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@ARTICLE{Sona:277315,
      author       = {Sona, Chandan and Yeh, Yu-Te and Li, Yunxiao and Liu,
                      Xiaoxuan and Ghosh, Adhideb and Hinte, Laura C and Ku,
                      Min-Chi and Rathjen, Thomas and Niendorf, Thoralf and Yu,
                      Guoxing and Jia, Shiqi and Kononenko, Natalia L and Hermann,
                      Andreas and Luo, Jiankai and Lin, Juntang and von Meyenn,
                      Ferdinand and Yan, Xin and Poy, Matthew N},
      title        = {{G}lutamatergic argonaute2 promotes the formation of the
                      neurovascular unit in mice.},
      journal      = {Science signaling},
      volume       = {18},
      number       = {875},
      issn         = {1945-0877},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DZNE-2025-00378},
      pages        = {eadl6745},
      year         = {2025},
      abstract     = {Proper formation of the complex neurovascular unit (NVU)
                      along with the blood-brain barrier is critical for building
                      and sustaining a healthy, functioning central nervous
                      system. The RNA binding protein argonaute2 (Ago2) mediates
                      microRNA (miRNA)-mediated gene silencing, which is critical
                      for many facets of brain development, including NVU
                      development. Here, we found that Ago2 in glutamatergic
                      neurons was critical for NVU formation in the developing
                      cortices of mice. Glutamatergic neuron-specific loss of Ago2
                      diminished synaptic formation, neuronal-to-endothelial cell
                      contacts, and morphogenesis of the brain vasculature,
                      ultimately compromising the integrity of the blood-brain
                      barrier. Ago2 facilitated miRNA targeting of phosphatase and
                      tensin homolog (Pten) mRNA, which encodes a phosphatase that
                      modulates reelin-dependent phosphatidylinositol 3-kinase
                      (PI3K)-Akt signaling within the glutamatergic subpopulation.
                      Conditionally deleting Pten in Ago2-deficient neurons
                      restored Akt2 phosphorylation as well as postnatal
                      development and survival. Several mutations in AGO2 impair
                      small RNA silencing and are associated with
                      Lessel-Kreienkamp syndrome, a neurodevelopmental disorder.
                      When expressed in a neuronal cell line, these human AGO2
                      loss-of-function variants failed to suppress PTEN, resulting
                      in attenuated PI3K-Akt signaling, further indicating that
                      dysregulation of Ago2 function may contribute to both
                      impaired development and neurological disorders. Together,
                      these results identify Ago2 as central to the engagement of
                      neurons with blood vessels in the developing brain.},
      keywords     = {Animals / Argonaute Proteins: metabolism / Argonaute
                      Proteins: genetics / PTEN Phosphohydrolase: metabolism /
                      PTEN Phosphohydrolase: genetics / Mice / Humans / Neurons:
                      metabolism / Reelin Protein / MicroRNAs: metabolism /
                      MicroRNAs: genetics / Signal Transduction / Blood-Brain
                      Barrier: metabolism / Proto-Oncogene Proteins c-akt:
                      metabolism / Proto-Oncogene Proteins c-akt: genetics /
                      Phosphatidylinositol 3-Kinases: metabolism /
                      Phosphatidylinositol 3-Kinases: genetics / Mice, Knockout /
                      Glutamic Acid: metabolism / Argonaute Proteins (NLM
                      Chemicals) / PTEN Phosphohydrolase (NLM Chemicals) / Ago2
                      protein, mouse (NLM Chemicals) / Reln protein, mouse (NLM
                      Chemicals) / Reelin Protein (NLM Chemicals) / RELN protein,
                      human (NLM Chemicals) / Pten protein, mouse (NLM Chemicals)
                      / MicroRNAs (NLM Chemicals) / Proto-Oncogene Proteins c-akt
                      (NLM Chemicals) / Phosphatidylinositol 3-Kinases (NLM
                      Chemicals) / AGO2 protein, human (NLM Chemicals) / Glutamic
                      Acid (NLM Chemicals)},
      cin          = {AG Hermann},
      ddc          = {500},
      cid          = {I:(DE-2719)1511100},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39999211},
      doi          = {10.1126/scisignal.adl6745},
      url          = {https://pub.dzne.de/record/277315},
}