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Vincent C. Hascall

Researcher at Cleveland Clinic

Publications -  206
Citations -  13815

Vincent C. Hascall is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Hyaluronic acid & Proteoglycan. The author has an hindex of 64, co-authored 193 publications receiving 12685 citations. Previous affiliations of Vincent C. Hascall include Abbott Northwestern Hospital & Shriners Hospitals for Children.

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Hyaluronan matrices in pathobiological processes

TL;DR: This article focuses on the discovery in recent studies that many cell stress responses initiate the synthesis of a monocyte‐adhesive hyaluronan extracellular matrix, which forms a central focus for subsequent inflammatory processes that are modulated by the dialogue between the matrix and the inflammatory cells.
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Role of UDP-N-Acetylglucosamine (GlcNAc) and O-GlcNAcylation of Hyaluronan Synthase 2 in the Control of Chondroitin Sulfate and Hyaluronan Synthesis

TL;DR: It is found that HAS2, the main synthase in aortic smooth muscle cells, can be O-GlcNAcylated on serine 221, which strongly increased its activity and its stability, and could explain the elevated matrix HA observed in diabetic vessels.
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Characterization of chondroitin sulfate isolated from trypsin-chymotrypsin digests of cartilage proteoglycans

TL;DR: The data in sum indicate that peptide fragments which contain from 1 to 8 polysaccharide chains are released when the proteoglycans are digested with trypsin-chymotrypsin digestion, which indicates that some peptides contain large numbers of keratan sulfate chains.
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Coding sequence, exon-intron structure and chromosomal localization of murine TNF-stimulated gene 6 that is specifically expressed by expanding cumulus cell-oocyte complexes.

TL;DR: Since TSG-6 binds to hyaluronan and interacts with inter-alpha-trypsin inhibitor (IalphaI), molecules that are essential for matrix formation by COCs, this protein may have a structural role in the matrix or may enhance the antiproteolytic effect of IalphaI to protect the matrix from degradation.
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Proinflammatory Cytokines Induce Hyaluronan Synthesis and Monocyte Adhesion in Human Endothelial Cells through Hyaluronan Synthase 2 (HAS2) and the Nuclear Factor-κB (NF-κB) Pathway

TL;DR: This study used human umbilical chord vein endothelial cells (HUVECs) as a model to study the mechanism that regulates hyaluronan synthesis after treatment with proinflammatory cytokines, and found that interleukin 1β and tumor necrosis factors α and β, but not transforming growth factors β and α, strongly induced HA synthesis by NF-κB pathway.