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)

Radiological and histological studies were made on retinoid-induced hyperostosis in rats. Vitamin A (VA) was administered intraperitoneally in rats for 6 months. Hyperostosis was observed in 94 percent of rats administered VA and in 38 percent of the control. Chondrocytes and vascular proliferation were observed in the attachment of the tendons and in the anterior corner of the vertebral body after 3 months. Hyperostosis was observed as osteophytes in the attachment of ligaments or tendons and as heterotopic ossification in the tendons or the joint capsules of the whole body after 6 months. Immature cells were observed around the osteophytes. These areas were stained with pH 4.1 toluidine blue and disappeared following streptomyces hyaluronidase treatment. This would indicate that hyaluronic acid increased around these areas. These results appear to demonstrate that hypervitaminosis A is capable of producing hyperostosis.
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PMID:[Experimental study of hyperostosis induced by hypervitaminosis A]. 128 Feb 97

The effects of all-trans retinoic acid on glycosaminoglycan (GAG) accumulation were determined in cultured primary human skin fibroblasts. Confluent cultures treated with retinoic acid accumulated less [3H]GAG than those without the compound, an effect with an apparent threshold of 10 nM which was dose dependent in the concentration range tested (0-10 microM). At 10 microM, the inhibition was 54%. Greater than 80% of the labeled macromolecular material was streptomyces hyaluronidase digestible in cultures labeled with [3H]acetate. The incorporation of H2[35S]O4 into chondroitin sulfate and dermatan sulfate was unaffected, as was total protein synthesis. Retinol also inhibited accumulation of [3H]GAG, but was far less potent. T3 and dexamethasone can inhibit [3H]hyaluronate synthesis. When retinoic acid was added to cultures treated with either of these hormones at concentrations that maximally inhibit [3H] GAG accumulation, there was a further decrease in the rate of macromolecular accumulation. The retinoic acid effect evolved over 24-48 h after addition to the culture medium. A pulse-chase study failed to demonstrate any effect on [3H]GAG degradation.
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PMID:Retinoic acid inhibition of hyaluronate synthesis in cultured human skin fibroblasts. 230 23

Immediate steps in the treatment of ureteral stone, beginning with the often acute onset, are relief of pain, urinalysis (including Gram stain), forcing fluids, examination of urine for the stone and urography at the earliest feasible time. If the stone causes continual pain or appears unlikely to be passed safely, it should be removed-with a cystoscope if possible; if not, by operation which may be done while the patient is still under anesthesia. To combat further stone formation a large fluid intake should be maintained, the extracted stone analyzed, an acid ash diet prescribed, serum calcium and phosphorus measured, urinary stasis corrected and urinary infection and distant foci of infection cured. Vitamin A, aluminum gels and particularly hyaluronidase appear promising as preventives to stone formation.
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PMID:Management of patients with ureteral stone. 1301 10

Numerous wrinkles are observed in the skin of streptozotocin (STZ)-induced type 1 diabetic rats, which are similar to those seen in vitamin A-deficient (VAD) rats. Retinoic acid (RA), the active form of vitamin A, promotes the production of collagen in dermis and induces cell growth and inhibition of epidermal differentiation in skin tissues. Normal skin function is maintained by the extracellular matrix (ECM)-degrading enzymes, matrix metalloproteinase (MMP) and hyaluronidase (HAase). This study is the first comparison of MMP and HAase activities in skin tissues of type 1 diabetic, VAD and RA-treated animal models. In skin tissues of type 1 diabetic and VAD rats or VAD mice, both MMP-2 and HAase activities increased as compared with controls. In contrast, MMP and HAase activities were reduced in the skin tissues of RA-treated mice. Blood retinol levels in type 1 diabetic rats were lower than controls. These results indicate a close relationship between type 1 diabetes and vitamin A-deficiency on MMP and HAase in skin tissues, suggesting that type 1 diabetic rats could be vitamin A-deficient. Vitamin A-derived RA might be a significant regulator of ECM-degrading enzyme expression and diabetic symptoms.
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PMID:A close relationship between type 1 diabetes and vitamin A-deficiency and matrix metalloproteinase and hyaluronidase activities in skin tissues. 2185 36