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@ARTICLE{Ungvari:128991,
      author       = {Ungvari, Z. and Tucsek, Zsuzsanna and Sosnowska, Danuta and
                      Toth, Peter and Gautam, Tripti and Podlutsky, Andrej and
                      Csiszar, Agnes and Losonczy, Gyorgy and Valcarcel-Ares, M
                      Noa and Sonntag, William E and Csiszar, Anna},
      title        = {{A}ging-{I}nduced {D}ysregulation of {D}icer1-{D}ependent
                      {M}icro{RNA} {E}xpression {I}mpairs {A}ngiogenic {C}apacity
                      of {R}at {C}erebromicrovascular {E}ndothelial {C}ells.},
      journal      = {The journals of gerontology / A},
      volume       = {68},
      number       = {8},
      issn         = {1758-535X},
      address      = {Oxford [u.a.]},
      publisher    = {Oxford Univ. Pr.},
      reportid     = {FZJ-2013-00514},
      pages        = {877-891},
      year         = {2013},
      abstract     = {Age-related impairment of angiogenesis is likely to play a
                      central role in cerebromicrovascular rarefaction and
                      development of vascular cognitive impairment, but the
                      underlying mechanisms remain elusive. To test the hypothesis
                      that dysregulation of Dicer1 (ribonuclease III, a key enzyme
                      of the microRNA [miRNA] machinery) impairs endothelial
                      angiogenic capacity in aging, primary cerebromicrovascular
                      endothelial cells (CMVECs) were isolated from young (3
                      months old) and aged (24 months old) Fischer 344 × Brown
                      Norway rats. We found an age-related downregulation of
                      Dicer1 expression both in CMVECs and in small cerebral
                      vessels isolated from aged rats. In aged CMVECs, Dicer1
                      expression was increased by treatment with polyethylene
                      glycol-catalase. Compared with young cells, aged CMVECs
                      exhibited altered miRNA expression profile, which was
                      associated with impaired proliferation, adhesion to
                      vitronectin, collagen and fibronectin, cellular migration
                      (measured by a wound-healing assay using electric
                      cell-substrate impedance sensing technology), and impaired
                      ability to form capillary-like structures. Overexpression of
                      Dicer1 in aged CMVECs partially restored miRNA expression
                      profile and significantly improved angiogenic processes. In
                      young CMVECs, downregulation of Dicer1 (siRNA) resulted in
                      altered miRNA expression profile associated with impaired
                      proliferation, adhesion, migration, and tube formation,
                      mimicking the aging phenotype. Collectively, we found that
                      Dicer1 is essential for normal endothelial angiogenic
                      processes, suggesting that age-related dysregulation of
                      Dicer1-dependent miRNA expression may be a potential
                      mechanism underlying impaired angiogenesis and
                      cerebromicrovascular rarefaction in aging.},
      cin          = {ICS-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-7-20110106},
      pnm          = {452 - Structural Biology (POF2-452)},
      pid          = {G:(DE-HGF)POF2-452},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23239824},
      UT           = {WOS:000322298700001},
      doi          = {10.1093/gerona/gls242},
      url          = {https://juser.fz-juelich.de/record/128991},
}