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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
E-mail(s) mollenkopf@mpiib-berlin.mpg.de
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
Relations
BioProject PRJNA140035

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

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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