Relationship of glycosaminoglycan and matrix changes to vascular smooth muscle cell phenotype modulation in rabbit arteries after acute injury  John A.

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Relationship of glycosaminoglycan and matrix changes to vascular smooth muscle cell phenotype modulation in rabbit arteries after acute injury  John A. Bingley, PhD, Ian P. Hayward, PhD, Gordon R. Campbell, PhD, Julie H. Campbell, PhD  Journal of Vascular Surgery  Volume 33, Issue 1, Pages 155-164 (January 2001) DOI: 10.1067/mva.2001.109774 Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 1 Normal rabbit carotid artery in cross section. a, Immunochemistry showing distribution of heparan sulphates. Primary antibody against heparan sulphates (10E4 Seikagaku Kyogo, Japan; requiring at least 1 N-sulphate residue as epitope18) visualized with Texas Red. b, Chondroitin sulphate distribution with primary antibody detecting CS-4 and CS-6 sulphates (CS56, Sigma) visualized with Texas Red. Arrows indicate internal elastic lamina. Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 2 Immunochemistry showing glycosaminoglycan distributions in rabbit carotid artery cross sections 4 days after injury. a, Heparan sulphates (antibody 10E4) visualized with Texas Red at 4 days. b, Chondroitin sulphates (antibody CS56) visualized with Texas Red at 4 days. Arrows indicate internal elastic lamina. Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 3 Immunochemistry showing glycosaminoglycan distributions in rabbit carotid artery cross sections 14 days after injury. a, Heparan sulphates (10E4) visualized with Texas Red at 14 days. b, Chondroitin sulphates (CS56) visualized with Texas Red at 14 days. Arrows indicate internal elastic lamina. Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 4 Electron photomicrographs showing smooth muscle cells (SMCs; ×1000) in rabbit carotid artery cross sections at various points after injury. a, At 2 days, SMCs have contracted away from elastic lamellae. b, At 4 days, SMCs appear smaller and dissociated from elastic lamellae. c, At 7 days, SMCs increased in size and were reassociating with elastic lamellae. e, Elastic lamellae; m, nonelastin matrix. Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 5 Histogram showing ultrastructural phenotype of rabbit carotid artery medial smooth muscle cells (SMCs) at various times after injury. Ultrastructural SMC phenotype was measured by means of point-counting morphometry to determine the cytoplasmic volume fraction of myofilaments (%Vvmyo), expressed as means (± SE). All points beyond 6 hours were significantly different from the control (P <.05). Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 6 Histogram showing the contribution of smooth muscle cells (SMCs) to overall medial cross-sectional area at various times after injury. The percentage areas were measured by means of point-counting morphometry and expressed as means (± SE). *Control significantly greater than all injured artery time points (P <.05). Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 7 Histogram showing the contribution of elastic lamellae, including internal elastic lamina, to overall medial cross-sectional area at various times after injury. The percentage areas were measured by means of point-counting morphometry and expressed as means (± SE). *Significantly different from the control (P <.05). Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 8 Histogram showing the contribution of extracellular matrix (excluding elastic components) to overall medial cross-sectional area at various times after injury. The percentage areas were measured by means of point-counting morphometry and expressed as means (± SE). *Control significantly less than all injured artery time points (P <.05). Journal of Vascular Surgery 2001 33, 155-164DOI: (10.1067/mva.2001.109774) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions