Influence of polyethylene terephthalate on the release of growth factors by human endothelial cells

Cenni, E.; Verri, E.; Granchi, Donatella; Gamberini, Simonetta; Corradini, Alessandra; Leo, Alessandro Di; Montanaro, Lucio; Pizzoferrato, Alberto

doi:10.1163/156856299x00513

Cited by 6 publications

(1 citation statement)

References 36 publications

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“…However, most of them do not occur physiologically and, therefore, might be only artificial. Such "nonphysiological" stimuli are UV light treatment (34), physico-mechanical treatments (like freeze-thawing, sonication, scrape-loading, or balloon catheter de-endothelialization) (10,(35)(36)(37)(38)(39), high density culture (40), and culture on artificial substrates (like polyethylene terephthalate or polytetrafluoroethylene) (41)(42)(43)(44). In vivo, one common and accepted hypothesis proposes that so called "sublethal" membrane disruptions may be responsible for the cellular bFGF release, which led to the idea that bFGF represents a kind of "wound hormone" (37).…”

Section: Discussionmentioning

confidence: 99%

Shear Stress-induced Release of Basic Fibroblast Growth Factor from Endothelial Cells Is Mediated by Matrix Interaction via Integrin αVβ3

Gloe¹,

Sohn²,

Meininger³

et al. 2002

Journal of Biological Chemistry

102

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Considering that chronic elevation of shear stress results in remodeling of the vasculature, we analyzed whether mechanical load could mediate basic fibroblast growth factor (bFGF) release and whether bFGF would act as mediator of shear stress-induced endothelial proliferation and differentiation. Supernatant media of shear stress-exposed endothelial cells (EC) contained significantly higher amounts of bFGF than medium from static cells. Released bFGF was fully intact with regard to its function as an inductor of proliferation and differentiation. Shear stress-conditioned media induced capillary-like structure formation, whereas static control medium did not. Likewise, only shear stress-conditioned medium induced proliferation of serum starved EC. Both capillary-like structure formation and proliferation could be inhibited by neutralization of bFGF or its receptor. The release of bFGF was subject to specific, integrin-mediated control, since inhibition of ␣ v ␤ 3 integrin prevented it, whereas inhibition of ␣ 5 ␤ 1 integrin had no effect. We conclude that shear stress induces the release of bFGF from EC in a tightly controlled manner. The release is dependent on specific cell-matrix interactions via ␣ v ␤ 3 integrins. The effects on cell proliferation and differentiation suggest that release of bFGF is functionally significant and may represent a necessary initial step in adaptive remodeling processes induced by shear stress.Chronic physical exercise leads to increases in the diameter of existing vessels as well as the formation of new vessels (angiogenesis), thereby enhancing the total number of vessels in the skeletal muscle (1-6). It is believed that shear stress represents an important stimulus for these vascular events. However, little is known about the mechanism of mechanosensing (the initial step) or about potential mediators involved in this shear stress response. Some growth factors controlling angiogenesis have similar vascular effects as shear stress. They are involved in a regulated time sequence of cell migration, proliferation, differentiation, and apoptosis. Therefore, growth factors might be sufficient to induce remodeling processes per se (3,7,8).In particular the basic fibroblast growth factor (bFGF) 1 may play a pivotal role in vascular remodeling. Several investigators have reported a critical participation of this cytokine in new vessel formation (4, 5, 9 -13). The expression of bFGF is not affected at the transcription level by shear stress, hypoxia, or hypertension (14), all of which have been shown to stimulate angiogenesis (3, 6), but bFGF is stored at significant concentrations within the endothelium and could well be released in amounts sufficient to initiate angiogenesis after exposure to high shear stress. Therefore, we hypothesized that shear stress could serve as an adequate stimulus for the release of bFGF from endothelial cells and that bFGF could function as a mediator of shear stress-induced angiogenesis. Because many investigators are claiming that part of the mechano-sensing...

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