Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental contact dermatitis has been induced in 2,4 dinitrochlorobenzene (DNCB) sensitized guinea pigs. The developing dermal infiltrate was excised and the infiltrating cells were obtained by mechanical extraction alone as well as by the combination with collagenase and elastase treatment. The most viable cells appeared in the elastase and mechanically extracted samples and the least in those subjected to mechanical treatment alone. The most cells in the enzyme-treated samples were present 24 h after re-exposure of the sensitized animals to DNCB consisting mainly of lymphocytes and of polymorphonuclear granulocytes. The optimum conditions for the action of enzymes including optimum duration of the treatment, buffer milieu, aspecific proteolytic effect on foreign substrate and action on T and B cell receptors have been elaborated. It was concluded that 80 min of collagenase treatment with gentle mechanical extraction under specified conditions does not affect any measurable immunologic properties of the liberated cells resulting in the second best yield. A comparison of these data with earlier reports and their significance is being discussed.
Arch Dermatol Res 1979 Mar 31
PMID:A new method for obtaining viable cells from dermal infiltrates. A study on 2,4 dinitrochlorobenzene induced contact dermatitis. 22 2

In 150 patients with different dermatoses and 15 controls the activity of collagen peptidase in serum was determined. No relation to specific skin diseases was found. Negative findings were also observed in the group of collagenoses: only 4 of 14 patients with progressive systemic sclerosis showed an increase of this enzyme activity. These negative results seem noteworthy because it thus is demonstrated that alterations of collagen structure are not necessaryly associated with alterations of collagen peptidase activity.
Arch Dermatol Forsch 1975
PMID:The behaviour of collagen peptidase in the serum of different dermatoses. 23 21

During keratinocyte maturation, individual cells undergo an orderly succession of biochemical and structural changes. In certain skin disorders alterations in keratinocyte numbers, volumes, and epidermal skin thickness occur. To assess such alterations and to provide base line values for normal human epidermis, a computer assisted histologic technique was developed. Skin biopsies were taken from normal skin on the forearm, back and thigh of 6 adult men. Whole specimens of epidermis were separated from the dermis with collagenase, fixed, stained, and mounted for microscopic examination. From the three dimensional coordinates of epidermal nuclei, epidermal cell volumes, surface density of epidermal cells, and epidermal thickness were determined. Measurement of cell volumes in this way compared favorably with electronic cell sizing of disaggregated epidermal cells in matched samples. The mean densities of nucleated cells per 10(4) mu2 surface area were 452, 483, and 487 for the forearm, back and thigh respectively. This technique will be used to make similar assessments in disorders of abnormal keratinocyte maturation.
J Invest Dermatol 1978 May
PMID:Counting and sizing of epidermal cells in normal human skin. 64 79

Human hair follicles were isolated from the scalp by dispase and collagenase treatment and dispersed into a cell suspension by trypsin. These cells proliferated well and could be subcultured 7 to 8 times. The medium used was MCDB 153 HAA medium further supplemented with some amino acids, hydrocortisone, insulin, EGF, and bovine brain extract. The concentration of Ca++ was adjusted to 0.1 mM. Immunohistochemically, these cells were proved to possess keratins specific to hair forming cells.
J Dermatol 1992 Nov
PMID:In vitro keratin expression of hair cells. 128 73

The effects of basic fibroblast growth factor (bFGF) and doxorubicin on cultured human skin fibroblasts were examined in order to determine their relevance to wound healing. bFGF is shown to stimulate fibroblast collagenase production per cell, and this effect in vitro seems to be one explanation for its efficacy in wound healing. Doxorubicin inhibited not only fibroblast proliferation but also collagen production by inactivating prolyl hydroxylase. This result may explain the reduced wound healing in patients undergoing treatment with doxorubicin. These studies indicate the importance of assessing the effects of growth factors on matrix metabolism in order to understand their roles in wound healing.
J Dermatol 1992 Nov
PMID:The effects of basic fibroblast growth factor and doxorubicin on cultured human skin fibroblasts: relevance to wound healing. 129 51

Pentoxifylline (PFN), analog of theobromine, which phenotypically and functionally alters various cell types including dermal fibroblasts, has been reported to inhibit tumor necrosis factor-alpha (TNF alpha) activation of neutrophils. We investigated the ability of PFN to alter constitutive and TNF alpha-induced biosynthetic activities of human normal dermal fibroblasts. The sixteenfold increase over constitutive intracellular 2'-5' oligo-adenylate synthetase (2'-5' A synthetase) activity induced by TNF alpha (400 U/ml) failed to occur when PFN (1 mg/ml) was added prior to cytokine treatment. This loss of biologic activity paralleled a reduction in 2'-5' A synthetase proteins and 2'-5' A synthetase-specific m-RNA. PFN failed to inhibit constitutive or TNF alpha-induced IL-6 hybridoma proliferative activity, IL-6 protein, or IL-6-specific m-RNA levels. The presence of PFN (1 mg/ml) in fibroblast cultures reduced constitutive synthesis of collagen and glycosaminoglycan (GAG) by 87% and 45%, respectively, and blocked induction of their synthesis by TNF alpha (10(4) U/ml). Total non-collagenous protein synthesis was not inhibited following PFN treatment (1 mg/ml). PFN did not inhibit TNF alpha induction of only those biosynthetic activities also susceptible to PFN in the constitutive state, with PFN failing to reduce constitutive collagenolytic activity but reducing TNF alpha-induced enhanced collagenolytic activity by 26% and collagenase m-RNA by 51%. Furthermore, PFN did inhibit, by 98%, TNF alpha-dependent murine and human fibroblast cytotoxicity. The selective nature of PFN inhibition of certain TNF alpha activities, the failure of PFN (1 mg/ml) to alter constitutive and TNF alpha-induced levels of type 1 and 2 TNF alpha receptor m-RNA, and the finding that PFN-treated fibroblasts express a similar number of receptors, of similar molecular weight and high affinity for TNF alpha as control, untreated cells, suggest that inhibitory activities of PFN are mediated at a locus other than receptors for TNF alpha.
J Invest Dermatol 1992 May
PMID:Pentoxifylline inhibits certain constitutive and tumor necrosis factor-alpha-induced activities of human normal dermal fibroblasts. 131 65

In order to identify structures in human skin that bind collagenase, sections from frozen or paraffin-embedded skin were incubated with either procollagenase or activated collagenase. After washing, bound procollagenase or collagenase was detected by immunofluorescence microscopy. In normal skin, procollagenase bound only to isolated granular dermal cells that were identified as mast cells on the basis of staining with fluoresceinated avidin and pinacyanol erythrosinate. When mast cells were degranulated by exposure to the ionophore A23187, extracellular granules bound procollagenase. Of various pathologic conditions examined, the highest binding of procollagenase occurred in specimens of urticaria pigmentosa. Procollagenase bound to granular cells and to abundant granules scattered throughout the dermis. Binding could be abolished by pre-treatment of tissue sections with heparinase or by pre-incubation of procollagenase with soluble heparin, suggesting that heparin is the binding agent in the granules. Activated collagenase also bound to dermal mast cells but in addition bound strongly to the dermal collagen. Enzymatic activity of activated collagenase was not inhibited by heparin in concentrations up to 10 mg/ml. There is evidence that mast cell tryptase can contribute to procollagenase activation. This study further supports a role for mast cells in collagenolysis by demonstrating that heparin from mast cells binds procollagenase and possibly serves as a reservoir for procollagenase, which may then subsequently be activated.
J Invest Dermatol 1992 May
PMID:Dermal mast cell granules bind interstitial procollagenase and collagenase. 137 47

The concept of mast cell heterogeneity has been studied extensively. Recently developed techniques to enzymatically disperse skin mast cells from human skin have shown that skin mast cells are somehow different from those of other organs such as lung and intestine. In this report, we have isolated and partially purified human skin mast cells from human neonatal foreskins by collagenase and hyaluronidase digestion. These mast cells are morphologically intact by histological, immunohistochemical and electron microscopic criteria. These human skin mast cells secrete histamine significantly (max. net histamine release, 20-30%) in a dose-related, temperature- and time-dependent fashion following stimulation with purified human C5a and C3a (over the ranges of 5 x 10(-8) M to 10(-7) M and 3 x 10(-7) M to 6 x 10(-6) M, respectively). On the other hand, interactions between human skin mast cells and other leukocytes have long been suspected of playing a very important role in cutaneous inflammation. Recently, a human neutrophil-derived histamine-releasing activity termed HRA-N was partially purified. HRA-N has been shown to cause human and rat basophil leukemia cells to degranulate. This study was also undertaken to assess the ability of HRA-N to directly induce histamine release from isolated human skin mast cells. HRA-N causes dose- and time-dependent histamine release as do human anaphylatoxins. These results suggest that HRA-N may lead to a better comprehension of allergic and inflammatory reactions and their modulation in the skin.
J Dermatol 1992 Jan
PMID:The effect of human anaphylatoxins and neutrophils on histamine release from isolated human skin mast cells. 137 10

Three patients with severe recessive dystrophic epidermolysis bullosa were treated with oral phenytoin and palliative and supportive measures for variable periods. Their progress was compared with that of three milder cases managed only with palliative and supportive measures. The phenytoin-treated group showed marked decrease in blister count, increase in trauma tolerance, a rise in hemoglobin level, and considerable weight gain. The results support earlier reports that collagenase inhibitors are useful in controlling blister formation in recessive dystrophic epidermolysis bullosa.
Int J Dermatol 1992 Oct
PMID:Recessive dystrophic epidermolysis bullosa treated with phenytoin. 139 6

This study was designed to investigate the biochemical mechanisms responsible for the connective tissue changes seen in actinically damaged skin, which is characterized histologically by diminution and ultrastructural alterations of collagen fibrils and deposition of elastotic material in the papillary dermis. We hypothesized that ultraviolet light could stimulate synthesis of interstitial collagenase in the skin, resulting in collagen degradation. Monolayer cultures of human fibroblasts or keratinocytes were irradiated with ultraviolet A (UVA) or ultraviolet B (UVB) radiation and interstitial collagenase or its inhibitor, TIMP (tissue inhibitor of metalloproteinases) assessed in the conditioned medium with Western immunoblots 24 h after irradiation. Northern blot analysis of the irradiated fibroblasts with a cDNA probe representing collagenase was also performed. Cell viability was greater than 90% with all doses of UV radiation studied. A dose-related increase in immunoreactive collagenase was detected in the medium of fibroblasts irradiated with 0-10 J/cm2 of UVA radiation as well as a parallel increase in the collagenase mRNA in the irradiated cells. UVA radiation stimulated collagenase synthesis in both neonatal and adult fibroblasts. TIMP production in UVA-irradiated fibroblasts increased to a lesser degree than did collagenase and its increase did not parallel the increase in collagenase. UVB (0-100 mJ/cm2) did not stimulate collagenase production by fibroblasts. In contrast to the stimulation of collagenase production by fibroblasts, a slight decrease in immunoreactive collagenase was seen in UVA-irradiated keratinocytes. These data suggest that direct stimulation of collagenase synthesis by human skin fibroblasts by UVA radiation may contribute to the connective tissue damage induced by ultraviolet radiation leading to photoaging.
J Invest Dermatol 1992 Oct
PMID:Ultraviolet A irradiation stimulates collagenase production in cultured human fibroblasts. 140 2


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