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Arteriogenesis in Gja5 (Connexin-40) deficient mice

von Dr. Haitao Wang

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Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
[1.] Haw/Fragment 009 01 - Diskussion
Zuletzt bearbeitet: 2014-10-12 16:44:04 Schumann
BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 9, Zeilen: 1-19
Quelle: Schaper and Scholz 2003
Seite(n): 1146, Zeilen: r. Spalte:17 ff.
[The same results can be obtained with] intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MCP-1 receptor (CC chemokines receptor-2) (CCR-2) in mice prevented almost all collateral growth after femoral artery occlusion[59], but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect[60]. We also discovered that the weak arteriogenic effects of chronically infused vascular endothelial growth factor-A (VEGF-A) is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes[61]. A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice [62] could be lifted by bone marrow transplantation, i.e., an effect of monocytes[62, 63]. Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation[64]. Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis[64]. Suppression of monocyte counts by treatment with 5-fluorouracil (5-FU) significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect[20, 59].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

59. Heil, M., et al., Blood monocyte concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol, 2002. 283(6): p. H2411-9.

60. Ito, W.D., et al., Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res, 1997. 80(6): p. 829-37.

61. Breier, G., et al., Transforming growth factor-beta and Ras regulate the VEGF/VEGF-receptor system during tumor angiogenesis. Int J Cancer, 2002. 97(2): p. 142-8.

62. Carmeliet, P., et al., Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nat Med, 2001. 7(5): p. 575-83.

63. Scholz, D., et al., Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol, 2003. 35(2): p. 177-84.

64. Pipp, F., et al., VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocyte-mediated mechanism. Circ Res, 2003. 92(4): p. 378-85.

The same results can be obtained with intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MPC-1 receptor (CCR-2) in mice prevents almost all collateral growth after femoral artery occlusion,43 but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect.44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.45 A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice46 could be lifted by bone marrow transplantation, ie, an effect of monocytes.46,47 Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.48 Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis.48

Suppression of monocyte counts by treatment with 5-fluorouracil significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect.49


43. Heil M, Ziegelhoeffer T, Helisch A, Wagner S, Martin S, Kuziel WA, Schaper W. Arteriogenesis (collateral artery growth) after femoral artery occlusion is reduced in mice lacking CC-chemokine-receptor-2. Circulation. 2002;106 (Suppl II):1390. Abstract.

44. Ito W, Arras M, Winkler B, Scholz D, Schaper J, Schaper W. Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res. 1997;80:829–837.

45. Breier G, Blum S, Peli J, Groot M, Wild C, Risau W, Reichmann E. Transforming growth factor-b1 and Ras regulate the VEGF/VEGF receptor system during tumor angiogenesis. Int J Cancer. 2002;97: 142–148.

46. Carmeliet P, Moons L, Luttun A, Vincenti V, Compernolle V, De Mol M, Wu Y, Bono F, Devy L, Beck H, Scholz D, Acker T, DiPalma T, Dewerchin M, Noel A, Stalmans I, Barra A, Blacher S, Vandendriessche T, Ponten A, Eriksson U, Plate K, Foidart J-M, Schaper W, Charnock-Jones DS, Hicklin DJ, Herbert J-M, Collen D, Persico G. Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nature Med. 2001;7:575–583.

47. Scholz D, Elsaesser H, Sauer A, Friedrich C, Luttun A, Carmeliet P, Schaper W. Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol. 2003;35:177–184.

48. Pipp F, Heil M, Issbrücker K, Ziegelhöffer T, Martin S, van den Heuvel J, Weich H, Fernandez B, Clauss M, Schaper W. VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocytemediated mechanism. Circ Res. 2003;92:378–385.

49. Heil M, Ziegelhoeffer T, Pipp F, Kostin S, Martin S, Clauss M, Schaper W. Blood monocytes concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol. 2002;283: H2411–H2419.

Anmerkungen

Die Quelle wird am Ende zusammen mit einem anderen Literaturverweis genannt. Der Umfang der Übernahme wird aber so nicht deutlich.

Sichter
(Hindemith), SleepyHollow02

[2.] Haw/Fragment 009 20 - Diskussion
Zuletzt bearbeitet: 2014-10-23 19:27:46 WiseWoman
BauernOpfer, Buschmann and Schaper 1999, Fragment, Gesichtet, Haw, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 9, Zeilen: 20-30
Quelle: Buschmann and Schaper 1999
Seite(n): 122, 123, Zeilen: 122: r. Spalte: 45ff: 123: l. Spalte: 6ff
Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor (GM-CSF)) provides the environment for a stable function of monocytes (Fig.1.3. C). These in turn produce fairly large amounts of growth factors, including VEGF, colony stimulating factor, transforming growth factor-β, in particular, FGF-2[20]. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its [diameter up to 20 times[21].]

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor) provides the environment for a stable function of monocytes (Fig. 1C). These in turn produce fairly large amounts of growth factors, in particular, fibroblast growth factor-2. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. [...]

[S. 123]

[...] The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its diameter up to 20 times.

Anmerkungen

Die Quelle ist am Ende des Absatzes genannt, aber es ist nicht klar, dass der gesamte Absatz aus ihr stammt.

Sichter
(Hindemith), WiseWoman


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