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The effect of hyaluronate and its oligosaccharides on endothelial cell proliferation and monolayer integrity

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Abstract

Hyaluronidase treatment of hyaluronic acid produced a series of oligosaccharides. Those between 3 and 16 disaccharides in length stimulated angiogenesis in vivo and the proliferation of tissue cultured endothelial cells in vitro. This effect appears to be cell type specific, as no stimulation of fibroblasts or smooth muscle cells was observed. Endothelial cells were found to endocytose both high- and low-molecular-mass hyaluronate, which might be receptor mediated. Fibroblasts and smooth muscle cells, cultured under the same conditions, showed negligible uptake of hyaluronate. Thus, the cell-specific effects may be due to the differences in internalization of hyaluronate. High-molecular-weight hyaluronate both inhibited endothelial cell proliferation and disrupted newly formed monolayers. These data are consistent with the ability of hyaluronate to inhibit new blood vessel formation in vivo and also suggest that hyaluronate metabolism plays a pivotal role in the regulation of angiogenesis.

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      As a glycosaminoglycan, hyaluronic acid has angiogenic effect depending its molecular weights. The low molecular weight enhances the proliferation and migration of endothelial cells, while the high molecular HAs inhibit angiogenesis (Sattar et al., 1994; West and Kumar, 1989). Hydrogels which can be chemically modified from HA are biocompatible with micropores and can retain and release angiogenic growth factors in vivo (Hosack et al., 2008).

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