TY - JOUR
T1 - Smooth muscle cell proliferation in response to co-culture with venous and arterial endothelial cells
AU - Waybill, Peter N.
AU - Chinchilli, Vernon M.
AU - Ballermann, Barbara J.
N1 - Funding Information:
Abbreviations: BBE = bovine brain extract, EC = endothelial cell, EC-GM = endothelial cell growth medium, FBS = fetal bovine serum, HA-EC = humzn aortic endothelial cell, HA-SMC = human aortic smooth muscle cell, hEGF = human recombinant epidermal growth factor, HSV-EC = human saphenous vein endothelial cell, MDCK = Mandin Darby canine kidney, OPT-GM = optimal growth medium, SMC = smooth muscle cell, SMC-GM = smooth muscle cell growth medium, TCA = trichloroacetic acid From the Department of Cardiovascular and Interventional Radiology, Room HG 300 K (P.N.W.) and Center for Biostatistics and Epidemiology (V.M.C.), Pennsylvania State University Hospital, Hershey, PA 17033, and the Division of Nephrology, Department of Medicine (B.J.B.), The Johns Hopkins University School of Medicine, Baltimore, Md. From the 1996 SCVIR annual meeting. Received March 9, 1996; revision requested April 5; revision received December 5, accepted December 7. This work was supported in part by a grant from the William Mayo Gatewood Fellowship Fund; and by the Division of Cardiovascular and Interventional Radiology of the Russell Morgan Department of Radiology and Radiological Sciences, The Johns Hopkins University Hospital. B.J.B. is an Established Investigator of the American Heart Association. Address correspondence to P.N.W.
PY - 1997
Y1 - 1997
N2 - PURPOSE: The critical role of endothelial cells (ECs) in arterial disease is well established, but little is known of their role in venous disease. Previous studies suggest inherent differences between arteries and veins: arterial stenoses demonstrate a large lipid component, whereas hemodialysis-related venous stenoses are characterized by marked smooth muscle cell (SMC) proliferation. This study compares effects of venous versus arterial ECs on SMC proliferation in co-culture. MATERIALS AND METHODS: Human saphenous vein ECs (HSV-ECs) or human aortic ECs (HA-ECs) were cultured on the under-side of 10-μn, porous polycarbonate membranes and allowed to grow to confluence for 48 hours. After EC confluence, human aortic SMCs (HA-SMCs) were cultured on the membranes opposite the EC (day 0). On days 0, 1, 2, 4, 6, and 8, membranes were harvested (n = 3 per day), stained with Hoechst dye, and HA-SMCs were counted by fluorescence microscopy. Controls were HA-SMCs cultured alone. Comparisons were made by two-way multivariate analysis of variance. RESULTS: During the entire 8-day period, there was significant induction of HA-SMC proliferation by both HSV-ECs (P = .0003) and HA-ECs (P = .0012). Maximal inductions were 88% ± 11% for HSV-ECs (P = .0015) and 24% ± 6% for HA-ECs (P = .0015). HSV-ECs exhibited a three- to ninefold greater induction than HA-ECs (P = .0003). CONCLUSION: HSV-ECs induce adjacent HA- SMC proliferation, possibly in a paracrine manner to a significantly greater extent than HA-ECs.
AB - PURPOSE: The critical role of endothelial cells (ECs) in arterial disease is well established, but little is known of their role in venous disease. Previous studies suggest inherent differences between arteries and veins: arterial stenoses demonstrate a large lipid component, whereas hemodialysis-related venous stenoses are characterized by marked smooth muscle cell (SMC) proliferation. This study compares effects of venous versus arterial ECs on SMC proliferation in co-culture. MATERIALS AND METHODS: Human saphenous vein ECs (HSV-ECs) or human aortic ECs (HA-ECs) were cultured on the under-side of 10-μn, porous polycarbonate membranes and allowed to grow to confluence for 48 hours. After EC confluence, human aortic SMCs (HA-SMCs) were cultured on the membranes opposite the EC (day 0). On days 0, 1, 2, 4, 6, and 8, membranes were harvested (n = 3 per day), stained with Hoechst dye, and HA-SMCs were counted by fluorescence microscopy. Controls were HA-SMCs cultured alone. Comparisons were made by two-way multivariate analysis of variance. RESULTS: During the entire 8-day period, there was significant induction of HA-SMC proliferation by both HSV-ECs (P = .0003) and HA-ECs (P = .0012). Maximal inductions were 88% ± 11% for HSV-ECs (P = .0015) and 24% ± 6% for HA-ECs (P = .0015). HSV-ECs exhibited a three- to ninefold greater induction than HA-ECs (P = .0003). CONCLUSION: HSV-ECs induce adjacent HA- SMC proliferation, possibly in a paracrine manner to a significantly greater extent than HA-ECs.
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U2 - 10.1016/S1051-0443(97)70575-X
DO - 10.1016/S1051-0443(97)70575-X
M3 - Article
C2 - 9152910
AN - SCOPUS:0030730479
SN - 1051-0443
VL - 8
SP - 375
EP - 381
JO - Journal of Vascular and Interventional Radiology
JF - Journal of Vascular and Interventional Radiology
IS - 3
ER -
