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Series GSE29388 Query DataSets for GSE29388
Status Public on Apr 03, 2012
Title H. pylori infection blocks DNA damage induced apoptosis by T4SS-dependent upregulation of miR-155
Organism Mus musculus
Experiment type Expression profiling by array
Summary The innate immune response against Helicobacter pylori is mainly controlled by pattern recognition receptors that lead to the up-regulation of pro-inflammatory cytokines. A new player in this field is the miR-155 being regulated by TLR ligands in monocytic derived cells influencing certain intracellular pathways by down-regulating targets involved in signaling and development. By using primary bone marrow derived macrophages (BMMs) from mice deficient in the key TLR signals the regulation of miR-155 was explored. Further on the biological impact of a lack of miR-155 in BMMs was analyzed by micro-array studies and apoptosis assays. We observed that miR-155 is up-regulated in response to H. pylori via TLR2 and TLR4 in a NF-╬║B dependent manner, but also identified a TLR2/TLR4 independent mechanism that was strongly connected to a functional TypeIV secretion system. Down-stream the high expression of miR-155 down-regulated many mRNA targets during H. pylori infection. Thereby we could validate Tspan14, Lpin1, and Pmaip1 as new targets of miR-155 and identified their binding site. These and other already published targets showed a substantial pro-apoptotic potential. We observed that H. pylori infected wild type BMMs were much more resistant to DNA damage induced apoptosis by cisplatin when compared to their respective miR-155-/- BMMs. Our data strongly suggests that there is an additional innate immune mechanism of BMMs leading to the upregulation of the anti-apoptotic miR-155 that causes resistance to DNA damage in BMMs.
Overall design Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, an independent dye-reversal color-swap was applied. Bone marrow derived macrophages were 'in vitro' infected with H.pylori P12 and the expression changes were measured.
Contributor(s) Koch M, Meyer TF, Mollenkopf H
Citation(s) 22509021
Submission date May 19, 2011
Last update date May 10, 2018
Contact name Hans-Joachim Mollenkopf
Phone +49 30 28460 482
Organization name Max-Planck-Institute for Infection Biology
Lab Microarray/Genomics Core Facility
Street address Charit├ęplatz 1
City Berlin
ZIP/Postal code 10117
Country Germany
Platforms (1)
GPL4134 Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Feature Number version)
Samples (4)
GSM726772 wt ni vs wt P12 [30 hpi]
GSM726773 wt P12 vs wt ni [30 hpi]
GSM726774 155 P12 vs wt P12
BioProject PRJNA140035

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Supplementary file Size Download File type/resource
GSE29388_RAW.tar 6.6 Mb (http)(custom) TAR
Processed data included within Sample table

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