% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Demolli:126419,
      author       = {S. Demolli and C. Doebele and A. Doddaballapur and V. Lang
                      and B. Fisslthaler and E. Chavakis and M. Vinciguerra and S.
                      Sciacca and R. Henschler and M. Hecker and S. Savant and H.
                      Augustin$^*$ and D. Kaluza and S. Dimmeler and R. A. Boon},
      title        = {{M}icro{RNA}-30 mediates anti-inflammatory effects of shear
                      stress and {KLF}2 via repression of angiopoietin 2.},
      journal      = {Journal of molecular and cellular cardiology},
      volume       = {88},
      issn         = {0022-2828},
      address      = {New York, NY [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-02448},
      pages        = {111 - 119},
      year         = {2015},
      abstract     = {MicroRNAs are endogenously expressed small noncoding RNAs
                      that regulate gene expression. Laminar blood flow induces
                      atheroprotective gene expression in endothelial cells (ECs)
                      in part by upregulating the transcription factor KLF2. Here,
                      we identified KLF2- and flow-responsive miRs that affect
                      gene expression in ECs. Bioinformatic assessment of mRNA
                      expression patterns identified the miR-30-5p seed sequence
                      to be highly enriched in mRNAs that are downregulated by
                      KLF2. Indeed, KLF2 overexpression and shear stress
                      stimulation in vitro and in vivo increased the expression of
                      miR-30-5p family members. Furthermore, we identified
                      angiopoietin 2 (Ang2) as a target of miR-30. MiR-30
                      overexpression reduces Ang2 levels, whereas miR-30
                      inhibition by LNA-antimiRs induces Ang2 expression.
                      Consistently, miR-30 reduced basal and TNF-α-induced
                      expression of the inflammatory cell–cell adhesion
                      molecules E-selectin, ICAM1 and VCAM1, which was rescued by
                      stimulation with exogenous Ang2. In summary, KLF2 and shear
                      stress increase the expression of the miR-30-5p family which
                      acts in an anti-inflammatory manner in ECs by impairing the
                      expression of Ang2 and inflammatory cell–cell adhesion
                      molecules. The upregulation of miR-30-5p family members may
                      contribute to the atheroprotective effects of shear stress.},
      keywords     = {C11orf2 protein, human (NLM Chemicals) / E-Selectin (NLM
                      Chemicals) / ICAM1 protein, human (NLM Chemicals) / KLF2
                      protein, human (NLM Chemicals) / Kruppel-Like Transcription
                      Factors (NLM Chemicals) / MIRN30 microRNA, human (NLM
                      Chemicals) / MicroRNAs (NLM Chemicals) / RNA, Messenger (NLM
                      Chemicals) / SELE protein, human (NLM Chemicals) / Tumor
                      Necrosis Factor-alpha (NLM Chemicals) / Vascular Cell
                      Adhesion Molecule-1 (NLM Chemicals) / Vesicular Transport
                      Proteins (NLM Chemicals) / Intercellular Adhesion Molecule-1
                      (NLM Chemicals)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26456066},
      doi          = {10.1016/j.yjmcc.2015.10.009},
      url          = {https://inrepo02.dkfz.de/record/126419},
}