{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T01:31:21Z","timestamp":1780450281708,"version":"3.54.1"},"reference-count":42,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2017,9,19]],"date-time":"2017-09-19T00:00:00Z","timestamp":1505779200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:p>Stroke is a dramatic complication of sickle cell disease (SCD), which is associated with cerebral vasculopathies including moya moya, intravascular thrombi, cerebral hyperemia, and increased vessel tortuosity. The spontaneous occurrence of these pathologies in the sickle cell mouse model has not been described. Here, we studied Townes humanized sickle cell and age-matched control mice that were 13 months old. We used in\u00a0vivo two-photon microscopy to assess blood flow dynamics, vascular topology, and evidence of cerebral vasculopathy. Results showed that compared to controls, sickle cell mice had significantly higher red blood cell (RBC) velocity (0.73\u2009mm\/s vs. 0.55\u2009mm\/s, p\u2009=\u20090.013), capillary vessel diameter (4.84\u2009\u00b5M vs. 4.50\u2009\u00b5M, p\u2009=\u20090.014), and RBC volume flux (0.015 nL\/s vs. 0.010 nL\/s, p\u2009=\u20090.021). Also, sickle cell mice had significantly more tortuous capillary vessels ( p\u2009&lt;\u20090.0001) and significantly shorter capillary vessel branches ( p\u2009=\u20090.0065) compared to controls. Sickle cell mice also had significantly higher number of capillary occlusive events (3.4% vs. 1.9%, p\u2009&lt;\u20090.0001) and RBC stalls (3.8% vs. 2.1%, p\u2009&lt;\u20090.0001) in the cerebral capillary bed. In post-mortem immunohistochemical analyses, sickle cell mice had a 2.5-fold higher frequency of cortical microinfarcts compared to control mice. Our results suggest that aged Townes sickle cell mice spontaneously develop SCD-associated cerebral vasculopathy.<\/jats:p>","DOI":"10.1177\/0271678x17732275","type":"journal-article","created":{"date-parts":[[2017,9,19]],"date-time":"2017-09-19T10:05:15Z","timestamp":1505815515000},"page":"342-351","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":29,"title":["Higher prevalence of spontaneous cerebral vasculopathy and cerebral infarcts in a mouse model of sickle cell disease"],"prefix":"10.1177","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1991-7463","authenticated-orcid":false,"given":"Hyacinth I","family":"Hyacinth","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Aflac Cancer and Blood Disorder Center of Children\u2019s Healthcare of Atlanta and Emory University, Atlanta, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Courtney L","family":"Sugihara","sequence":"additional","affiliation":[{"name":"Neuroscience and Behavioral Biology Program, Emory University, Atlanta, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas L","family":"Spencer","sequence":"additional","affiliation":[{"name":"Department of Mechanical Engineering, Georgia Technical Institute, Atlanta, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David R","family":"Archer","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Aflac Cancer and Blood Disorder Center of Children\u2019s Healthcare of Atlanta and Emory University, Atlanta, GA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andy Y","family":"Shih","sequence":"additional","affiliation":[{"name":"Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA"},{"name":"Center for Biomedical Imaging, Medical University of South Carolina, Charleston, SC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,9,19]]},"reference":[{"key":"bibr1-0271678X17732275","doi-asserted-by":"publisher","DOI":"10.1126\/science.110.2865.543"},{"key":"bibr2-0271678X17732275","first-page":"628","volume-title":"Robins and cotran pathologic basis of disease","author":"Aster 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PM, Hartmann DA, Hui ES, et\u00a0al\n                      .\n                      Functional deficits induced by cortical microinfarcts.\n                      J Cereb Blood Flow Metab.\n                      Epub ahead of print 1 January 2017. 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