Arteriogenesis by Wolfgang Schaper, Jutta Schaper

By Wolfgang Schaper, Jutta Schaper

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This‚ however‚ is only possible when the basement membranes of the SMCs are dissolved so that the cells can move. This is obvious in numerous SMCs in the tunica media and intima. The basement membrane reappears in redifferentiated SMCs of mature collateral vessels. These observations Collateral vessel‚ actively growing. The IEL is absent‚ numerous smaller and larger SMCs are migrating towards the lumen. Note the large amount of ECM but absence of collagen fibrils between the migrating SMCs Structural Remodeling during Growth of Collateral Vessels 29 strengthen the notion that laminin and other basement membrane components promote the differentiation of vascular SMCs11‚12‚ which may occur via receptormediated interaction and generation of signals that affect cell behavior.

J Cell Biochem. 1996;61:543-553. Structural Remodeling during Growth of Collateral Vessels 49 16. PALECEK SP‚ LOFTUS JC‚ GINSBERG MH‚ LAUFFENBURGER DA‚ HORWITZ AF. integrin-ligand binding properties govern cell migration speed through cell-substratum adhesiveness. Nature. 1997;385:537-40. 17. WOLF C‚ CAI W-J‚ VOSSCHULTE R‚ KOLTAI S‚ MOUSAVIPOUR D‚ SCHOLZ D‚ AFSAH-HEDJRI A‚ SCHAPER W‚ SCHAPER J. Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol.

Apoptosis may be caused by increased stretch of SMCs and is mediated by the betal–integrinrac-p38-p53 pathway18. The balance between the number of cells undergoing mitosis and the rate of cells dying will decide the final outcome of the vascular growth process17. Usually‚ the balance is in favor of cell division‚ which results in the formation of a multilayered neointima where the SMCs are arranged either circumferentially or in the direction of the longitudinal axis of the vessel. Proliferation of SMCs can be promoted by stretch19‚ lack of elastin20 as discussed below and by the direct action of growth factors (discussed in Vascular wall of a growing collateral vessel characterized by almost complete absence of the IEL and presence chapter 10).

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