Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The apparent intensity of hyaluronan (HA) staining in tissue sections can vary as a function of fixation techniques. We examined the histochemical distribution of HA in normal human skin using an HA-specific binding peptide derived from bovine nasal cartilage. The HA, particularly in the dermis, was best preserved in sections fixed in 10% acid-formalin with 70% ethanol. In contrast, sections fixed in the routine 10% neutral-buffered formalin had a much weaker intensity of HA staining. Furthermore, acid-formalin/ethanol-fixed sections retained much of their apparent HA after incubation with saline, in contrast to the neutral formalin-fixed sections, in which most of the stainable HA was lost. Such marked differences in staining intensity were not observed in slides stained with Alcian blue, a procedure presumed to stain HA as well as other glycosaminoglycans. Staining using the HA binding peptide was entirely absent when sections were first preincubated in hyaluronidase, whereas similar Alcian blue-stained sections retained most of their staining intensity. Caution should be exercised in evaluating the distribution of HA in tissues using the HA binding peptide, particularly when different fixation techniques among several laboratories are being compared. In addition, the ability to evaluate the HA content of tissues using Alcian blue staining should be reconsidered. The sulfated glycosaminolglycans of the "ground substance" appear to be the predominant substrates for Alcian blue.
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PMID:Patterns of hyaluronan staining are modified by fixation techniques. 926 76

Hyaluronan (HA) is a polysaccharide component in the parenchyma and stroma of human esophageal squamous cell carcinoma (ESCC). Clinically, esophageal cancer represents a highly aggressive tumor type with poor prognosis resulting in a 5-year survival rate of 5%. The aim of the present study was the detailed analysis of the role of HA synthesis for ESCC phenotype in vitro using the ESCC cell line OSC1. In OSC1 cells, pericellular HA-matrix surrounding extended actin-dependent filopodia was detected. The small molecule inhibitor of HA synthesis, 4-methylumbelliferone (4-MU, 0.3 mm) caused loss of these filopodia and focal adhesions and inhibited proliferation and migration. In search of the underlying mechanism cleavage of focal adhesion kinase (FAK) was detected by immunoblotting. In addition, displacing HA by an HA-binding peptide (Pep-1, 500 mug/ml) and digestion of pericellular HA by hyaluronidase resulted in cleavage of focal adhesions. Furthermore, real-time reverse transcription PCR revealed that HA synthase 3 (HAS3) > HAS2 are the predominant HA-synthases in OSC1. Lentiviral transduction with shHAS3, and to a lesser extent with shHAS2, reduced intact FAK protein and filopodia as well as proliferation and migration. Furthermore, down-regulation by lentiviral shRNA of RHAMM (receptor of HA-mediated motility) but not CD44 induced loss of filopodia and caused FAK cleavage. In contrast, knockdown of both HA receptors inhibited proliferation and migration of OSC1. In conclusion, HA synthesis and, in turn, RHAMM and CD44 signaling promoted an activated phenotype of OSC1. Because RHAMM appears to support both filopodia, FAK, and the proliferative and migratory phenotype, it may be promising to explore RHAMM as a potential therapeutic target in esophageal cancer.
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PMID:Hyaluronan stabilizes focal adhesions, filopodia, and the proliferative phenotype in esophageal squamous carcinoma cells. 2046 12