{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T15:25:07Z","timestamp":1787757907352,"version":"build-2784847793"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Pericytes play essential roles in blood-brain barrier regulation and stroke pathogenesis. Given that pericytes are embedded in the ECM (extracellular matrix), it is speculated that ECM-receptor interactions are involved in these functions. Integrin-\u03b21, the most common integrin subunit that can engage multiple ECM proteins, is highly expressed in pericytes. The function of pericytic integrin \u03b21, however, remains unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      To address this question, we generated brain pericyte-specific integrin-\u03b21 knockout mice by crossing the\n                      <jats:italic toggle=\"yes\">Atp13a5 (ATPase type 13A5)-CreER<\/jats:italic>\n                      with the\n                      <jats:italic toggle=\"yes\">Itgb1<\/jats:italic>\n                      floxed mice and characterized their phenotypes under homeostatic conditions and after intracerebral hemorrhage.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>Under homeostatic conditions, pericyte-specific integrin-\u03b21 knockout mice were grossly normal and failed to show blood-brain barrier disruption or pericyte\/astrocyte defects. In the collagenase-induced intracerebral hemorrhage model, however, the pericyte-specific integrin-\u03b21 knockout mice exhibited larger hematoma volume, enhanced brain edema, aggravated blood-brain barrier damage caused by both paracellular and transcellular mechanisms, reduced pericyte number\/coverage and aquaporin-4 coverage, increased neuronal death, elevated gliosis, and worsened neurological outcomes. Interestingly, hypertensive pericyte-specific integrin-\u03b21 knockout mice demonstrated similar changes in the autologous blood model of intracerebral hemorrhage.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>These results suggest that brain pericyte-derived integrin-\u03b21 is dispensable under homeostatic conditions but plays a protective role in intracerebral hemorrhage, likely through repairing blood-brain barrier damage and regulating gliosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/strokeaha.126.055631","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T09:00:14Z","timestamp":1783501214000},"page":"2839-2852","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Loss of Pericytic Integrin-\u03b21 Exacerbates Blood-Brain Barrier Damage and 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