Flow-dependent remodeling in the carotid artery of fibroblast growth factor-2 knockout mice.

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Abstract
Objective — Fibroblast growth factor-2 (FGF2) has been implicated as a mediator in the structural remodeling of arteries. Chronic changes in blood flow are known to cause reorganization of the vessel wall, resulting in permanent changes in artery size (flow-dependent remodeling). Using FGF2 knockout ( Fgf2 −/− ) mice, we tested the hypothesis that FGF2 is required during flow-dependent remodeling of the carotid arteries. Methods and Results — All branches originating from the left common carotid artery (LCCA), except for the left thyroid artery, were ligated to reduce flow in the LCCA and increase flow in the contralateral right common carotid artery (RCCA). Age- and sex-matched control animals did not undergo ligation of the LCCA branches. Morphometric analysis showed that by day 7, vessel diameter was significantly greater in the high-flow RCCA of FGF2 wild-type ( Fgf2 +/+ ) and Fgf2 −/− mice versus the respective control RCCA, demonstrating outward remodeling. In contrast, vessel diameter was decreased by day 7 in the low-flow LCCA of both genotypes compared with the control LCCA, showing inward remodeling. No differences were observed between Fgf2 +/+ and Fgf2 −/− mice in either high-flow or low-flow remodeling. Conclusions — Given these results, we demonstrate that FGF2 is not essential for flow-dependent remodeling of the carotid arteries.