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Tumors of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Growth factor and growth factor receptor overexpression are common in malignant gliomas and may accelerate tumorigenesis and tumor progression. Most of these are found predominantly in diffuse, high-grade, astrocytic tumors and include the following: EGFR.Platelet-derived growth factor (PDGF).Vascular endothelial growth factor (VEGF).Insulin-like growth factor (IGF-1).Basic fibroblast growth factor (bFGF, FGF-2).Transforming growth factor (TGF)-alpha.
Immune Function in Exercise-Induced Injuries
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
Louis C. Almekinders, Sally V. Almekinders
In addition to phagocytosis, the cellular immune response also appears to play a critical role in the induction of the fibroblast healing response. IL-1 and TNF can be produced by macrophages, and appear to stimulate the subsequent fibroblast proliferation and synthetic activity.23,24 These cytokines may be responsible in part for modulating the fibroblastic scarring response that occurs at the site of injury. Fibronectin (a glycoprotein), derived from the initial clot, and macrophages attract fibroblasts and allow adherence of matrix and cellular elements.25 Transforming growth factor-beta (TGF-β) is another macrophage-derived cytokine with profound effects on matrix proliferation.26 TNF and TGF also influence the ingrowth of new capillaries into the injured area.27 Besides macrophages and lymphocytes, platelets in the clot that forms in the injured area can induce a healing response. Platelet-derived growth factor may be responsible for some of these effects.28 Finally, prostaglandins may also modulate the fibroblast response, directly or through other cytokines. The fibroblasts, through their collagen production, are responsible for the eventual recovery of mechanical strength. Modulation of their activity can result in a change in strength. Dahners et al.29 found an early increase in strength in healing rat ligaments treated with NSAIDs.
Cellular Oncogenes as Biotherapeutic Targets for the Differentiation and Inhibition of Cancer Cells
Published in Robert I. Glazer, Developments in Cancer Chemotherapy, 2019
Robert I. Glazer, Angelo Aquino, Gang Yu
Recent studies have determined that several cellular oncogene products are closely related to growth factor receptors (Figure 3). The v-sis oncogene product resembles platelet-derived growth factor (PDGF), which plays an important role in wound healing.85,86 Similarly, the human EGF receptor is closely related to the product of the v-erb B oncogene. In the latter instance, the overproducing epidermoid carcinoma cell line A431 has been used almost exclusively to study the EGF receptor tyrosine protein kinase87-93 and the messenger RNAs94-96 encoding the normal and aberrant EGF receptor in these cells. This cell line is also the only one thus far possessing amplified receptor-gene sequences and an aberrant truncated form of the EGF receptor which is devoid of tyrosine protein kinase.97 Although the latter mutant EGF receptor can be considered a result of a rearrangement and amplification in the gene, its presence has not provided any clue to the neoplastic properties of this cell line.
Pathophysiology and management of saphenous vein graft disease
Published in Expert Review of Cardiovascular Therapy, 2023
Elizabeth C. Ghandakly, Aaron E. Tipton, Faisal G. Bakaeen
Intimal hyperplasia of vein grafts is a primary driver of graft failure. This process begins at a cellular level within the layers of the graft. The composition of a vein graft is an internal layer of the intima followed outwardly by the media and adventitia. Within the media are vascular smooth muscle cells (VSMCs) and fibroblasts. When the vein grafts undergo stress, these cells will proliferate to help strengthen the graft. The different forms of stress experienced by a vein graft are sheer, circumferential, and mechanical manipulation. These events are converted into biochemical signaling by the release of platelet-derived growth factor, transforming growth factor beta, and epidermal growth factor from the endothelium, platelets, and macrophages. The process is called mechanotransduction [29]. VSMCs receive these signals and migrate into the intima. They begin to proliferate and deposit extracellular matrix. Fibroblasts translocate into the intima as well and differentiate into myofibroblasts. This cellular process begins immediately and noticeable changes can be seen within 4 to 6 weeks with a decrease in graft lumen by 25% [30].
The measurement of wound tensile strength and the effect of PRP on wound tensile force: an experimental investigation on rabbits
Published in Journal of Plastic Surgery and Hand Surgery, 2022
Ali Gökkaya, Metin Görgü, Jehat Kızılkan, Ertuğrul Karanfil, Ali Doğan
Platelets start the inflammation phase of wound healing and manage it. Inflammatory, proliferative and remodeling are stages of wound healing. After activation by tissue damage, platelets initiate hemostasis and wound healing. Activated platelets promote wound healing by releasing biologically active proteins and growth factors (such as platelet-derived growth factor, transforming growth factor-b, fibroblast growth factor, epidermal growth factor, keratinocyte growth factor, and vascular endothelium growth factors) resulting in connective tissue healing, epithelial development, angiogenesis, and deposition of the collagen matrix. During the wound healing process, the tensile strength of the wound increases progressively. This increase is greater in the first week; later on, it is directly related to the increase in collagen production, and it stabilizes when collagen production and destruction are in balance. Weak crosslinks change to strong crosslinks and tensile strength increases progressively until the tensile force reaches an optimum strength. The stages of wound healing directly affect the tensile strength of the wound.
The use of platelet-rich products for skin graft donor site healing: a systematic review and meta-analysis
Published in Journal of Plastic Surgery and Hand Surgery, 2021
Christopher F. Brewer, Alexander Smith, Ben H. Miranda
Platelet-rich plasma (PRP) is an autologous mixture of concentrated platelets and growth factors derived from centrifuged blood [2]. It is purported to accelerate soft tissue wound healing [3] and axonal regeneration [4,5], thereby reducing the morbidity associated with acute and chronic wounds [6–10]. These effects are attributed to the release of cytokines and growth factors from activated platelets including platelet derived growth factor (PDGF), endothelial growth factor (EGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and platelet derived growth factor (PDGF) [11]. These anabolic substances stimulate cellular proliferation and epithelial cell migration at the wound site [12], and modulate the inflammatory to reduce prolonged inflammation [13].