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@ARTICLE{He:182641,
      author       = {H. He and W. Yang and N. Su and C. Zhang and J. Dai and F.
                      Han and M. Singhal and W. Bai and X. Zhu and J. Zhu and Z.
                      Liu and W. Xia and X. Liu and C. Zhang and K. Jiang and W.
                      Huang and D. Chen and Z. Wang and X. He and F. Kirchhoff and
                      Z. Li and C. Liu and J. Huan and X. Wang and W. Wei and J.
                      Wang and H. Augustin$^*$ and J. Hu},
      title        = {{A}ctivating {NO}-s{GC} crosstalk in the mouse vascular
                      niche promotes vascular integrity and mitigates acute lung
                      injury.},
      journal      = {Journal of experimental medicine},
      volume       = {220},
      number       = {2},
      issn         = {0022-1007},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DKFZ-2022-02818},
      pages        = {e20211422},
      year         = {2023},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Disruption of endothelial cell (ECs) and pericytes
                      interactions results in vascular leakage in acute lung
                      injury (ALI). However, molecular signals mediating
                      EC-pericyte crosstalk have not been systemically
                      investigated, and whether targeting such crosstalk could be
                      adopted to combat ALI remains elusive. Using comparative
                      genome-wide EC-pericyte crosstalk analysis of healthy and
                      LPS-challenged lungs, we discovered that crosstalk between
                      endothelial nitric oxide and pericyte soluble guanylate
                      cyclase (NO-sGC) is impaired in ALI. Indeed, stimulating the
                      NO-sGC pathway promotes vascular integrity and reduces lung
                      edema and inflammation-induced lung injury, while
                      pericyte-specific sGC knockout abolishes this protective
                      effect. Mechanistically, sGC activation suppresses
                      cytoskeleton rearrangement in pericytes through inhibiting
                      VASP-dependent F-actin formation and MRTFA/SRF-dependent de
                      novo synthesis of genes associated with cytoskeleton
                      rearrangement, thereby leading to the stabilization of
                      EC-pericyte interactions. Collectively, our data demonstrate
                      that impaired NO-sGC crosstalk in the vascular niche results
                      in elevated vascular permeability, and pharmacological
                      activation of this crosstalk represents a promising
                      translational therapy for ALI.},
      keywords     = {Mice / Animals / Soluble Guanylyl Cyclase: genetics /
                      Soluble Guanylyl Cyclase: metabolism / Pericytes / Nitric
                      Oxide: metabolism / Lipopolysaccharides: pharmacology /
                      Acute Lung Injury: genetics / Acute Lung Injury: metabolism
                      / Soluble Guanylyl Cyclase (NLM Chemicals) / Nitric Oxide
                      (NLM Chemicals) / Lipopolysaccharides (NLM Chemicals)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36350314},
      doi          = {10.1084/jem.20211422},
      url          = {https://inrepo02.dkfz.de/record/182641},
}