Early changes in phosphatidylinositol and arachidonic acid metabolism in quiescent swiss 3T3 cells stimulated to divide by platelet-derived growth factor.

Habenicht, Andreas J. R.; Glomset, John A.; King, Weiling C.; Nist, Cynthia; Mitchell, Carolyn D.; Ross, Russell

doi:10.1016/s0021-9258(18)43275-9

Cited by 467 publications

(24 citation statements)

References 33 publications

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“…Animal studies have demonstrated that the hypertrophic response is mediated by classic signal transduction mechanisms 1' 2, 4-6 involving protooncogene activation and intracellular signaling through a classic protein kinase C pathway. 7 The human heart has also been shown to undergo molecular adaptation to pressure overload. 23 Induction of LVT-I, both in experimental models and in human beings, can be mediated by the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic benefits of the Toronto stentless valve

Rizzo¹,

Goldman²,

Christakis³

et al. 1996

The Journal of Thoracic and Cardiovascular Surgery

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We report on 254 consecutive patients (170 male, 84 female) undergoing aortic valve replacement with the Toronto SPV Stentless Valve (St. Jude Medical, Inc., St. Paul, Minn.). Mean age (+/- standard deviation) was 62.1 +/- 11.6 years. Three patients (1%) received sizes 21 or 22 mm, 24 (9%) received size 23 mm, and 227 patients (89%) received sizes 25, 27, or 29 mm. Serial echocardiography was used to assess valve performance during a 3-year follow-up. Mean gradient decreased by 35.8% (p < 0.0001; 95% confidence interval -39.6%, -31.7%) from postoperative values to the 3- to 6-month follow-up and by 6.1% (p = 0.004; 95% confidence interval -10.1%, -2%) at each subsequent interval; effective orifice area increased by 17.2% (p = 0.0001; 95% confidence interval 12.0%, 22.6%) initially and by 4.4% (p < 0.001; 95% confidence interval 1.8%, 7.0%) thereafter. At 2 years of follow-up, mean gradient was 3.3 +/- 2.1 mm Hg and mean effective orifice area was 2.2 +/- 0.8 cm2. Studies on left ventricular mass were carried out on 84 patients. Left ventricular mass decreased by 14.3% (37.8 +/- 57.9 gm; p < 0.0001; 95% confidence interval -53.7, -21.9 gm) and left ventricular mass index decreased by 15.2% (21.1 +/- 30.5 gm/m2; p < 0.0001; 95% confidence interval -29.5, -12.7 gm/m2) from postoperative values to the 3- to 6-month follow-up interval. The reduction in residual gradient and potential regression in left ventricular hypertrophy may have a beneficial prognostic implication. We believe that the unique stentless design of the Toronto SPV Stentless Valve allows this to occur.

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Section: Discussionmentioning

confidence: 99%

Hemodynamic benefits of the Toronto stentless valve

Rizzo¹,

Goldman²,

Christakis³

et al. 1996

The Journal of Thoracic and Cardiovascular Surgery

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“…It has been reported (Lopez-Rivas et al, 1987) that highly purified PDGF from pig platelets, even at saturating concentrations, caused little if any increase in IP3 production compared with the pronounced response seen with bombesin. Those authors point out that previous studies (Habenicht et al, 1981;Berridge et al, 1984;Hasegawa-Sasaki, 1985) have generally used partially purified PDGF, and imply that this may explain the difference in results. The results presented here indicate that this is not the explanation, since both highly purified human PDGF and pure recombinant PDGF are both very effective stimulators of production of inositol phosphates.…”

Section: Discussionmentioning

confidence: 99%

“…Other early events associated with the binding of PDGF, bombesin or vasopressin to Swiss 3T3 cells include stimulation of polyphosphoinositide hydrolysis (Habenicht et al, 1981;Berridge et al, 1984;Brown et al, 1984Brown et al, , 1987Chu et al, 1985;Heslop et al, 1986;Besterman et al, 1986b;Takuwa et al, 1987), Ca2" mobilization (Berridge et al, 1984;Mendoza et al, 1986b;Brown et al, 1987;Takuwa et al, 1987) and activation of protein kinase C (Isacke et al, 1986;Zachary et al, 1986). It remains to be established whether stimulated phosphoinositide hydrolysis is a necessary event for the stimulation of DNA synthesis and cell proliferation by these mitogens.…”

Section: Introductionmentioning

confidence: 99%

Bombesin and platelet-derived growth factor stimulate formation of inositol phosphates and Ca2+ mobilization in Swiss 3T3 cells by different mechanisms

Blakeley¹,

Corps²,

Brown³

1989

Biochemical Journal

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Highly purified platelet-derived growth factor (PDGF) or recombinant PDGF stimulate DNA synthesis in quiescent Swiss 3T3 cells. The dose-response curves for the natural and recombinant factors were similar, with half-maximal responses at 2-3 ng/ml and maximal responses at approx. 10 ng/ml. Over this dose range, both natural and recombinant PDGF stimulated a pronounced accumulation of [3H]inositol phosphates in cells labelled for 72 h with [3H]inositol. In addition, mitogenic concentrations of PDGF stimulated the release of 45Ca2+ from cells prelabelled with the radioisotope. However, in comparison with the response to the peptide mitogens bombesin and vasopressin, a pronounced lag was evident in both the generation of inositol phosphates and the stimulation of 45Ca2+ efflux in response to PDGF. Furthermore, although the bombesin-stimulated efflux of 45Ca2+ was independent of extracellular Ca2+, the PDGF-stimulated efflux was markedly inhibited by chelation of external Ca2+ by using EGTA. Neither the stimulation of formation of inositol phosphates nor the stimulation of 45Ca2+ efflux in response to PDGF were affected by tumour-promoting phorbol esters such as 12-O-tetradecanoylphorbol 13-acetate (TPA). In contrast, TPA inhibited phosphoinositide hydrolysis and 45Ca2+ efflux stimulated by either bombesin or vasopressin. Furthermore, whereas formation of inositol phosphates in response to both vasopressin and bombesin was increased in cells in which protein kinase C had been down-modulated by prolonged exposure to phorbol esters, the response to PDGF was decreased in these cells. These results suggest that, in Swiss 3T3 cells, PDGF receptors are coupled to phosphoinositidase activation by a mechanism that does not exhibit protein kinase C-mediated negative-feedback control and which appears to be fundamentally different from the coupling mechanism utilized by the receptors for bombesin and vasopressin.

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“…One of the earliest results of pd gf binding to its receptor is activation of phospholipase type A (Shier 1980;Shier & Durkin 1982) and phospholipase C (Habenicht 1981(Habenicht , 1985(Habenicht , 1986. Such phospholipase activation leads to release of free arachidonic acid, formation of diacylglycerol (Coughlin et al 1980;Habenicht et al 1981;Sawyer & Cohen et al 1983), breakdown of phosphatidylinositol, and turnover of phosphatidylinositol 4-5bisphosphate (PIP2) (Chu etal. 1985 ;Hasegawa-Sasaki 1985 ;Matuoka et al 1988).…”

Section: Pdgf Moleculesmentioning

confidence: 99%

Platelet-derived growth factor and its role in health and disease

Ross

Bowen‐Pope

Raines

1990

Phil. Trans. R. Soc. Lond. B

102

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Platelet-derived growth factor (PDGF) was first discovered in platelets because they are the principal source of mitogenic activity in whole blood serum for mesenchymal cells in culture. PDGF is ubiquitous in that it can be formed by a large number of normal cells as well as many varieties of transformed cells. However, its expression and biological activity appear to be controlled at a number of different levels. The molecule consists of two peptide chains (termed 'A' and 'B') and is found as one of at least three possible isoforms, (AB, AA or BB). Each of these isoforms binds to a high-affinity cell-surface receptor that is composed of two different subunits, each of which has specificity for one or the other of the peptide chains of PDGF. The two receptor subunits are present in differing amounts on different cell types, and therefore the capacity of the different isoforms of PDGF to induce mitogenesis depends on the specific PDGF isoform and the relative numbers of receptor subunits present on the responding cell. In addition to inducing cell replication, PDGF elicits a number of intracellular signals related to mitogenesis, is chemotactic, is a vasoconstrictor, activates leukocytes, and modulates extracellular matrix turnover. This growth factor is probably involved in a number of biologically important events including wound repair, embryogenesis and development, and inflammation, leading to fibrosis, atherosclerosis and neoplasia.

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Early changes in phosphatidylinositol and arachidonic acid metabolism in quiescent swiss 3T3 cells stimulated to divide by platelet-derived growth factor.

Cited by 467 publications

References 33 publications

Hemodynamic benefits of the Toronto stentless valve

Hemodynamic benefits of the Toronto stentless valve

Bombesin and platelet-derived growth factor stimulate formation of inositol phosphates and Ca2+ mobilization in Swiss 3T3 cells by different mechanisms

Platelet-derived growth factor and its role in health and disease

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