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| Autor | Anne Limbourg, Thomas Korff, L Christian Napp, Wolfgang Schaper, Helmut Drexler, Florian P Limbourg |
| Titel | Evaluation of postnatal arteriogenesis and angiogenesis in a mouse model of hind-limb ischemia |
| Zeitschrift | Nature Protocols |
| Ausgabe | 4 |
| Jahr | 2009 |
| Seiten | 1737-1748 |
| URL | http://www.nature.com/nprot/journal/v4/n12/full/nprot.2009.185.html |
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| During embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins[4]. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions[5]. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.
4. Adams, R.H. and K. Alitalo, Molecular regulation of angiogenesis and lymphangiogenesis. Nat Rev Mol Cell Biol, 2007. 8(6): p. 464-78. 5. Carmeliet, P., Angiogenesis in health and disease. Nat Med, 2003. 9(6): p. 653-60. |
During the embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins2. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions3. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.
2. Adams, R.H. & Alitalo, K. Molecular regulation of angiogenesis and lymphangiogenesis. Nat. Rev. Mol. Cell. Biol. 8, 464–478 (2007). 3. Carmeliet, P. Angiogenesis in health and disease. Nat. Med. 9, 653–660 (2003). |
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| [Arteriogenesis is defined as the enlargement of pre-existing collateral arteries and their remodelling into conductance vessels[8]. This process is driven by an] increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress[9-11]. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth[12-17]. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs[18, 19].
8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21. 9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58. 10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55. 11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62. 12. Limbourg, A., et al., Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ Res, 2007. 100(3): p. 363-71. 13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6. 14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50. 15. Jacobi, J., et al., Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation, 2004. 110(16): p. 2424-9. 16. Kondoh, K., et al., Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc Res, 2004. 61(1): p. 132-42. 17. Ziegelhoeffer, T., et al., Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ Res, 2004. 94(2): p. 230-8. 18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87. 19. Simons, M., Angiogenesis: where do we stand now? Circulation, 2005. 111(12): p. 1556-66. |
Arteriogenesis, on the other hand, is defined as the enlargement of pre-existing collateral arteries and their remodelling to conductance vessels5. This process is driven by an increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress6–8. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth9–14. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs15,16.
5. Schaper, W. Collateral circulation: past and present. Basic Res. Cardiol. 104, 5–21 (2009). 6. Heil, M. & Schaper, W. Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ. Res. 95, 449–458 (2004). 7. Heil, M., Eitenmuller, I., Schmitz-Rixen, T. & Schaper, W. Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55 (2006). 8. Eitenmuller, I. et al. The range of adaptation by collateral vessels after femoral artery occlusion. Circ. Res. 99, 656–662 (2006). 9. Limbourg, A. et al. Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ. Res. 100, 363–371 (2007). 10. Schaper, W., Jageneau, A. & Xhonneux, R. The development of collateral circulation in the pig and dog heart. Cardiologia 51, 321–335 (1967). 11. Arras, M. et al. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101, 40–50 (1998). 12. Jacobi, J. et al. Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation 110, 2424–2429 (2004). 13. Kondoh, K. et al. Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc. Res. 61, 132–142 (2004). 14. Ziegelhoeffer, T. et al. Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ. Res. 94, 230–238 (2004). 15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002). 16. Simons, M. Angiogenesis: where do we stand now? Circulation 111, 1556–1566 (2005). |
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| Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue[3]. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.
3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95. |
Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue4. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.
4. Carmeliet, P. Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395 (2000). |
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| Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42. |
Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html). |
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| Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest. | Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest. |
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| The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin[131]. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images[132]. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion[132]. We therefore take LDI measurements from the feet, which correlate with other measures of limb perfusion[18, 133].
18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87. 131. Jakobsson, A. and G.E. Nilsson, Prediction of sampling depth and photon pathlength in laser Doppler flowmetry. Med Biol Eng Comput, 1993. 31(3): p. 301-7. 132. Chalothorn, D., et al., Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol Genomics, 2007. 30(2): p. 179-91. 133. Helisch, A., et al., Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler Thromb Vasc Biol, 2006. 26(3): p. 520-6. |
The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin22. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images23. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion23. We therefore
[Seite 1739] take LDI measurements from the feet, which correlate with other measures of limb perfusion15,24. 15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002). 22. Jakobsson, A. & Nilsson, G.E. Prediction of sampling depth and photon path length in laser Doppler flowmetry. Med. Biol. Eng. Comput. 31, 301–307 (1993). 23. Chalothorn, D., Clayton, J.A., Zhang, H., Pomp, D. & Faber, J.E. Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol. Genomics 30, 179–191 (2007). 24. Helisch, A. et al. Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler. Thromb. Vasc. Biol. 26, 520–526 (2006). |
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| Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and MicroCT imaging. | Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and angiogenesis or whole-mount visualization of arteries in limb muscles. |
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| Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42. |
Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html). |
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