Fibrin Gel Induces the Migration of Smooth Muscle Cells from Rabbit Aortic Explants

1999 ◽  
Vol 82 (10) ◽  
pp. 1347-1352 ◽  
Author(s):  
Hideki Nomura ◽  
Akihisa Iguchi ◽  
W. Douglas Thompson ◽  
Elspeth Smith ◽  
Michitaka Naito
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Thrombin Inhibitors ◽  
Positive Staining ◽  
Αvβ3 Integrin ◽  
Major Step ◽  
Fibrin Gel ◽  
Vitro Assay ◽  
Fibrin Gels

SummaryA major step in the pathogenesis of atherosclerosis is the vectorial migration of smooth muscle cells (SMCs) from the arterial media into the intima. Although subcultured SMCs usually show synthetic phenotype, the behaviour of contractile SMCs may be crucial for the subsequent migration of the cells. In the present study, we utilized an in vitro assay system to evaluate the effects of fibrin gels on the migration of SMCs from explants taken from rabbit aorta. After cultured for 5-7 days in a serum-free condition, SMCs appeared from explants covered with fibrin gel. The cells were positive on immunostaining for SMC specific α-actin. No migration of SMCs from the control explants without fibrin gel was observed. Then the percentage of explants showing cell migration and the number of migrating cells increased with time. The migration of SMCs into fibrin gels was not dependent on the concentration of fibrinogen used for the preparation of fibrin gel in the range of 1.5-3 mg/ml. Variations of thrombin concentration in the range of 0.25-1.25 U/ml had no significant effect. However, there was less migration of SMCs with higher concentrations of thrombin. Thrombin inhibitors, hirudin and PPACK had no significant effect on the migration of SMCs. An RGD-containing peptide, GRGDS inhibited the migration of SMCs although a control peptide GRGES at the same concentration had no significant effect. A monoclonal antibody to αvβ3, LM609, completely inhibited the migration of SMCs from the explants, suggesting that αvβ3 integrin is involved in the migration of SMCs into fibrin gels. SMCs which migrated from the explants showed the positive staining with the monoclonal antibodies against SMC myosin heavy chain isoforms, SMemb, SM1 and SM2, suggesting that they are in an intermediate state changing from contractile to synthetic state. In conclusion, the present study showed that fibrin gel induces the migration of SMCs from explants into itself and the process may not need other growth factors or cytokines.

Effect of Crosslinking by Factor XIIIa on the Migration of Vascular Smooth Muscle Cells into Fibrin Gels

1998 ◽  
Vol 90 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Michitaka Naito ◽  
Hideki Nomura ◽  
Akihisa Iguchi ◽  
W.Douglas Thompson ◽  
Elspeth B Smith
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Factor Xiiia ◽  
Fibrin Gels

scholarly journals Human iPSC-Derived Vascular Smooth Muscle Cells in a Fibronectin Functionalized Collagen Hydrogel Augment Endothelial Cell Morphogenesis

2021 ◽  
Vol 8 (12) ◽  
pp. 223
Author(s):  
Kaiti Duan ◽  
Biraja C. Dash ◽  
Daniel C. Sasson ◽  
Sara Islam ◽  
Jackson Parker ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanistic Study ◽  
Αvβ3 Integrin ◽  
Factor Secretion ◽  
Growth Factor Secretion

Tissue-engineered constructs have immense potential as autologous grafts for wound healing. Despite the rapid advancement in fabrication technology, the major limitation is controlling angiogenesis within these constructs to form a vascular network. Here, we aimed to develop a 3D hydrogel that can regulate angiogenesis. We tested the effect of fibronectin and vascular smooth muscle cells derived from human induced pluripotent stem cells (hiPSC-VSMC) on the morphogenesis of endothelial cells. The results demonstrate that fibronectin increases the number of EC networks. However, hiPSC-VSMC in the hydrogel further substantiated the number and size of EC networks by vascular endothelial growth factor and basic fibroblast growth factor secretion. A mechanistic study shows that blocking αvβ3 integrin signaling between hiPSC-VSMC and fibronectin impacts the EC network formation via reduced cell viability and proangiogenic growth factor secretion. Collectively, this study set forth initial design criteria in developing an improved pre-vascularized construct.

Human Umbilical Vein Smooth Muscle Cells as a Model to Study Thrombin Generation and Function: Effect of Thrombin Inhibitors

1996 ◽  
Vol 76 (04) ◽  
pp. 603-609 ◽  
Author(s):  
Rose-Marie Catalioto ◽  
Paola Cucchi ◽  
Anna Rita Renzetti ◽  
Marco Criscuoli ◽  
Alessandro Subissi
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Human Plasma ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Thrombin Inhibitors ◽  
Coagulation Cascade ◽  
Thrombin Inhibitor ◽  
Fibrinopeptide A ◽  
Human Umbilical Vein

SummaryThe aim of the present work was to study how human umbilical vein smooth muscle cells (HUVSMC) can initiate the coagulation process and to investigate the responses of these cells to thrombin. Exposure of HUVSMC to recalcified human plasma led to a time-dependent production of thrombin, measured both as amidolytic activity and as release of fibrinopeptide A. Thrombin activity was dose-dependently reduced by an anti-human tissue factor antibody (76 ± 3% at 10 Μg/ml) and by inhibitors like heparin, rec-hirudin, hirulog-1, Napap and hiru-norm, a novel hirudin-like thrombin inhibitor (IC50 = 2 ± 0.4, 8 ± 1, 130 ± 22, 199 ± 29 and 68 ± 8nM, respectively). The release of fibrinopeptide A was similarly prevented (IC50 = 14 ± 1,132 ± 25 and 50 ± 8 nM for rec-hirudin, Napap and hirunorm, respectively). Exogenously added thrombin increased thymidine incorporation into HUVSMC to 240 ± 30% of basal (EC50 = 0.49 ± 0.09 nM) and thrombin inhibitors blocked this effect (IC50 = 10 ± 3, 37 ± 17, 343 ± 165 and 1402 ± 758 nM for rec-hirudin, hirunorm, Napap and hirulog-1, respectively). Also recalcified human plasma was mitogenic for HUVSMC and its effect was mainly due to endogenously generated thrombin, as shown by the use of thrombin inhibitors. In conclusion, HUVSMC are capable of initiating the extrinsic coagulation cascade, leading to the formation of thrombin which promotes clotting and stimulates DNA synthesis. Thrombin inhibitors prevent both coagula-tive and cellular effects of thrombin.

Decorin synthesized by arterial smooth muscle cells is retained in fibrin gels and modulates fibrin contraction

2007 ◽  
Vol 101 (2) ◽  
pp. 281-294 ◽  
Author(s):  
Pamela Y. Johnson ◽  
Susan Potter-Perigo ◽  
Michel D. Gooden ◽  
Robert B. Vernon ◽  
Thomas N. Wight
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Fibrin Gels ◽  
Arterial Smooth Muscle Cells

Role of D and E domains in the migration of vascular smooth muscle cells into fibrin gels

Life Sciences ◽  
2002 ◽  
Vol 71 (10) ◽  
pp. 1139-1148 ◽  
Author(s):  
Michiteru Kodama ◽  
Michitaka Naito ◽  
Hideki Nomura ◽  
Akihisa Iguchi ◽  
W.Douglas Thompson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Fibrin Gels

scholarly journals Insulin-Like Growth Factor-I Signaling in Smooth Muscle Cells Is Regulated by Ligand Binding to the 177CYDMKTTC184 Sequence of the β3-Subunit of αVβ3

2006 ◽  
Vol 20 (2) ◽  
pp. 405-413 ◽  
Author(s):  
Laura A. Maile ◽  
Walker H. Busby ◽  
Kevin Sitko ◽  
Byron E. Capps ◽  
Tiffany Sergent ◽  
...  
Keyword(s):  
Amino Acids ◽  
Smooth Muscle ◽  
Ligand Binding ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Αvβ3 Integrin ◽  
Ligand Specificity ◽  
Igf I ◽  
Important Regulator ◽  
Critical Residues

Abstract The response of smooth muscle cells to IGF-I requires ligand occupancy of the αVβ3 integrin. We have shown that vitronectin (Vn) is required for IGF-I-stimulated migration or proliferation, whereas the anti-αVβ3 monoclonal antibody, LM609, which inhibits ligand binding, blocks responsiveness of these cells to IGF-I. The amino acids 177–184 (177CYDMKTTC184) within the extracellular domain of β3 have been proposed to confer the ligand specificity of αVβ3; therefore, we hypothesized that ligand binding to the 177–184 cysteine loop of β3 may be an important regulator of the cross talk between αVβ3 and IGF-I in SMCs. Here we demonstrate that blocking ligand binding to a specific amino acid sequence within the β3 subunit of αVβ3 (i.e. amino acids 177–184) blocked Vn binding to the β3 subunit of αVβ3 and correspondingly β3 phosphorylation was decreased. In the presence of this antibody, IGF-I-stimulated Shc phosphorylation and ERK 1/2 activation were impaired, and this was associated with an inhibition in the ability of IGF-I to stimulate an increase in migration or proliferation. Furthermore, in cells expressing a mutated form of β3 in which three critical residues within the 177–184 sequence were altered β3 phosphorylation was decreased. This was associated with a loss of IGF-I-stimulated Shc phosphorylation and impaired smooth muscle cell proliferation in response to IGF-I. In conclusion, we have demonstrated that the 177–184 sequence of β3 is necessary for Vn binding to αVβ3 and that ligand occupancy of this site is necessary for an optimal response of smooth muscle cells to IGF-I.

scholarly journals iPSC-derived Vascular Smooth Muscle Cells in a Fibronectin Functionalized Collagen Scaffold Augment Endothelial Cell Morphogenesis

2021 ◽  
Author(s):  
Kaiti Duan ◽  
Biraja C. Dash ◽  
Daneil Sasson ◽  
Henry Hsia
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Network Formation ◽  
Collagen Scaffold ◽  
Muscle Cells ◽  
Mechanistic Study ◽  
Αvβ3 Integrin ◽  
3D Scaffold

Tissue-engineered constructs have immense potential as autologous grafts for wound healing. Despite the rapid advancement in fabrication technology, the major limitation is controlling angiogenesis within these constructs to form a vascular network. Here, we aimed to develop a 3D scaffold that can regulate angiogenesis. We tested the effect of fibronectin and vascular smooth muscle cells derived from human induced pluripotent stem cells (hiPSC-VSMC) on the morphogenesis of endothelial cells. The results demonstrate that fibronectin increases the number of endothelial networks. However, hiPSC-VSMC in the presence of fibronectin further substantiated the number and size of endothelial networks. A mechanistic study shows that blocking αvβ3 integrin signaling between hiPSC-VSMC and fibronectin impacts the endothelial network formation. Collectively, this study set forth initial design criteria in developing an improved pre-vascularized construct.

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