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@ARTICLE{Chen:293803,
      author       = {J. Chen and E. E. Crouch and M. E. Zawadzki and K. A.
                      Jacobs and L. N. Mayo and J. J. Choi and P.-Y. Lin and S.
                      Shaikh and J. Tsui and S. Gonzalez-Granero and S. Waller and
                      A. Kelekar and G. Kang and E. J. Valenzuela and J. O.
                      Birrueta and L. N. Diafos and K. Wedderburn-Pugh and B. Di
                      Marco$^*$ and W. Xia and C. Z. Han and N. G. Coufal and C.
                      K. Glass and S. P. J. Fancy and J. Alfonso$^*$ and A. R.
                      Kriegstein and M. C. Oldham and J. M. Garcia-Verdugo and M.
                      L. Kutys and M. K. Lehtinen and A. J. Combes and E. J.
                      Huang},
      title        = {{P}roinflammatory immune cells disrupt angiogenesis and
                      promote germinal matrix hemorrhage in prenatal human brain.},
      journal      = {Nature neuroscience},
      volume       = {27},
      number       = {11},
      issn         = {1097-6256},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DKFZ-2024-01961},
      pages        = {2115-2129},
      year         = {2024},
      note         = {2024 Nov;27(11):2115-2129},
      abstract     = {Germinal matrix hemorrhage (GMH) is a devastating
                      neurodevelopmental condition affecting preterm infants, but
                      why blood vessels in this brain region are vulnerable to
                      rupture remains unknown. Here we show that microglia in
                      prenatal mouse and human brain interact with nascent
                      vasculature in an age-dependent manner and that ablation of
                      these cells in mice reduces angiogenesis in the ganglionic
                      eminences, which correspond to the human germinal matrix.
                      Consistent with these findings, single-cell transcriptomics
                      and flow cytometry show that distinct subsets of CD45+ cells
                      from control preterm infants employ diverse signaling
                      mechanisms to promote vascular network formation. In
                      contrast, CD45+ cells from infants with GMH harbor activated
                      neutrophils and monocytes that produce proinflammatory
                      factors, including azurocidin 1, elastase and CXCL16, to
                      disrupt vascular integrity and cause hemorrhage in
                      ganglionic eminences. These results underscore the brain's
                      innate immune cells in region-specific angiogenesis and how
                      aberrant activation of these immune cells promotes GMH in
                      preterm infants.},
      cin          = {A230},
      ddc          = {610},
      cid          = {I:(DE-He78)A230-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39349662},
      doi          = {10.1038/s41593-024-01769-2},
      url          = {https://inrepo02.dkfz.de/record/293803},
}