{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shaligram SS"],"funding":["National Institute of Neurological Disorders and Stroke","Michael Ryan Zodda Foundation","American Heart Association-American Stroke Association","Fondation Leducq","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","U.S. Department of Defense","NINDS NIH HHS","Barrow Neurological Foundation","American Health Assistance Foundation"],"pagination":["494-504"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9021325"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(3)"],"pubmed_abstract":["We have previously demonstrated that deletion of activin receptor-like kinase 1 (Alk1) or endoglin in a fraction of endothelial cells (ECs) induces brain arteriovenous malformations (bAVMs) in adult mice upon angiogenic stimulation. Here, we addressed three related questions: (1) could Alk1<sup>-</sup> mutant bone marrow (BM)-derived ECs (BMDECs) cause bAVMs? (2) is Alk1<sup>-</sup> ECs clonally expended during bAVM development? and (3) is the number of mutant ECs correlates to bAVM severity? For the first question, we transplanted BM from PdgfbiCreER;Alk1<sup>2f/2f</sup> mice (EC-specific tamoxifen-inducible Cre with Alk1-floxed alleles) into wild-type mice, and then induced bAVMs by intra-brain injection of an adeno-associated viral vector expressing vascular endothelial growth factor an"],"journal":["Translational stroke research"],"pubmed_title":["Bone Marrow-Derived Alk1 Mutant Endothelial Cells and Clonally Expanded Somatic Alk1 Mutant Endothelial Cells Contribute to the Development of Brain Arteriovenous Malformations in Mice."],"pmcid":["PMC9021325"],"funding_grant_id":["ATTRACT","HL122774","20POST35120371","PR161205","NS027713","NS112819","R01 HL122774","R01 NS112819","R01 NS027713"],"pubmed_authors":["Shaligram SS","do Prado L","Ma L","Arnold T","Tang C","Li Q","Zhang R","Oh SP","Su H","Santander N","Luo M","Pan F","Pan P","Zhu W","Weiss M","Liang R"],"additional_accession":[]},"is_claimable":false,"name":"Bone Marrow-Derived Alk1 Mutant Endothelial Cells and Clonally Expanded Somatic Alk1 Mutant Endothelial Cells Contribute to the Development of Brain Arteriovenous Malformations in Mice.","description":"We have previously demonstrated that deletion of activin receptor-like kinase 1 (Alk1) or endoglin in a fraction of endothelial cells (ECs) induces brain arteriovenous malformations (bAVMs) in adult mice upon angiogenic stimulation. Here, we addressed three related questions: (1) could Alk1<sup>-</sup> mutant bone marrow (BM)-derived ECs (BMDECs) cause bAVMs? (2) is Alk1<sup>-</sup> ECs clonally expended during bAVM development? and (3) is the number of mutant ECs correlates to bAVM severity? For the first question, we transplanted BM from PdgfbiCreER;Alk1<sup>2f/2f</sup> mice (EC-specific tamoxifen-inducible Cre with Alk1-floxed alleles) into wild-type mice, and then induced bAVMs by intra-brain injection of an adeno-associated viral vector expressing vascular endothelial growth factor an","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-26T23:03:07.168Z","creation":"2025-04-06T17:24:33.159Z"},"accession":"S-EPMC9021325","cross_references":{"pubmed":["34674144"],"doi":["10.1007/s12975-021-00955-9"]}}