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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1948.)
© 2001 American Heart Association, Inc.

Vascular Biology

Differential Cell Cycle Progression Patterns of Infiltrating Leukocytes and Resident Cells After Balloon Injury of the Rat Carotid Artery

Carl Hay; Connie Micko; Margaret Forney Prescott; Gene Liau; Keith Robinson; Hector De Leon

From Genetic Therapy, Inc (C.H., G.L., H.D.L.), Gaithersburg, Md; Atlanta Cardiovascular Research Institute (C.M., K.R., H.D.L.), Norcross, Ga; and Novartis Pharmaceuticals (M.F.P.), East Hanover, NJ.

Correspondence to Hector De Leon, MD, PhD, Atlanta Cardiovascular Research Institute, 3155 Northwoods Place, Norcross, GA 30071. E-mail hdeleon{at}acri.com

The heterogeneous nature of the cell populations involved in vascular repair remains a major hurdle for the assessment of the cellular events that take place in injured arteries. The present experiments were designed to estimate the proportions and cell cycle progression of infiltrating leukocytes versus resident vascular cells after balloon injury of the rat common carotid artery. After tissue disaggregation, cell suspension samples from each artery were analyzed by flow cytometry. Cells were stained with anti-CD45 or anti–-smooth muscle actin antibodies to identify leukocytes and smooth muscle cells, respectively. A day after injury, a 12-fold increase in CD45+ leukocytes was found. Double labeling with CD45 and CD-3, ED-1, or granulocyte markers revealed that most infiltrating cells were monocytes and granulocytes. Approximately 14% of infiltrating leukocytes were found to enter apoptosis at day 1, and 17% entered S phase at day 3. In contrast, the highest proliferation rate of resident -smooth muscle actin–positive cells was observed at day 7 (19%). The present results demonstrate that infiltrating leukocytes and resident vascular smooth muscle cells have dissimilar cell cycle profiles. Furthermore, our study demonstrates the feasibility of using flow cytometry to quantitatively determine the cell types and their relative activation state in injured arteries.

Key Words: restenosis • vascular remodeling • inflammation • flow cytometry • apoptosis

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