FGF-2 Promotes Disassembly of Actin Cytoskeleton and Shape Changes in Murine Vascular Cells

Cavallaro, Ugo; Perilli, Alessandra; Castelli, Vera; Pepper, Michael Sean; Soria, Marco R.

doi:10.1006/mvre.2000.2299

Cited by 3 publications

(2 citation statements)

References 9 publications

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“…We have recently shown that TTB and SIE cells, which are poorly differentiated microvascular endothelial cells, respond to exogenous FGF‐2 with dramatic changes in the cytoskeleton and morphology, very similar to those observed in BME cells [Cavallaro et al, 2001]. However, while FGF‐2‐stimulated BME cells to form capillary‐like structures when cultured on 3‐D collagen matrices [Montesano et al, 1986], TTB and SIE cells fail to do so [Cavallaro et al, 2000, and our unpublished observations].…”

Section: Discussionmentioning

confidence: 82%

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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Section: Discussionmentioning

confidence: 82%

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

Self Cite

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“…In this respect, several studies have indicated that a number of growth factors, including bFGF or FGF‐2, TGFβ, and platelet‐derived growth factor (PDGF), play roles in the re‐endothelialization process. bFGF, known to stimulate the production of plasminogen activator and endothelial cell migration (Montesano et al, 1986; Tsuboi et al, 1990), has recently been shown to induce changes in shape and cytoskeletal alterations in vascular cells (Cavallaro et al, 2001a, b). Additionally, immunolocalization studies have shown that this growth factor is located in the nucleus and cytoplasm of endothelial cells in culture, suggesting that such locations are associated with the activity of these cells (Renko et al, 1990; Dell'Era et al, 1991; Muthukrishnan et al, 1991; Acevedo et al, 1993; Yu et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Mechanically altered embryonic chicken endothelial cells change their phenotype to an epithelioid phenotype

2002

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Monolayers of retracted endothelial cells exhibiting wounds or zones denuded of cells were obtained from aortic explants from 10-to 12-day-old chicken embryos. Using time-lapse videomicroscopy, we investigated the sequence of events that occurred both during and after closure of the monolayer wounds. Such wound closure (re-endothelialization process) occurred 4 -12 hr after removing the explants, depending on wound width and presence of serum. The cells from along the wound edges appeared to move toward one another. We suggest an important role for bFGF and TGF␤-2 and -3 during this process. Twenty-five hours after removal there were still some areas of retracted cells, and many of the cells displayed a weak von Willebrand's Factor (vWf) immunoreactivity. Surprisingly, after 63-65 hr many of the endothelial cells had become epithelioid in shape and the vWf immunoreactivity appeared increased. This epithelioid phenotype is currently considered typical of cultured vascular non-muscle-like cells and intimal thickening cells. By 5-7 days, the vast majority of cells in the monolayer had acquired an epithelioid morphology, showing a cobblestone appearance. These cells were significantly smaller than polygonal cells. Most importantly, they showed strong vWf immunoreactivity. At the edge of the monolayers we found that the majority of the cells had become epithelioid. Some of them detached from their neighbors and became round in shape and acquired mesenchymal characteristics, some expressing smooth muscle ␣-actin (SM ␣-actin). These findings demonstrate not only that embryonic endothelial cells that are transiently mechanically altered may change their phenotype to an epithelioid phenotype, but also that these cells may eventually transdifferentiate into mesenchymal cells expressing SM ␣-actin. Since some aspects of endothelial cell behavior have been shown to be regulated by locally released growth factors such as TGF␤ and FGF, we also investigated TGF␤-2 and -3 and bFGF expression. Presence of TGF␤-2 and -3 and bFGF-immunoreactive epithelioid and mesenchymal cells indicates that these growth factors may be involved in the changes described. Anat Rec Part A 270A: 67-81, 2003.

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Human eosinophil cationic protein enhances stress fiber formation in Balb/c 3T3 fibroblasts and differentiation of rat neonatal cardiomyocytes

et al. 2009

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We found that eosinophil cationic protein (ECP) stimulated the growth of mouse Balb/c 3T3 fibroblasts. ECP-treated 3T3 cells were more flattened and exhibited enhanced stress fiber formation. The enhancement of cytoskeleton after addition of recombinant ECP appeared stable and was able to inhibit disassembly of actin filaments that was induced by fibroblast growth factor-2. The ROCK inhibitor, Y-27632, abrogated this enhancement on stress fiber formation that was induced by ECP indicating the involvement of Rho/ROCK signaling pathway. The effect of ECP was assessed on the differentiation of primary cardiomyocytes derived from rat neonatal heart since the development of actin filaments is significantly related with organization of stress fibers. As the result, both beating rate and the expression of cardiac muscle specific markers such as atrial natriuretic factor were enhanced in the presence of ECP. Thus ECP may also function as a cardiomyocyte differentiation factor.

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FGF-2 Promotes Disassembly of Actin Cytoskeleton and Shape Changes in Murine Vascular Cells

Cited by 3 publications

References 9 publications

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

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

Mechanically altered embryonic chicken endothelial cells change their phenotype to an epithelioid phenotype

Human eosinophil cationic protein enhances stress fiber formation in Balb/c 3T3 fibroblasts and differentiation of rat neonatal cardiomyocytes

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