{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T08:08:47Z","timestamp":1790755727006,"version":"4.1.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2016,8,5]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Endothelial Notch signaling is critical for early vascular development and survival. Yet, previously described mice lacking endothelial a disintegrin and metalloproteinase 10 (ADAM10), a key regulator of Notch signaling, survived into adulthood with organ-specific vascular defects. These findings raised questions about whether these vascular defects were related to Notch signaling or other functions of ADAM10.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              The aims of the study are to determine whether compensatory or redundant functions of ADAM17 in Notch signaling can explain the survival of\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice, explore the contribution of different\n              <jats:italic>Tie2-Cre<\/jats:italic>\n              transgenes to the differences in survival, and establish whether the\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC vascular phenotypes can be recapitulated by inactivation of Notch receptors in endothelial cells.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Mice lacking ADAM10 and ADAM17 in endothelial cells (\n              <jats:italic>Adam10\/Adam17<\/jats:italic>\n              \u0394EC), which survived postnatally with organ-specific vascular defects, resembled\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice. In contrast,\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice generated with the\n              <jats:italic>Tie2Cre<\/jats:italic>\n              transgene previously used to inactivate endothelial Notch (\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC\n              <jats:sup>Flv<\/jats:sup>\n              ) died by E10.5. Quantitative polymerase chain reaction analysis demonstrated that Cre-mediated recombination occurs earlier in\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC\n              <jats:sup>Flv<\/jats:sup>\n              mice than in the previously described\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice. Finally, mice lacking endothelial Notch1 (\n              <jats:italic>Notch1<\/jats:italic>\n              \u0394EC) share some organ-specific vascular defects with\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice, whereas\n              <jats:italic>Notch4<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice lacking endothelial Notch1 (\n              <jats:italic>Notch1<\/jats:italic>\n              \u0394EC\n              <jats:italic>\/Notch4<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) had defects in all vascular beds affected in\n              <jats:italic>Adam10<\/jats:italic>\n              \u0394EC mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Our results argue against a major role for ADAM17 in endothelial Notch signaling and clarify the difference in phenotypes of previously described mice lacking ADAM10 or Notch in endothelial cells. Most notably, these findings uncover new roles for Notch signaling in the development of organ-specific vascular beds.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.115.307738","type":"journal-article","created":{"date-parts":[[2016,6,29]],"date-time":"2016-06-29T05:26:30Z","timestamp":1467177990000},"page":"519-531","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":52,"title":["ADAM10-Dependent Signaling Through Notch1 and Notch4 Controls Development of Organ-Specific Vascular Beds"],"prefix":"10.1161","volume":"119","author":[{"given":"Rolake O.","family":"Alabi","sequence":"first","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY (S.M.); Institute for Advanced Study, Technical University Munich, Munich, Germany (C.P.B.); and..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krzysztof","family":"Glomski","sequence":"additional","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY (S.M.); Institute for Advanced Study, Technical University Munich, Munich, Germany (C.P.B.); and..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Coline","family":"Haxaire","sequence":"additional","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY (S.M.); Institute for Advanced Study, Technical University Munich, Munich, Germany (C.P.B.); and..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gisela","family":"Weskamp","sequence":"additional","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY (S.M.); Institute for Advanced Study, Technical University Munich, Munich, Germany (C.P.B.); and..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00e9bastien","family":"Monette","sequence":"additional","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, Weill Cornell Medicine, Rockefeller University, New York, NY (S.M.); Institute for Advanced Study, Technical University Munich, Munich, Germany (C.P.B.); and..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carl P.","family":"Blobel","sequence":"additional","affiliation":[{"name":"From the Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY (R.O.A., K.G., C.H., G.W., C.P.B.); Weill Cornell\/Rockefeller\/Sloan-Kettering Tri-Institutional MD-PhD Program, New York, NY (R.O.A., K.G., C.P.B.); 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