Human arterial smooth muscle cells in culture

Fager, Gunnar; Hansson, Göran K.; Ottosson, Pia; Dahllöf, Björn; Bondjers, Göran

doi:10.1016/0014-4827(88)90334-5

Cited by 66 publications

(13 citation statements)

References 33 publications

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“…Preparation of HS from Smooth Muscle Cells-Human arterial smooth muscle cells (hASMC) derived from the inner media of uterine arteries were prepared and maintained as described previously (34). Cells were labeled metabolically with 100 Ci/ml of 35 SO 4 (DuPont NEN) in sulfate-free medium.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Heparin and Heparan Sulfate Domains Binding to the Long Splice Variant of Platelet-derived Growth Factor A Chain

Feyzi

Lustig

Fager

et al. 1997

Journal of Biological Chemistry

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128

100

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Section: Methodsmentioning

confidence: 99%

Characterization of Heparin and Heparan Sulfate Domains Binding to the Long Splice Variant of Platelet-derived Growth Factor A Chain

Feyzi

Lustig

Fager

et al. 1997

Journal of Biological Chemistry

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128

100

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“…Dose responses have been elucidated in cell culture preparations, wherein a well described and controlled pharmacologic environment exists (1)(2)(3)(4)(5)(6). These data are invaluable but reflect an essentially static situation, in the absence of drug consumption or degradation, without the complex pharmacokinetics or concentration gradients across target tissues observed in vivo.…”

mentioning

confidence: 99%

“…Many studies have shown that heparin inhibits smooth muscle cell (SMC) proliferation in culture (1)(2)(3)(4)(5)(6) and intimal hyperplasia in models of arterial injury (7)(8)(9)(10)(11)(12)). Yet, the clinical efficacy of heparin in modulating the response to vascular injury is mixed at best.…”

mentioning

confidence: 99%

Tissue concentration of heparin, not administered dose, correlates with the biological response of injured arteries in vivo

Lovich

Edelman

1999

Proc. Natl. Acad. Sci. U.S.A.

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Drug activity is often studied in well controlled and characterized cellular environments in vitro. However, the biology of cells in culture is only a part of the tissue behavior in vivo. Quantitative studies of the dose response to drugs in vivo have been limited by the inability to reliably determine or predict the concentrations achieved in tissues. We developed a method to study the dose response of injured arteries to exogenous heparin in vivo by providing steady and predictable arterial levels of drug. Controlled-release devices were fabricated to direct heparin uniformly and at a steady rate to the adventitial surface of balloon-injured rat carotid arteries. We predicted the distribution of heparin throughout the arterial wall by using computational simulations of intravascular drug binding and transport, and we correlated these concentrations with the biologic response of the tissues. This allowed the estimation of the arterial concentration of heparin required to maximally inhibit intimal hyperplasia after injury in vivo, 0.3 mg͞ml. This estimation of the required concentration of drug seen by a specific tissue is independent of the route of administration and holds for all forms of drug release. In this way we may now be able to evaluate the potential of widely disparate forms of drug release and to finally create some rigorous criteria by which to guide the development of particular delivery strategies for local diseases.

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“…SMC were obtained from human uterine arteries as described (35) or from umbilical veins as follows. Umbilical cords < 48 h old were cannulated, rinsed ofblood with 37°C PBS, and filled with 0.1% collagenase (Type IV; Sigma) for 15 min.…”

Section: Introductionmentioning

confidence: 99%

“…After several lumenal rinses with RPMI 1640 (Gibco) to remove the endothelial cells, fresh collagenase was introduced for 15 min. The liberated SMC were collected in RPMI, pelleted, and resuspended in RPMI containing antibiotics, 10% heat-inactivated FCS and 10% heat-inactivated normal human serum (35). Seeding densities were 4 X 105 cells/ml and medium was changed every 4 d. Cells were grown in standard tissue culture flasks (Nunc, Roskilde, Denmark) and passaged at near confluence at a 1:3 ratio using a 0.25% trypsin-EDTA solution (Gibco).…”

Section: Introductionmentioning

confidence: 99%

Decay-accelerating factor is expressed on vascular smooth muscle cells in human atherosclerotic lesions.

Seifert

Hansson²

1989

J. Clin. Invest.

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Decay-accelerating factor (DAF) is a constitutively expressed plasma membrane glycoprotein on blood cells and endothelium that inhibits cell surface C3/C5 convertase formation, thus inhibiting complement activation and protecting cells from lysis by the terminal complement components. Using monoclonal anti-DAF antibodies in conjunction with anti-smooth muscle cell (SMC)-specific myosin antibodies, it was found by immunohistochemistry that vascular SMC in advanced human carotid atherosclerotic lesions express DAF antigen. The percentage of DAF-positive SMC ranged from 20 to 60% between different patient samples and SMC DAF expression was limited to SMC in the lesion proper. Normal arterial wall SMC exhibited no DAF-specific immunostaining. Essentially 100% of passaged cultured vascular SMC derived from normal human uterine artery, or from umbilical vein, expressed DAF as assessed by immunocytochemistry. A 68-kD band was observed on SDS-PAGE autoradiograms of DAF-immunoprecipitated radiolabeled cultured SMC extracts. Sensitization of rabbit erythrocytes with DAF-containing SMC extracts conferred protection against complement-mediated hemolysis in normal human serum and the protective effect could be reversed by treatment with anti-DAF antibodies. We conclude that DAF is induced on vascular SMC during atherogenesis and in culture.

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Human arterial smooth muscle cells in culture

Cited by 66 publications

References 33 publications

Characterization of Heparin and Heparan Sulfate Domains Binding to the Long Splice Variant of Platelet-derived Growth Factor A Chain

Characterization of Heparin and Heparan Sulfate Domains Binding to the Long Splice Variant of Platelet-derived Growth Factor A Chain

Tissue concentration of heparin, not administered dose, correlates with the biological response of injured arteries in vivo

Decay-accelerating factor is expressed on vascular smooth muscle cells in human atherosclerotic lesions.

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