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)

Immunohistochemical studies of the hyaluronan (HA)-receptor (R), originally found on liver endothelial cells (LEC) and related to the intercellular adhesion molecule 1 (ICAM-1), showed that polyclonal antibodies against HARLEC (HA receptor on LEC) also stain structures in mouse mastocytomas, mainly vessels. To test if intravenously administered HA might target the tumour receptors in vivo, mice carrying an inoculated mastocytoma in one hind leg muscle were injected in the tail vein with 125I-tyrosine (T)-labelled HA and killed 75 min after injection when organs and tissues were checked for radioactivity. When doses exceeding the binding capacity of the liver were injected, a significant increase in radioactivity (up to five-fold) within the tumour tissue was found. The weight adjusted difference between control and tumour tissue was greater for smaller tumours, probably due to necrosis in the larger. HA-staining of tumours from animals receiving 125I-T-HA, showed HA in areas that also stained weakly for ICAM-1 using monoclonal antibodies. ICAM-1 staining was dramatically increased after hyaluronidase treatment of the sections, indicating that the HA is bound to these receptors and thereby blocks antibody recognition.
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PMID:Accessible hyaluronan receptors identical to ICAM-1 in mouse mast-cell tumours. 749 49

Asthma is a disease of airway inflammation and hyperreactivity that is associated with a lymphocytic infiltrate in the bronchial submucosa. The interactions between infiltrating T lymphocytes with cellular and extracellular matrix components of the airway and the consequences of these interactions have not been defined. We demonstrate the constitutive expression of CD44 on human airway smooth muscle (ASM) cells in culture as well as in human bronchial tissue transplanted into severe combined immunodeficient mice. In contrast, basal levels of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) expression are minimal but are induced on ASM by inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha). Activated, but not resting T cells, adhere to cultured ASM; stimulation of the ASM with TNF-alpha enhanced this adhesion. Adhesion was partially blocked by monoclonal antibodies (mAb) specific for lymphocyte function-associated antigen 1 (LFA-1) and very late antigen 4 (VLA-4) on T cells and ICAM-1 and VCAM-1 on ASM cells. The observed integrin-independent adhesion was mediated by CD44/hyaluronate interactions as it was inhibited by anti-CD44 mAb 5F12 and by hyaluronidase. Furthermore, the adhesion of activated T lymphocytes induced DNA synthesis in growth-arrested ASM cells. Thus, the interaction between T cells and ASM may provide insight into the mechanisms that induce bronchial inflammation and possibly ASM cell hyperplasia seen in asthma.
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PMID:T lymphocytes adhere to airway smooth muscle cells via integrins and CD44 and induce smooth muscle cell DNA synthesis. 752 Apr 73

Histochemical stainings of frozen sections of human normal and psoriatic skin were used to study the localization of hyaluronan (HA) and intercellular adhesion molecule 1 (ICAM-1). HA staining was found in all areas of the skin, with the exception of the stratum corneum, in both normal and psoriatic cases without any apparent quantitative differences between the conditions. The staining for ICAM-1 was detected in vessels in normal skin and at lower levels in normal areas of the skin in patients with psoriasis. However, in these patients the staining increased to about the same level as in normal skin after hyaluronidase treatment of the sections prior to staining. In psoriatic lesions, distinct staining for ICAM-1 was localized mainly to vessels and infiltrating leukocytes. Treatment of the sections with hyaluronidase increased the staining of vessels only slightly, but more strongly around leukocytes. These findings show that ICAM-1 is predominantly free from bound HA on vessel endothelium in psoriasis lesions but not on vessels in normal areas of the skin, and suggests that systematically administered HA, previously shown to reduce chronic inflammation in animal models, might have a beneficial effect in psoriasis via blocking of endothelial ICAM-1 and thereby causing a reduced invasion of leukocytes into the skin.
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PMID:Histochemical studies of hyaluronan and the hyaluronan receptor ICAM-1 in psoriasis. 886 47