Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.37 (neutrophil elastase)
 4,078 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hairless (SKH-1) mice were mated with beige (C57BL/bb) mice to produce a hairless mouse deficient in neutrophil elastase (hhbb). These mice were exposed to 0.09 J UVB radiation for 5 months to see if neutrophil elastase was an important factor in the development of solar elastosis. Analysis of peritoneal neutrophils confirmed that the hhbb mouse was deficient in elastase, retaining only 10% of the activity of the normal littermates (hhHb). Skin myeloperoxidase activity was equally elevated in all the mice receiving UVB indicating a similar influx of inflammatory cells. The absolute breaking strength of the skin in both the hhBb and hhbb mice was not altered by UVB treatment over the 5 month exposure period. Elastin quantitated biochemically as desmosine, or visualized histologically, was increased following UVB exposure in the normal mice. In the elastase-deficient mice, however, the elastin fibres appeared to be unaffected by exposure to UVB radiation at this level. The results suggest that neutrophil elastase is an important mediator in the development of solar elastosis resulting from continued exposure to UVB.
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PMID:A role for neutrophil elastase in solar elastosis. 857 66

In this study we investigated whether a reduction in neutrophil elastase activity in mice would alter the development of ultraviolet B or chemically induced skin tumors. A mutant strain of neutrophil elastase-deficient mice was developed by crossing beige mice with SKH 1 hairless mice. Ultraviolet irradiation three times per week for 20 wk developed an average of 10 tumors per normal mouse, whereas elastase-deficient hairless mice receiving the same treatment developed only 0.4 tumors per mouse. Benzopyrene administered topically for 20 wk resulted in an average of seven tumors per control mouse, while similar treatment to elastase-deficient hairless mice reduced the tumor count to 0.2 per mouse. Two small molecular weight elastase inhibitors, which were shown to inhibit mouse neutrophil elastase, were administered subcutaneously to normal SKH-1 mice during 16 wk of ultraviolet B exposure. Both inhibitors significantly reduced the incidence of ultraviolet B-induced tumors. When control and elastase-deficient mice were immunized with 2,4,6-trinitrochlorobenzene and oxazolone, both molecules elicited a significant contact hypersensitivity response. Ultraviolet B irradiation prior to immunization at a nonirradiated site completely suppressed the induction of contact hypersensitivity in both the normal and the deficient mice, suggesting that prevention of systemic immunosuppression was not the reason for the resistance to skin tumors observed in the elastase-deficient mice. The results suggest that neutrophil elastase can be an important factor in squamous cell tumor development.
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PMID:Inhibition of neutrophil elastase suppresses the development of skin tumors in hairless mice. 875 56

Neutrophil infiltration and epidermal hyperproliferation are major histopathologic changes observed in psoriasis. Neutrophils contain human leukocyte elastase, which is thought to be released during neutrophil infiltration of the epidermis. As active human leukocyte elastase is known to be present in psoriatic lesions we were interested whether human leukocyte elastase induces hyperproliferation in keratinocytes in vitro and in vivo. In the cultured murine keratinocyte cell line PAM-212 concentrations of human leukocyte elastase from 1 to 30 nM induced significant proliferation as determined by 5-bromo-2'-deoxy-uridine-incorporation. Daily topical application of 0.043-434.8 pmol human leukocyte elastase per cm2 skin on hairless mice induced a concentration-dependent epidermal hyperproliferation and an increase in 5-bromo-2'-deoxy-uridine incorporation of up to 5-fold in basal keratinocytes within 3 d. Hyperproliferation resulted in a up to 2-fold increase of keratinocyte layers. Histologic analysis revealed marked vasodilatation but no inflammatory infiltrate. Application of porcine pancreatic elastase (3-300 pmol per cm2 skin) resulted in similar epidermal changes as observed for human leukocyte elastase. Hyperproliferative effects of human leukocyte elastase in vitro and in vivo were abolished by the addition of elastase inhibitors, such as elafin, anti-leukoprotease, and alpha1-protease inhibitor. In summary, human leukocyte elastase induces proliferation in murine keratinocytes in concentrations, which can be found on the skin surface of psoriatic lesions. These results may provide an explanation for the epidermal hyperproliferation observed in psoriasis.
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PMID:Human leukocyte elastase induces keratinocyte proliferation in vitro and in vivo. 1185 75

Hairless (SKH-1) mice were mated with Beige (C57B/bb) mice to produce a hairless mouse deficient in neutrophil elastase (hhbb). These mice were exposed to 0.09J UVB irradiation for 5 months to see if neutrophil elastase was an important factor in elastin remodeling and development of solar elastoses. Analysis of peritoneal neutrophils confirmed that the hhbb mouse was deficient in elastase, retaining only 10% as much activity as the normal littermates (hhHb). Skin MPO activity was equally elevated in all the mice receiving UVB suggesting an equal influx of inflammatory cells. The absolute breaking strength of the skin in both the hhBb and hhbb mice was not altered by UVB treatment over the 5 month exposure period. Elastin quantitated biochemically as desmosine, or visualized histologically, was increased following UVB exposure in the normal mice. In the elastase deficient mice, however, the elastin fibers appeared to be unaffected by exposure to UVB irradiation at this level. The results suggest that neutrophil elastase is an important mediator in the development of solar elastosis resulting from continued exposure to UVB irradiation.
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PMID:A role for neutrophil elastase in the progression of solar elastosis. 1561 29