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PDGFs, found in several types of human cells but mostly in platelets, were the first type of growth factor discovered in alpha granules.²⁷ PDGF adheres only to target cells with receptive surface membranes. When a wound is treated with concentrated platelets, the release of PDGF triggers activity in fibroblasts, neutrophils, and macrophages, stimulating the latter to additionally release growth factors that help to heal injured tissues.^70–72 Specifically, the target cells’ transmembrane receptors are activated by the platelet-released growth factors, and the receptors’ intracytoplasmic qualities activate the signal transducer proteins, one of which migrates to the target cell’s nucleus. There, the protein initiates a particular, regulated gene sequence—which may, for example, include the production of osteoid.

Alternatively, the sequence might lead to the synthesis of collagen. The regulated nature of the sequence precludes an “overdose” of concentrated growth factors. Growth factors’ amutagenic qualities testify to their ability as natural proteins to initiate and participate in the regular genetic activities associated with the controlled mechanisms for wound healing.^1,73–76 As isomers of a single protein, and functioning as mitogens, PDGFs—the most common growth factors—perform different but often complementary tasks (Fig 1-6). This prompts certain cells to replicate, specifically mesenchymal stem cells, osteoblasts (producing osteoid), endothelial cells (secreting basal lamina), and fibroblasts (producing collagen).^77–83

FIG 1-5 Wound healing and tissue regeneration cycle.

FIG 1-6 Roles of PDGF.

FIG 1-7 TGF-β stimulates the proliferation and migration of fibroblasts and the process of epithelial-mesenchymal transition, but it also stimulates fibrotic responses, which can lead to end-stage organ failure in the heart, kidney, etc.

FIG 1-8 Fibroblasts have different origins at different developmental stages (EMT, epithelial-mesenchymal transition; MET, mesenchymal-epithelial transition).