Fibroblast Growth Factor 2 Enhances Early Stages of in Vitro Endothelial Repair by Microfilament Bundle Reorganization and Cell Elongation

Wang, David I.; Gotlieb, Avrum I.

doi:10.1006/exmp.1999.2265

Cited by 19 publications

(9 citation statements)

References 27 publications

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“…Therefore, the newly formed blood vessels could supply oxygen and nutrients, thereby facilitating collagen synthesis. However, at day 11 after surgery, the expression levels of VEGF and CD31 were lower than those in the other groups, demonstrating downregulation of growth factors to form normal skin tissues 49 , 50 .…”

Section: Discussionmentioning

confidence: 91%

Effects of incorporation of granule-lyophilised platelet-rich fibrin into polyvinyl alcohol hydrogel on wound healing

Zou

Dai

et al. 2018

Sci Rep

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Dressings are commonly used to treat skin wounds. In this study, we aimed to develop a new scaffold composed of a polyvinyl alcohol (PVA) hydrogel containing granule-lyophilised platelet-rich fibrin (G-L-PRF) as a dressing. G-L-PRF was prepared by freeze-drying and was then incorporated into PVA hydrogel by freezing-thawing. Notably, the mechanical strength and degradation rate of the scaffold were found to be related to G-L-PRF concentrations, reaching 6.451 × 10−2 MPa and 17–22%, respectively, at a concentration of 1%. However, the strength decreased and the degradation was accelerated when the G-L-PRF concentration was over 1%. The elastic properties and biocompatibility of the scaffold were independent of G-L-PRF concentration, and both showed excellent elasticity and biocompatibility. The release of vascular endothelial growth factor and platelet-derived growth factor-AB was no significant time dependent. Additionally, application of 1% G-L-PRF/PVA to acute full-thickness dorsal skin wounds accelerated wound closure at days 7 and 9. Healing also increased on day 11. Histological and immunohistochemical analyses showed that the scaffold enhanced granulation tissue, maturity, collagen deposition, and new vessel formation. These results demonstrated that the prepared G-L-PRF/PVA scaffolds accelerated wound healing in acute full-thickness skin wounds, suggesting potential applications as an ideal wound dressing.

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Section: Discussionmentioning

confidence: 91%

Effects of incorporation of granule-lyophilised platelet-rich fibrin into polyvinyl alcohol hydrogel on wound healing

Zou

Dai

et al. 2018

Sci Rep

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“…Early changes in the actin cytoskeleton in the bFGF-mediated scratch wound repair model were characterized by Wang and Gotlieb in the endothelial cells [40]. They demonstrated that bFGF-treated cells at the leading edge were more elongated and had more prominent perpendicular actin microfilaments as compared to the non-treated cells at 4 h after wounding.…”

Section: Discussionmentioning

confidence: 97%

bFGF Regulates PI3-Kinase-Rac1-JNK Pathway and Promotes Fibroblast Migration in Wound Healing

et al. 2010

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Fibroblast proliferation and migration play important roles in wound healing. bFGF is known to promote both fibroblast proliferation and migration during the process of wound healing. However, the signal transduction of bFGF-induced fibroblast migration is still unclear, because bFGF can affect both proliferation and migration. Herein, we investigated the effect of bFGF on fibroblast migration regardless of its effect on fibroblast proliferation. We noticed involvement of the small GTPases of the Rho family, PI3-kinase, and JNK. bFGF activated RhoA, Rac1, PI3-kinase, and JNK in cultured fibroblasts. Inhibition of RhoA did not block bFGF-induced fibroblast migration, whereas inhibition of Rac1, PI3-kinase, or JNK blocked the fibroblast migration significantly. PI3-kinase-inhibited cells down-regulated the activities of Rac1 and JNK, and Rac1-inhibited cells down-regulated JNK activity, suggesting that PI3-kinase is upstream of Rac1 and that JNK is downstream of Rac1. Thus, we concluded that PI3-kinase, Rac1, and JNK were essential for bFGF-induced fibroblast migration, which is a novel pathway of bFGF-induced cell migration.

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“…This implies that FGF‐2‐induced cytoskeletal reorganization requires a high number of FGFRs on the surface of PAE (and, possibly, BAE) cells. Neither Wang and Gotlieb [1999] nor Coomber [1991] observed disassembly of stress fibers or formation of cellular processes in FGF‐2‐treated PAE or bovine pulmonary artery endothelial cells. Actually, Wang and Gotlieb [1999] reported PAE cell elongation and microfilament reorganization very similar to our bFGF‐treated BAE cells.…”

Section: Discussionmentioning

confidence: 99%

Response of bovine endothelial cells to FGF‐2 and VEGF is dependent on their site of origin: Relevance to the regulation of angiogenesis

Cavallaro

Tenan²,

Castelli

et al. 2001

J of Cellular Biochemistry

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Angiogenesis, the formation of new capillary blood vessels, occurs almost exclusively in the microcirculation. This process is controlled by the interaction between factors with positive and negative regulatory activity. In this study, we have compared the effect of two well described positive regulators, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF-2) on bovine adrenal cortex-derived microvascular endothelial (BME) and bovine aortic endothelial (BAE) cells. The parameters we assessed included (a) cellular reorganization and lumen formation following exposure of the apical cell surface to a three-dimensional collagen gel; (b) organization of the actin cytoskeleton; (c) expression of thrombospondin-1 (TSP-1), an endogenous negative regulator of angiogenesis; and (d) extracellular proteolytic activity mediated by the plasminogen activator (PA)/plasmin system. We found that (a) collagen gel overlay induces rapid reorganization and lumen formation in BME but not BAE cells; (b) FGF-2 but not VEGF induced dramatic reorganization of actin microfilaments in BME cells, with neither cytokine affecting BAE cells; (c) FGF-2 decreased TSP-1 protein and mRNA expression in BME cells, an effect which was specific for FGF-2 and BME cells, since TSP-1 protein levels were unaffected by VEGF in BME cells, or by FGF-2 or VEGF in BAE cells; (d) FGF-2 induced urokinase-type PA (uPA) in BME and BAE cells, while VEGF induced uPA and tissue-type PA in BME cells with no effect on BAE cells. Taken together, these findings reveal endothelial cell-type specific responses to FGF-2 and VEGF, and point to the greater specificity of these cytokines for endothelial cells of the microvasculature than for large vessel (aortic) endothelial cells. Furthermore, when viewed in the context of our previous observation on the synergistic interaction between VEGF and FGF-2, our present findings provide evidence for complementary mechanisms which, when acting in concert, might account for the synergistic effect.

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Fibroblast Growth Factor 2 Enhances Early Stages of in Vitro Endothelial Repair by Microfilament Bundle Reorganization and Cell Elongation

Cited by 19 publications

References 27 publications

Effects of incorporation of granule-lyophilised platelet-rich fibrin into polyvinyl alcohol hydrogel on wound healing

Effects of incorporation of granule-lyophilised platelet-rich fibrin into polyvinyl alcohol hydrogel on wound healing

bFGF Regulates PI3-Kinase-Rac1-JNK Pathway and Promotes Fibroblast Migration in Wound Healing

Response of bovine endothelial cells to FGF‐2 and VEGF is dependent on their site of origin: Relevance to the regulation of angiogenesis

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