Published online before print June 1, 2006, doi: 10.1161/01.RES.0000229657.83816.a7
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© 2006 American Heart Association, Inc.
Integrative Physiology |
Flow-Dependent Remodeling of Small Arteries in Mice Deficient for Tissue-Type Transglutaminase
Possible Compensation by Macrophage-Derived Factor XIII
From the Departments of Medical Physics (E.N.T.P.B., A.P., J.A.E.S., T.R., E.V.) and Medical Biochemistry (C.J.d.V.), Cardiovascular Research Institute Amsterdam, Academic Medical Center; Department of Molecular Cell Biology (N.v.R.), Faculty of Medicine, Vrije Universiteit, Amsterdam, the Netherlands; and Biochemistry Laboratory (E.C.), IDI-IRCCS, c/o Department of Experimental Medicine, University of Rome Tor Vergata, Italy.
Correspondence to Erik N. T. P. Bakker, Department of Medical Physics, Academic Medical Center and Cardiovascular Research Institute Amsterdam, PO Box 22700; 1100 DE Amsterdam, the Netherlands. E-mail n.t.bakker{at}amc.uva.nl
Chronic changes in blood flow induce an adaptation of vascular caliber. Thus, arteries show inward remodeling after a reduction in blood flow. We hypothesized that this remodeling depends on the crosslinking enzyme tissue-type transglutaminase (tTG). Flow-dependent remodeling was studied in wild-type (WT) and tTG-null mice using a surgically imposed change in blood flow in small mesenteric arteries. WT mice showed inward remodeling after 2 days of low blood flow, which was absent in arteries from tTG-null mice. Yet, after continued low blood flow for 7 days, inward remodeling was similar in arteries from WT and tTG-null mice. Studying the alternative pathways of remodeling, we identified a relatively high expression of the plasma transglutaminase factor XIII in arteries of WT and tTG-null mice. In addition, vessels from both WT and tTG-null mice showed the presence of transglutaminase-specific crosslinks. An accumulation of adventitial monocytes/macrophages was found in vessels exposed to low blood flow in tTG-null mice. Because monocytes/macrophages may represent a source of factor XIII, tTG-null mice were treated with liposome-encapsulated clodronate. Elimination of monocytes/macrophages with liposome-encapsulated clodronate reduced both the expression of factor XIII and inward remodeling in tTG-null mice. In conclusion, tTG plays an important role in the inward remodeling of small arteries associated with decreased blood flow. Adventitial monocytes/macrophages are a source of factor XIII in tTG-null mice and contribute to an alternative, delayed mechanism of inward remodeling when tTG is absent.
Key Words: vascular remodeling • transglutaminase • resistance arteries • macrophages • blood flow
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