{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yan L"],"funding":["NCATS NIH HHS","Howard Hughes Medical Institute","NHLBI NIH HHS"],"pagination":["1399-411"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4108264"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34(7)"],"pubmed_abstract":["Objective
S100A12 and fibroblast growth factor 23 are biomarkers of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). We tested the hypothesis that human S100/calgranulin would accelerate cardiovascular disease in mice subjected to CKD.Approach and results
A bacterial artificial chromosome of the human S100/calgranulin gene cluster containing the genes and regulatory elements for S100A8, S100A9, and S100A12 was expressed in C57BL/6J mouse (hBAC-S100) to generate a novel humanized mouse model. CKD was induced by ureteral ligation, and hBAC-S100 mice and wild-type mice were studied after 10 weeks of chronic uremia. hBAC-S100 mice with CKD showed increased fibroblast growth factor 23 in the hearts, left ventricular hypertrophy, diastolic dys"],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["S100/Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products-dependent manner."],"pmcid":["PMC4108264"],"funding_grant_id":["1R01HL4821","UL1 TR000430","R01 HL114821"],"pubmed_authors":["Yan L","Earley J","Puri TS","Hofmann Bowman MA","Mathew L","Gardner B","Chellan B"],"additional_accession":[]},"is_claimable":false,"name":"S100/Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products-dependent manner.","description":"Objective
S100A12 and fibroblast growth factor 23 are biomarkers of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). We tested the hypothesis that human S100/calgranulin would accelerate cardiovascular disease in mice subjected to CKD.Approach and results
A bacterial artificial chromosome of the human S100/calgranulin gene cluster containing the genes and regulatory elements for S100A8, S100A9, and S100A12 was expressed in C57BL/6J mouse (hBAC-S100) to generate a novel humanized mouse model. CKD was induced by ureteral ligation, and hBAC-S100 mice and wild-type mice were studied after 10 weeks of chronic uremia. hBAC-S100 mice with CKD showed increased fibroblast growth factor 23 in the hearts, left ventricular hypertrophy, diastolic dys","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jul","modification":"2025-04-19T04:55:59.033Z","creation":"2019-03-27T01:32:38Z"},"accession":"S-EPMC4108264","cross_references":{"pubmed":["24855059"],"doi":["10.1161/ATVBAHA.114.303508","10.1161/atvbaha.114.303508"]}}