Abstract
Studies of growth control have focused on the role of low-molecular-weight proteins that stimulate growth. Like other hormones or cytokines, these small proteins, including platelet-derived growth factor (PDGF) and epidermal growth factor (EGF), bind to receptors in target cell membranes and initiate a set of events leading to DNA synthesis. The existence of these growth factors is consistent with the usual view of growth stimulus and response, which occurs when a tissue proliferates during wound repair. That is, we usually think of a wound as disrupting a resting environment. Cytokines and lymphokines released at sites of injury might be thought of as wound-repair hormones, initiating margination of leukocytes, chemotaxis, release of proteases, hemostasis, and so on. In a similar manner, it is reasonable to imagine that growth factors released at a wound site would stimulate cells in the wounded tissue to begin replicating. This idea is well supported by studies showing that many of the blood cells responding to a wound can release mitogens (Ross et al., 1974) and by more recent studies showing that these agents can be effective when released in a wound chamber in vivo (Sporn et al, 1983; Assoian et al, 1984) (see Chapter 9-12).
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Heimark, R.L., Schwartz, S.M. (1988). The Role of Cell-Cell Interaction in the Regulation of Endothelial Cell Growth. In: Clark, R.A.F., Henson, P.M. (eds) The Molecular and Cellular Biology of Wound Repair. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1795-5_16
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DOI: https://doi.org/10.1007/978-1-4615-1795-5_16
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