl C5-epimerase expression in normal and tumor breast tissues2012In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 7, no 10, p. 1109-1114Article in journal (Refereed)
    Abstract [en]

    microRNAs (miRNAs) are key posttranscriptional regulators of gene expression. In the present study, regulation of tumor-suppressor gene D-glucuronyl C5-epimerase (GLCE) by miRNA-218 was investigated. Significant downregulation of miRNA-218 expression was shown in primary breast tumors. Exogenous miRNA-218/anti-miRNA-218 did not affect GLCE mRNA but regulated GLCE protein level in MCF7 breast carcinoma cells in vitro. Comparative analysis showed a positive correlation between miRNA-218 and GLCE mRNA, and negative correlation between miRNA-218 and GLCE protein levels in breast tissues and primary tumors in vivo, supporting a direct involvement of miRNA-218 in posttranscriptional regulation of GLCE in human breast tissue. A common scheme for the regulation of GLCE expression in normal and tumor breast tissues is suggested.

  • 5.
    Pértille, Fábio
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering. Univ Sao Paulo, Brazil.
    Da Silva, Vinicius H.
    Wageningen Univ and Res, Netherlands; Netherlands Inst Ecol NIOO KNAW, Netherlands; Swedish Univ Agr Sci, Sweden.
    Johansson, Anna M.
    Swedish Univ Agr Sci, Sweden.
    Lindström, Tom
    Linköping University, Department of Physics, Chemistry and Biology, Theoretical Biology. Linköping University, Faculty of Science & Engineering.
    Wright, Dominic
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Coutinho, Luiz L.
    Univ Sao Paulo, Brazil.
    Jensen, Per
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Guerrero Bosagna, Carlos
    Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
    Mutation dynamics of CpG dinucleotides during a recent event of vertebrate diversification2019In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308Article in journal (Refereed)
    Abstract [en]

    DNA methylation in CpGs dinucleotides is associated with high mutability and disappearance of CpG sites during evolution. Although the high mutability of CpGs is thought to be relevant for vertebrate evolution, very little is known on the role of CpG-related mutations in the genomic diversification of vertebrates. Our study analysed genetic differences in chickens, between Red Junglefowl (RJF; the living closest relative to the ancestor of domesticated chickens) and domesticated breeds, to identify genomic dynamics that have occurred during the process of their domestication, focusing particularly on CpG-related mutations. Single nucleotide polymorphisms (SNPs) and copy number variations (CNVs) between RJF and these domesticated breeds were assessed in a reduced fraction of their genome. Additionally, DNA methylation in the same fraction of the genome was measured in the sperm of RJF individuals to identify possible correlations with the mutations found between RJF and the domesticated breeds. Our study shows that although the vast majority of CpG-related mutations found relate to CNVs, CpGs disproportionally associate to SNPs in comparison to CNVs, where they are indeed substantially under-represented. Moreover, CpGs seem to be hotspots of mutations related to speciation. We suggest that, on the one hand, CpG-related mutations in CNV regions would promote genomic flexibility in evolution, i.e., the ability of the genome to expand its functional possibilities; on the other hand, CpG-related mutations in SNPs would relate to genomic specificity in evolution, thus, representing mutations that would associate with phenotypic traits relevant for speciation.

  • 6.
    Skinner, Michael K
    et al.
    Center for Reproductive Biology, School of Biological Sciences, Washingston State University, Pullman, WA USA.
    Guerrero-Bosagna, Carlos
    Center for Reproductive Biology, School of Biological Sciences, Washingston State University, Pullman, WA USA.
    Haque, M Muksitul
    Center for Reproductive Biology, School of Biological Sciences, Washingston State University, Pullman, WA USA.
    Environmentally induced epigenetic transgenerational inheritance of sperm epimutations promote genetic mutations.2015In: Epigenetics, ISSN 1559-2294, E-ISSN 1559-2308, Vol. 10, no 8, p. 762-771Article in journal (Refereed)
    Abstract [en]

    A variety of environmental factors have been shown to induce the epigenetic transgenerational inheritance of disease and phenotypic variation. This involves the germline transmission of epigenetic information between generations. Exposure specific transgenerational sperm epimutations have been previously observed. The current study was designed to investigate the potential role genetic mutations have in the process, using copy number variations (CNV). In the first (F1) generation following exposure, negligible CNV were identified; however, in the transgenerational F3 generation, a significant increase in CNV was observed in the sperm. The genome-wide locations of differential DNA methylation regions (epimutations) and genetic mutations (CNV) were investigated. Observations suggest the environmental induction of the epigenetic transgenerational inheritance of sperm epimutations promote genome instability, such that genetic CNV mutations are acquired in later generations. A combination of epigenetics and genetics is suggested to be involved in the transgenerational phenotypes. The ability of environmental factors to promote epigenetic inheritance that subsequently promotes genetic mutations is a significant advance in our understanding of how the environment impacts disease and evolution.

1 - 6 of 6
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