Abnormalities in adenyl cyclase in psoriasis, a hyperproliferative skin disease
| Autor: | Mei Mei Mui, Kenneth M. Halprin, Reba K. Wright Hurst, S.L. Hsia |
|---|---|
| Rok vydání: | 1974 |
| Předmět: |
Cancer Research
medicine.medical_specialty Epinephrine Uninvolved skin Human skin Cyclase Fluorides Psoriasis Internal medicine Cyclic AMP Genetics medicine Humans Molecular Biology Incubation Skin chemistry.chemical_classification Epidermis (botany) medicine.disease Lipids Kinetics Glucose Enzyme Endocrinology chemistry Molecular Medicine Cell Division Adenylyl Cyclases medicine.drug |
| Zdroj: | Advances in Enzyme Regulation. 12:205-216 |
| ISSN: | 0065-2571 |
| DOI: | 10.1016/0065-2571(74)90015-6 |
| Popis: | Adenyl cyclase was demonstrated in slices of human skin and in the 650 × g pellet of skin homogenates. The slices were obtained with a keratome, and consisted mostly of epidermis. After the incubation of the slices with [ 3 H] adenine, 3 H was found in cyclic AMP. The accumulation of 3 H in cyclic AMP was enhanced 10–35-fold by the addition of 3.3 μ m epinephrine to the incubation medium, and could also be enhanced up to 4-fold by 10 m m NaF. In skin homogenates, adenyl cyclase was assayed by the formation of [ 32 P] cyclic AMP from [α- 32 P] ATP. More than 70% of the enzyme was found associated with the 650 × g pellet. The enzyme in the membrane preparation had an apparent K m for ATP of 1 m m . The activity was stimulated about 40% by 11 μ m epinephrine and 100% by 10 m m NaF. Skin specimens from psoriatic lesions had less adenyl cyclase activity as assayed in both the tissue slices and the 650 × g pellet of the homogenates. The enzyme in the slices of the diseased skin was less responsive to epinephrine or NaF, and in the 650 × g pellet prepared from psoriatic lesions, was not responsive to epinephrine or NaF. The uninvolved skin of the patients had normal enzymic activity and normal responses to epinephrine and NaF. As psoriasis is characterized by increased proliferation of epidermal cells, it is suggestive that the loss of control of cellular proliferation may be related to defects in the adenyl cyclase system. |
| Databáze: | OpenAIRE |
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