title: Inducing myointimal hyperplasia versus atherosclerosis in mice: an introduction of two valid models.
abstract: Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque formation and stenosis, as observed for example in ischemic heart disease. Two highly reproducible mouse models - both resulting in artery stenosis but each underlying a different pathway of development - are introduced here. The models represent the two most common causes of artery stenosis; namely one mouse model for each myointimal hyperplasia, and atherosclerosis are shown. To induce myointimal hyperplasia, a balloon catheter injury of the abdominal aorta is performed. For the development of atherosclerotic plaque, the ApoE -/- mouse model in combination with western fatty diet is used. Different model-adapted options for the measurement and evaluation of the results are named and described in this manuscript. The introduction and comparison of these two models provides information for scientists to choose the appropriate artery stenosis model in accordance to the scientific question asked.
authors.affiliation: Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg.
authors.forename: Mandy
authors.initials: M
authors.lastname: Stubbendorff
authors.affiliation: Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg.
authors.forename: Xiaoqin
authors.initials: X
authors.lastname: Hua
authors.affiliation: Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg; Department of Cardiovascular Surgery, University Heart Center Hamburg.
authors.forename: Tobias
authors.initials: T
authors.lastname: Deuse
authors.affiliation: Center for Interventional Vascular Therapy, Division of Cardiology, Columbia University; Cardiovascular Research Foundation, New York.
authors.forename: Ziad
authors.initials: Z
authors.lastname: Ali
authors.affiliation: Cardiovascular Research Center (CVRC) and DZHK University Hamburg; Department of Cardiovascular Surgery, University Heart Center Hamburg.
authors.forename: Hermann
authors.initials: H
authors.lastname: Reichenspurner
authors.affiliation: Karolinska Institute, Stockholm.
authors.forename: Lars
authors.initials: L
authors.lastname: Maegdefessel
authors.affiliation: Department of Cardiothoracic Surgery, Stanford University School of Medicine, Falk Cardiovascular Research Center.
authors.forename: Robert C
authors.initials: RC
authors.lastname: Robbins
authors.affiliation: Transplant and Stem Cell Immunobiology Lab, Cardiovascular Research Center, University Hospital Hamburg; Cardiovascular Research Center (CVRC) and DZHK University Hamburg; Department of Cardiovascular Surgery, University Heart Center Hamburg; Center for Interventional Vascular Therapy, Division of Cardiology, Columbia University; schrepfer@stanford.edu.
authors.forename: Sonja
authors.initials: S
authors.lastname: Schrepfer
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency; D050197:Atherosclerosis / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D006965:Hyperplasia / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D058226:Plaque, Atherosclerotic / Q000473:pathology; D015203:Reproducibility of Results; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D001057:Apolipoproteins E