Published online before print June 1, 2006, doi: 10.1161/01.RES.0000229657.83816.a7
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Submitted on August 26, 2005
Revised on May 12, 2006
Accepted on May 19, 2006
Flow-Dependent Remodeling of Small Arteries in Mice Deficient for Tissue-Type Transglutaminase. Possible Compensation by Macrophage-Derived Factor XIII
Erik N.T.P. Bakker *;
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.
* To whom correspondence should be addressed. 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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