title: Mebendazole reduces vascular smooth muscle cell proliferation and neointimal formation following vascular injury in mice.
abstract: Mebendazole is an antihelminthic drug that exerts its effects via interference with microtubule function in parasites. To determine the utility of mebendazole as a potential treatment for vascular diseases involving proliferation of vascular smooth muscle cells, the effects of mebendazole on vascular smooth muscle cell proliferation were tested in vitro and in a mouse model of arterial injury. In vitro, mebendazole inhibited proliferation and migration of murine vascular smooth muscle cells and this was associated with altered intracellular microtubule organization. To determine in vivo effects of mebendazole following vascular injury, femoral arterial wire injury was induced in wild-type mice treated with either mebendazole or placebo control. Compared with placebo-treated mice, mebendazole-treated mice formed less neointima at the site of injury. Mebendazole is effective at inhibiting vascular smooth muscle cell proliferation and migration, and neointimal formation following arterial injury in mice.
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Jintao
authors.initials: J
authors.lastname: Wang
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Chiao
authors.initials: C
authors.lastname: Guo
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Wei
authors.initials: W
authors.lastname: Luo
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Alyssa
authors.initials: A
authors.lastname: Lawler
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Aswin
authors.initials: A
authors.lastname: Reddy
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Julia
authors.initials: J
authors.lastname: Wang
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Eddy B
authors.initials: EB
authors.lastname: Sun
authors.affiliation: University of Michigan, Department of Internal Medicine, Cardiovascular Research Center, Ann Arbor, Michigan, United States of America.
authors.forename: Daniel T
authors.initials: DT
authors.lastname: Eitzman
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D004195:Disease Models, Animal; D006965:Hyperplasia; D008297:Male; D008463:Mebendazole / Q000008:administration & dosage / Q000494:pharmacology*; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D032389:Myocytes, Smooth Muscle / Q000187:drug effects*; D058426:Neointima / Q000188:drug therapy* / Q000473:pathology; D057772:Vascular System Injuries / Q000188:drug therapy* / Q000473:pathology
chemical_list: D008463:Mebendazole