Effect of heparin on proliferation and signalling in BC3H‐1 muscle cells

Vannucchi, Simonetta; Pasquali, Franca; Fiorelli, G; Biabchini, Pietro; Ruggiero, Marco

doi:10.1016/0014-5793(90)80723-v

Cited by 16 publications

(9 citation statements)

References 29 publications

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“…However, low molecular weight heparins differ from high molecular weight heparin in their binding to proteins (Lane, 1989): they have lower affinity for proteins such as fibronectin (Dawes & Pavuk, 1991) or Platelet factor 4 and histidine-rich glycoprotein (Lane et al, 1986). Moreover, they have much lower affinity for the heparin-binding sites on endothelial cells (Vannucchi et al, 1988) and BC3H-l muscle cells (Vannucchi et al, 1990b). In this paper we show that confluent cultures of Balb/c 3T3 cells bear high affinity binding sites for heparin with Kd values of the same magnitude as the IC50 shown in the antiproliferative experiments.…”

Section: Discussionsupporting

confidence: 52%

“…We have previously demonstrated that heparin inhibited seruminduced phosphoinositide turnover in BC3H-1 muscle cells and the interference with serum growth factors was proposed as a possible mechanism (Vannucchi et al, 1990b). PDGF accounts for approximately 50% of the platelet derived mitogenic activity of serum; the remaining activity appears to be due to other growth factors (Ross et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

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Binding and growth‐inhibitory effect of heparin and oligo‐heparin (2 kDa) in Balb/c 3T3 cells: lack of effect on PDGF‐ or serum‐induced inositol lipid turnover

Cavari¹,

Fiorelli²,

Vannucchi³

1994

British J Pharmacology

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1 The ability of heparins (bovine heparin sm 1026, Av. mol. wt. 36.9 kDa and bovine heparin EP 756, Av. mol. wt. 12.9 kDa) and heparin fractions of different molecular weights (low molecular weight heparin, LMW 2123/OP, Av. mol. wt. 4.5 kDa and oligo-heparin, Av. mol. wt. 2 kDa) to inhibit the proliferation and signalling of Balb/c 3T3 fibroblasts was investigated. 6 Both heparin and oligo-heparin exert their inhibitory effects on Balb/c 3T3 DNA synthesis stimulated by PDGF or serum. However these molecules did not affect the inositol lipid turnover triggered by PDGF at a concentration which did not produce maximal response. The increase of inositol phosphate metabolism produced by 20% serum was also unaffected by heparin. This concentration of serum elicited a response comparable to that induced by a submaximal concentration of PDGF.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Binding and growth‐inhibitory effect of heparin and oligo‐heparin (2 kDa) in Balb/c 3T3 cells: lack of effect on PDGF‐ or serum‐induced inositol lipid turnover

Cavari¹,

Fiorelli²,

Vannucchi³

1994

British J Pharmacology

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“…It could be intracellular, extracellular, or both. Heparin is taken into cells, such as fibroblasts, 18 by a process of cell-surface binding 19,20 followed by internalization and metabolism of the glycosaminoglycan into oligosaccharides. 21,22 Internalized heparin or its metabolites could change cellular metabolism, 23 resulting in an alteration in the production of extracellular matrix proteins.…”

Section: Discussionmentioning

confidence: 99%

Effect of Heparin on Production of Basic Fibroblast Growth Factor and Transforming Growth Factor-Beta1 by Human Normal Skin and Hyperplastic Scar Fibroblasts

Fan

Qin

Cai

et al. 2007

Journal of Burn Care & Research

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Heparin affects both dermal fibroblast proliferation and collagen and may mediate these effects by altering the levels of basic fibroblast growth factor (bFGF) and transforming growth factor-beta1 (TGF-beta1) production as a wound healing modulator. The purpose of this study is to probe the effect of heparin on bFGF and TGF-beta1 production by human normal skin and hyperplastic scar fibroblasts. This research investigates the effect of heparin on bFGF and TGF-beta1 production by human normal skin and hyperplastic scar fibroblasts with exposure to 0, 100, 300, or 600 microg/ml heparin for 24, 48, 72, or 96 hours in a serum-free in vitro model. Levels of bFGF and TGF-beta1 in the supernatants were determined by enzyme-linked immunosorbant assay. All doses of heparin significantly stimulated production of bFGF by normal skin (393% to 1019% increase) and hyperplastic scar fibroblasts (405% to 899% increase) at all time points (P < .05). Heparin (300 and 600 microg/ml) also stimulated TGF-beta1 production by normal skin (26% to 83%) and hyperplastic scar fibroblasts (63% to 85%) with statistical significance (P < .05) at various time points. These effects of heparin on normal skin and hyperplastic scar fibroblasts may have implications for hyperplastic scar formation and wound healing in vivo.

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“…Specific heparin-binding sites have been shown to occur in a smooth muscle cell type (BC3H-1), and binding is considered a preliminary to cellular internalization (46). Possible intracellular sites for heparin action are inhibition of IP 3 -dependent intracellular calcium mobilization after phospholipase C activation (47), which may affect calcium-dependent phospholipase A 2 secondarily.…”

Section: Discussionmentioning

confidence: 99%

Fibronectin-Induced Increase in Mesangial Cell Prostaglandin Release: Effect of Hyperglycemia and PKC Inhibition

1993

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Glomerular accumulation of extracellular matrix in diabetes is a potential regulator of mesangial cell-matrix interactions through transmembrane matrix receptors. We now provide evidence that PG production from rat glomerular mesangial cells is increased by Fn. An increase in PG (measured as PGE) was demonstrated in mesangial cell-enriched glomerular cores after 1-h exposure (149 +/- 8% of timed control) and was sustained over a 24-h period (214 +/- 7%). Increased PG production followed exposure to a chymotryptic fragment (120,000 M(r)) of Fn and occurred concomitant with an increase in particulate PKC activity. A tetrapeptide (Arg-Gly-Asp-Ser) with the Arg-Gly-Asp sequence, contained in Fn and the chymotryptic fragment and recognized by specific membrane receptors (integrin matrix-binding proteins), also raised PG levels. As has been shown previously, exposure to high glucose concentration can increase mesangial cell PGE production (from 677 +/- 61 pg.mg protein-1.2 h-1 at 5.6 mM glucose to 1561 +/- 132 pg.mg protein-1.2 h-1 at 50 mM glucose, P < 0.001). The response to the chymotryptic fragment of Fn also was enhanced by concurrent exposure to high glucose concentration (from 2560 +/- 199 pg.mg protein-1.2 h-1 at 5.6 mM glucose to 4672 +/- 358 pg.mg protein-1.2 h at 50 mM glucose, P < 0.001). Coincubation with H-7, an inhibitor of PKC, abolished the PG response to glucose and the chymotryptic fragment. Involvement of PKC was supported further by abrogation of the effect of chymotryptic fragment in mesangial cells cultured for a prior prolonged period with phorbol ester.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of heparin on proliferation and signalling in BC3H‐1 muscle cells

Cited by 16 publications

References 29 publications

Binding and growth‐inhibitory effect of heparin and oligo‐heparin (2 kDa) in Balb/c 3T3 cells: lack of effect on PDGF‐ or serum‐induced inositol lipid turnover

Binding and growth‐inhibitory effect of heparin and oligo‐heparin (2 kDa) in Balb/c 3T3 cells: lack of effect on PDGF‐ or serum‐induced inositol lipid turnover

Effect of Heparin on Production of Basic Fibroblast Growth Factor and Transforming Growth Factor-Beta1 by Human Normal Skin and Hyperplastic Scar Fibroblasts

Fibronectin-Induced Increase in Mesangial Cell Prostaglandin Release: Effect of Hyperglycemia and PKC Inhibition

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