Modulation of smooth muscle cell behaviour by platelet‐derived factors and the extracellular matrix

Wren, Fiona E.; Schor, Ana M.; Schor, Seth L.; Grant, Michael E.

doi:10.1002/jcp.1041270217

Cited by 24 publications

(8 citation statements)

References 23 publications

(19 reference statements)

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“…In the present investigation, smooth muscle cell prolifera tion was significantly accelerated when cells were grown on tissue culture dishes precoated with extracellular ma trix compared with uncoated plastic ware. Similar growth-stimulatory effects of extracellular matrix were observed previously for bovine aortic endothelial and smooth muscle cells in vitro [22][23][24], Interestingly, the growth stimulatory effects of extracellular matrix was dependent on the phenotype of the vascular smooth mus- cle cells: matrix derived from adult smooth muscle cells was less growth stimulatory than matrix produced by neo natal or neointimal cells. Biochemical analysis of the matrices revealed significant differences in the amount and species of glycosaminoglvcans deposited by different vascular smooth muscle cells.…”

Section: Discussionsupporting

confidence: 61%

Vascular Smooth Muscle Cell Phenotype Influences Glycosaminoglycan Composition and Growth Effects of Extracellular Matrix

Hein

Fischer²,

Kim³

et al. 1996

J Vasc Res

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Rat neonatal and neointimal vascular smooth muscle cells differ dramatically from adult medial vascular smooth muscle cells in their growth properties, with the neonatal and neointimal cells exhibiting growth in the absence of exogenously added growth factors. Since it has been hypothesized that extracellular matrix proteoglycans may influence the growth and differentiation of vascular smooth muscle cells, we examined the ability of matrix derived from these cells to influence vascular smooth muscle cell proliferation. To produce test matrices, cells were grown to confluence and removed by brief alkali treatment. Test cells were seeded onto these matrices and the rates of growth in a growth-factor-deficient medium determined. Compared to plastic wells, matrix from neonatal or neointimal cells stimulated the growth of vascular smooth muscle cells. Interestingly, matrix from adult cells was less efficient at promoting growth. Enzymatic digestion of extracellular matrix heparan sulfate, but not of other glycosaminoglycans, further increased the growth-stimulatory effect of extracellular matrix, suggesting that matrix heparan sulfate acts as a growth inhibitor. Consistent with this, biochemical analysis showed that the adult matrix contained a higher percentage of heparan sulfate compared with neonatal or neointimal matrix. These results suggest that autocrine production of heparan sulfate proteoglycans may play an important role in growth regulation of vascular smooth muscle cells during normal vascular development and differentiation as well as in pathological response to injury.

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Section: Discussionsupporting

confidence: 61%

Vascular Smooth Muscle Cell Phenotype Influences Glycosaminoglycan Composition and Growth Effects of Extracellular Matrix

Hein

Fischer²,

Kim³

et al. 1996

J Vasc Res

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“…Collagen gels were used as matrices for cancer cell invasion, and prepared according to the method of Wren et al 18…”

Section: Collagen Gel Invasion Modelmentioning

confidence: 99%

Fibroblast Growth Factor‐2 Accelerates Invasion of Oral Squamous Cell Carcinoma

Hase¹,

Kawashiri²,

Tanaka³

et al. 2005

Oral Science International

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IntroductionMany recent studies have investigated substances that are involved in the interaction between solid cancer cells and their induced fi broblasts 1 6 . Among them, basic fi broblast growth factor FGF-2 was discovered by Gospodarowicz 7 in 1974 as a protein that strongly promotes the proliferation of fi broblasts. Later studies reported its overexpression in highly malignant cancer cells, and malignant transformation of normal cells transfected with the FGF-2 gene 8,9 . These results suggest that FGF-2 is involved in the invasion of cancer cells and the proliferation of fi broblasts around cancer cells in an autocrine or paracrine fashion ; however, the details are largely unknown.Previously, we reported that in an immunohistochemical study of oral squamous cell carcinoma tissue, the expression or non-expression of FGF-2 in fi broblasts was associated with cancer invasion and metastasis, and the prognosis 10 .In this study, we examined the effects of FGF-2 on cancer cell invasion and on fi broblast proliferation in an in vitro model of invasion.Abstract : The aim of this study was to examine the effects of fi broblast growth factor-2 FGF-2 on cancer cell invasion and on fi broblast proliferation in an in vitro model of invasion. Three kinds of human oral squamous cell carcinoma cell lines with different invasive activity were used : OSC-20, OSC-19 lower invasive type , and HOC313 higher invasive type . FGF-2 and its high-affi nity receptors FGFR-1 and FGFR-2 were detected by western blotting. The expression of FGF-2 and FGFRs mRNA was examined in cultured human oral squamous cell carcinoma cells by reverse transcriptase polymerase chain reaction RT-PCR . Furthermore, recombinant human FGF-2 rhFGF-2 was reacted with each cell line, and the invasion rate was determined by invasion assay. We also observed the behavior of cancer cell invasion in the collagen gel invasion model in the presence or absence of FGF-2-neutralizing antibody anti-FGF-2 . HOC313 cells showed higher expression of FGF-2 than OSC-20 and OSC-19 cells. The addition of rhFGF-2 promoted not only the proliferation of fi broblasts, but also the invasion of all cancer cell lines. In contrast, the addition of anti-FGF-2 completely inhibited the invasion of OSC-20 and OSC-19 cells. These results suggest that a higher invasiveness of squamous carcinoma cells is associated with higher production of FGF-2, which acts in an autocrine fashion to promote cancer cell invasion, and in a paracrine fashion to promote fi broblast proliferation.

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“…Three dimensional collagen matrices were constructed in 12-well dishes or 100 mm plates using a modification of previously described methods (Boudreau et al, 1991;Wren et al, 1986). Vitrogen 100 (Celtrix, Santa Clara, California), a solution of nondenatured, pepsin-solubilized bovine dermal collagen with an intact triple-helical structure, was combined with 1ϫ and 10ϫ M199 medium (GIBCO, Grand Island, New York) in 3.5:1 ratio (Boudreau et al, 1991), for a final collagen concentration of 2 mg/ml, and adjusted to pH 7.4.…”

Section: Extracellular Matricesmentioning

confidence: 99%

Osteopontin Deficiency in Rat Vascular Smooth Muscle Cells is Associated with an Inability to Adhere to Collagen and Increased Apoptosis

Weintraub

Schnapp

Lin

et al. 2000

Laboratory Investigation

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SUMMARY: Osteopontin (OPN) is an extracellular matrix protein that has been implicated in vascular smooth muscle cell (VSMC) adhesion. We have previously described the generation of OPN-deficient VSMC that displayed altered adhesion to collagen. We have examined further the causes and consequences of this altered adhesion. OPN-deficiency was associated with a significant reduction in surface expression of ␣1 and ␤1 integrins (mean fluorescence intensity ␣1: OPN-deficient 0.135 Ϯ 0.04 vs. control 0.313 Ϯ 0.05, p Ͻ 0.0001; ␤1: OPN-deficient 0.398 Ϯ 0.09 vs. control 0.570 Ϯ 0.05, p Ͻ 0.004). Treatment of normal VSMC with antibody to ␣1 recapitulated the adhesion defect. OPN-deficient cells without collagen exposure had an apoptotic fraction of 1.9%, which increased to 95.7% after 24 hours exposure to collagen. Exogenous OPN added to cultures within 15 minutes of plating restored normal cell adhesion, but did not prevent cells from undergoing apoptosis. Normal VSMC had no detectable apoptosis after 24 hours incubation in suspension, whereas OPN-deficient cells had an apoptotic fraction of 37.5% when incubated in suspension under the same conditions. The data suggest that OPN-deficient VSMC have two distinct abnormalities: an ␣1␤1-mediated inability to adhere normally to collagen and an increased propensity for apoptosis. (Lab Invest 2000, 80:1603-1615.

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Modulation of smooth muscle cell behaviour by platelet‐derived factors and the extracellular matrix

Cited by 24 publications

References 23 publications

Vascular Smooth Muscle Cell Phenotype Influences Glycosaminoglycan Composition and Growth Effects of Extracellular Matrix

Vascular Smooth Muscle Cell Phenotype Influences Glycosaminoglycan Composition and Growth Effects of Extracellular Matrix

Fibroblast Growth Factor‐2 Accelerates Invasion of Oral Squamous Cell Carcinoma

Osteopontin Deficiency in Rat Vascular Smooth Muscle Cells is Associated with an Inability to Adhere to Collagen and Increased Apoptosis

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