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)

Selective destruction of connective tissue may be a useful therapeutic tool in conditions associated with abnormal deposition of scar tissue. We have investigated intradermal injections of clostridial collagenase and bovine testicular hyaluronidase alone and in combination in Yucatan miniature hairless pigs. Collagenase in combination with hyaluronidase was quite efficient at destroying the connective tissue matrix, although elastic tissue appeared to be completely spared. Collagenase alone at higher doses degraded collagen, but hyaluronidase had little effect on connective tissue architecture.
Br J Dermatol 1986 Oct
PMID:Degradation of porcine dermal connective tissue by collagenase and hyaluronidase. 302 82

Patients diagnosed as suffering from erysipelas or cellulitis were subjected to bacteriological and serological investigations. The serological tests used included the anti-streptolysin O reaction (ASO), the anti-deoxyribonuclease B test (ADB) and the anti-hyaluronidase tests (AHT) that are specific both for the group A streptococcus (Streptococcus pyogenes) and for the human pyogenic streptococci of group C or group G. Antibody tests to the alpha-lysin and the nuclease of Staphylococcus aureus were also employed. Conventional bacteriological culture methods were used plus needle aspiration of injected saline in most patients with erysipelas, but recognized pathogens were isolated in only 42% of cases. Our results indicate the limitations of these tests for making initial diagnoses and deciding treatment. Serial serological testing was very successful in differentiating cellulitis due to group A, C or G haemolytic streptococci, or occasionally Staphylococcus aureus, but was positive in only 40% of cases of erysipelas.
Br J Dermatol 1985 May
PMID:The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. 400 55

Frozen sections of newborn rat skin were treated with a variety of buffers, enzymes, and proteinase inhibitors in order to modify the reactivity of antigenic sites of histidine-rich protein and keratin. By indirect immunofluorescence, we found that antiserum to histidine-rich protein purified from granular cells reacted with keratohyalin granules but not cornified cells treated with hyaluronidase. The same antiserum reacted less distinctly with keratohyalin granules treated with neuraminidase; in contrast, it showed strong reactivity in cornified cells after the neuraminidase digestion. However, the enzyme digestions did not unmask the antigenic site(s) of keratohyalin granules to anti-keratin serum, as did saline in 0.1 M Tris-HCl buffer, pH 8.0. These results suggest that the antigenic site of histidine-rich protein is masked in keratohyalin granules by different mechanisms from the masking of keratin. Histindine-rich protein may be masked primarily with hyaluronic acid in keratohyalin granules, but the sugar moiety appears to be changed to sialic acid in cornified cells.
J Invest Dermatol 1981 Jun
PMID:Effects of hyaluronidase and neuraminidase on immunoreactivity histidine-rich protein in newborn rat epidermis. 616 81

Fourteen patients with necrotizing fasciitis are described. In thirteen the cause was Streptococcus pyogenes [Group A beta haemolytic streptococcus (BHS)]; in the fourteenth, Staphylococcus aureus was responsible. In the acute fulminating form of the disease, BHS can be cultured from the affected tissues. In the less acute form, particularly when the patient has been previously treated with antibiotics, other bacteria colonize the tissues and the BHS cannot be isolated. Serological evidence of infection with Streptococcus pyogenes can be ascertained in all such patients by finding high levels of anti-desoxyribonuclease B and anti-hyaluronidase. Measurement of the anti-streptolysin O titre is not helpful. Once the diagnosis is made, surgical removal of all necrotic tissue is still the treatment of choice.
Br J Dermatol 1983 Jul
PMID:The value of bacteriology and serology in the diagnosis of necrotizing fasciitis. 634 5

A recently described mammalian wound hyaluronidase is successfully characterized and partially purified in the current study. Peak enzyme activity occurred on postwound day 7, pH optimum 4.5. Both crude and purified wound enzyme exhibited endoglycosidic activity against hyaluronate and chondroitin-4-sulfate but not against chondroitin-6-sulfate or dermatan sulfate. A 5.3-fold increase in activity was obtained by the DEAE-Sephadex purification technique described. Polyacrylamide gel electrophoresis yielded a single major band near the gel's midrange and one minor band of lesser electrophoretic mobility. These enzyme characteristics support a biochemical analogy between tissue repair in skin and numerous developmental systems and may also provide a simple means for enzymatic differentiation among chondroitin sulfate isomers.
J Invest Dermatol 1982 Dec
PMID:Identification, characterization, and partial purification of mammalian skin wound hyaluronidase. 714 44

Scanning electron microscope findings of solar elastosis were compared with those of normal dermis in specimens digested by hyaluronidase and by autoclaving. Solar elastosis showed amorphous masses and broad fibres with irregular shapes and sizes in specimens digested by hyaluronidase, while it showed only fibrous structures in those after autoclaving. It is suggested that the origin of solar elastosis is elastic tissue.
Br J Dermatol 1980 Sep
PMID:Scanning electron microscope studies of solar elastosis. 742 27

Previously, we have shown that CD44 (the hyaluronan receptor) was involved in the degradation of hyaluronan. In the present study, we examined the distribution of CD44 and hyaluronan in the skin of embryonic and mature mice. During embryonic development, CD44 was prominently expressed by the condensed mesenchymal cells involved in the formation of the hair follicles, but was absent from the surrounding interstitial cells. The cells of the dermal condensation expressed CD44 throughout the development of the hair follicle; however, once the hair follicle reached maturity, the mesenchymal cells of the dermal papilla no longer expressed this molecule. In contrast to the above, the distribution of hyaluronan was reversed from that of CD44. Hyaluronan was widespread throughout the embryonic dermis, but was conspicuously absent from the regions of the dermal condensation. This arrangement persisted through the development of the hair follicle; however, in the mature hair follicle, hyaluronan reappeared in the dermal papilla. Thus, in the embryonic dermis, the expression of CD44 and hyaluronan were complementary to each other. However, in the adult skin, only minor changes were detected in the levels of CD44 and hyaluronan associated with the cells of the dermal condensation during the hair cycle. When organ cultures of embryonic mouse skin were treated with Streptomyces hyaluronidase, the interstitial mesenchymal cells became compacted, indicating that the removal of hyaluronan leads to the condensation of these cells. The results of this study are consistent with the hypothesis that the expression of CD44 by the inductive mesenchymal cells allows them to degrade hyaluronan in a localized region, leading to formation and maintenance of the dermal condensation.
J Invest Dermatol 1993 Dec
PMID:Hyaluronan is inversely correlated with the expression of CD44 in the dermal condensation of the embryonic hair follicle. 750 26

A proposed role for antigen-presenting dermal dendrocytes in the pathogenesis of many dermal inflammatory skin diseases remains speculative. We therefore sought to determine the phenotype and functional characteristics of antigen-presenting cells isolated from normal human dermis. Normal adult human skin was incubated overnight with dispase at 4 degrees C, the epidermis was removed, and the residual dermal preparation was then minced and digested with a mixture of hyaluronidase, collagenase, and DNAase at 37 degrees C, prior to filtration through mesh. Dermal cell suspensions thus obtained were stained using specific monoclonal antibodies, and analysed by fluorescence microscopy or flow cytometry. Mean values were as follows: CD45+ leucocytes 39%, HLA-DR+ cells 39%, Ulex europaeus agglutinin I+ endothelial cells 26%, CD1a+ cells 3.9%, CD11b+ cells 16%, CD11c+ cells 6%. Mitomycin C-treated crude dermal cell suspensions induced allostimulation of peripheral blood mononuclear cells in a 7-day culture, as assessed by 3H-TdR incorporation. Depletion of CD1a+ Langerhans-like cells from the dermal cell preparation, by 95, 74 and 90% in three separate experiments using immunomagnetic beads, reduced 3H-TdR incorporation at optimal responder-to-stimulator cell ratios by 90, 64, and 87%, respectively. Our findings suggest that, in normal human dermis, the great majority of the alloantigen-presenting capacity resides in the CD1a+ Langerhans cell-like dendritic antigen-presenting cell population, and not to any great extent in either CD1a- macrophage-like cells, or HLA-DR+ endothelial cells. The relationship of the CD1a+ dermal antigen-presenting cells to the Langerhans cell lineage remains to be determined.
Br J Dermatol 1994 Jul
PMID:Antigen-presenting capacity in normal human dermis is mainly subserved by CD1a+ cells. 754 20

We have identified a novel ligand for CD44, a cell surface glycoprotein implicated in tumor metastasis and lymphocyte homing. When the mouse T cell line CTLL-2 was transfected with cDNA encoding a hemopoietic form of mouse CD44, CTLL-2 cells exhibited a new self-adhesive phenotype, forming large aggregates. The aggregation was blocked by neutralizing anti CD44 monoclonal antibody but unaffected by hyaluronidase, indicating the involvement of CD44 and its non-hyaluronate ligand in the cell aggregation. The ability to induce CD44-dependent aggregation was found in culture supernatants of CTLL-2 and its CD44 transfectants. The use of CD44-immunoglobulin chimeric protein revealed that CTLL-2 and its transfectants synthesized a large-molecular weight protein (gp600) which bound specifically to CD44. The gp600 was readily labeled with radioactive sulfate, and treatment of gp600 with chondroitinase ABC or ACII generated a lower molecular weight species (18-22 kDa), suggesting that gp600 consists of a small core protein with chondroitin sulfate glycosaminoglycan side chains. However, binding of CD44 to glycosaminoglycans such as chondroitin 4-sulfate, chondroitin 6-sulfate, and dermatan sulfate was undetectable, suggesting either that a novel chondroitin-type glycosaminoglycan is recognized by CD44 or that a particular configuration of the glycosaminoglycan is required for recognition by CD44.
J Dermatol 1994 Nov
PMID:A sulfated proteoglycan as a novel ligand for CD44. 2292 40

Collagen was isolated from human placenta by pepsin digestion and salt precipitation. This collagen was similar in its electrophoretic mobility and immunological reactivity with monoclonal antibody to form B of type VI collagen in the literature (Trueb B, Schreier T, Bruckner P and Winterhalter K. 1987. Eur. J. Biochem. 166: 699-703). We prepared polyclonal rabbit antiserum against alpha 2 chain of type VI collagen and performed an immunohistochemical study using this polyclonal antibody. It reacted in fat tissue and around vessels and peripheral nerves in normal human skin. To confirm the presence of type VI collagen in fat tissue, we isolated collagen from human subcutaneous tissue. This collagen showed a similar pattern in polyacrylamide gel electrophoresis with that from human placenta and cross-reacted with monoclonal or polyclonal antibody against type VI collagen. By immunohistochemical staining, abundant type VI collagen was observed in the septum of subcutaneous fat tissue in morphea or systemic sclerosis. In the mild hyalinizing areas or after treatment with 6M urea or hyaluronidase in highly hyalinized areas, the staining of type VI collagen increased. These data suggest that the amount of type VI collagen in subcutaneous tissue is involved in the early phases of these fibrosing disorders and that type VI collagen accumulates even more in hyalinizing tissue in late phases of these diseases.
J Dermatol 1995 Jul
PMID:Human type VI collagen: purification from human subcutaneous fat tissue and an immunohistochemical study of morphea and systemic sclerosis. 756 Apr 37


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