title: Direct or indirect endothelial cell transforming growth factor-β receptor activation initiates arteriolar hyalinosis.
abstract: Tacrolimus (FK-506) controls organ rejection; however, arteriolar hyalinosis is a frequent complication. By use of mice lacking FK-506-binding protein-12 in endothelial cells, Chiasson and co-workers explored the contribution of endothelial cells and the transforming growth factor-β pathway to define mechanisms of hyalinosis. Absence of this binding protein removed a tonic inhibition to activate the transforming growth factor-β system, causing arteriolar hyalinosis. However, tacrolimus can have effects on any biologic process involving receptors with a GS domain.
authors.affiliation: Division of Clinical and Translational Research, Department of Anesthesiology, School of Medicine, Washington University in St Louis, St Louis, Missouri 63110, USA. morrisse@wustl.edu
authors.forename: Jeremiah J
authors.initials: JJ
authors.lastname: Morrissey
mesh_terms: D000818:Animals; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects*; D008297:Male; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism*; D016559:Tacrolimus / Q000633:toxicity*
chemical_list: D018125:Receptors, Transforming Growth Factor beta; D016559:Tacrolimus