Defects and deficiency of adenyl cyclase in psoriatic skin

Wright, R. K.

doi:10.1001/archderm.107.1.47

Cited by 22 publications

(14 citation statements)

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“…Our data do agree with those of Wright et al (1973). Their work was based on the prelabclling with radioactive adenine of the ATP pool in epidermal slices, and after the prelabelling the addition of the hormone (plus theophylline) to be tested.…”

Section: Discussionsupporting

confidence: 89%

“…Voorhees et al (1973) reported that adenyl cyclase in psoriatic lesions did not appear to be defective in its response to a /^agonist, isoproterenol. But Wright et al (1973) demonstrated a sluggish response of adenyl cyclase in psoriatic epidermis towards another /(-agonist, adrenaline. This study was undertaken to determine whether the hormonal regulation is defective in psoriasis.…”

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confidence: 97%

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On the lack of response to catecholamine stimulation by the adenyl cyclase system in psoriatic lesions*

et al. 1975

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When epidermis from the uninvolved skin of psoriatic patients was incubated for 5 min in Hank's medium containing adrenaline and theophylline, the cyclic AMP level consistently increased 20-30 times over the level observed when adrenaline was not added to the medium. On the other hand, when epidermis from the involved skin of psoriatic patients was incubated under the same experimental conditions, the cyclic AMP level increased only 2-5 times. Even when theophylline, and inhibitor of specific cyclic AMP-phosphodiesterase, was omitted from the medium, a clearly demonstrable difference in sensitivity to adrenaline was evident in normal appearing and lesional psoriatic epidermis. These results indicate a faulty adenyl cyclase system in the involved epidermis of psoriatic lesions rather than a defective degradation process by the specific phosphodiesterase. Since the Km for adrenaline activation of adenyl cyclase was approximately the same in both the uninvolved and the involved epidermis and since the cyclic AMP increase by adrenaline was abolished by the addition of propranolol, the basic nature of the beta-receptor (specifically the binding affinity to adrenaline) in the involved epidermis does not appear to be defective. On the other hand, the finding that the Vmax for adrenaline activation is 10-20 times higher in the uninvolved than in the involved epidermis suggests that the poor response in the involved epidermis may be due to fewer available binding sites for adrenaline in the psoriatic lesion.

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 97%

On the lack of response to catecholamine stimulation by the adenyl cyclase system in psoriatic lesions*

et al. 1975

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“…Biochemical data on adenyl cyclase activity in psoriasis are contradictory (Hsia et al, 1972;Harkonen, Hopsu-Havu & Ray, 1974). The present results confirm and extend the biochemical observations of Wright et al (1973), who found that in psoriatic plaques the adenyl cyclase was unresponsive to NaF and less responsive than normally to adrenaline. In agreement with the data of Harkonen ei al.…”

Section: (I) Atp Hydrolasessupporting

confidence: 93%

“…However, little or no activity of adenyl cyclase was found in human skin without stimulation, probably because adenyl cyclase is less active in epidermal cells than in liver cells (Mier & Urselmann, 1970). The addition of fluoride had no stimulatory effect on adenyl cyclase in intact human epidermis and may do so only in broken cells (Wright et al, 1973). Nevertheless, using other specific stimulatory agents such as glucagon (Mier & Urselmann, 1970) and isoproterenol (Duell et al, 1971) we found additional electron-dense deposits at the cell surfaces in the upper layers and, more distinctly, in the lower layers of normal epidermis.…”

Section: (I) Atp Hydrolasesmentioning

confidence: 95%

Ultrastructural localization and differentiation of membrane-bound ATP utilizing enzymes including adenyl cyclase in normal and psoriatic epidermis*

Mahrle

Orfanos

1975

Br J Dermatol

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The total membrane-bound ATP hydrolytic activity in human epidermis is due to the activities of at least three differently located enzymes, namely Mg++-activated ATPase, phosphomonoesterase and adenyl cyclase. Cytochemical studies on psoriatic epidermis with various inhibitory and stimulatory substances showed reduced activities of ATPase and phosphomonoesterase, and a lack of sensitivity of adenyl cyclase to specific stimulators such as isoproterenol and glucagon. Since no differences of basal adenyl cyclase activity were observed between normal and psoriatic human skin without stimulation, it seems likely that in psoriasis a latent defect of adenyl cyclase may exist, resulting in a deficient response of this enzyme to regulatory agents. In conclusion, the present study reveals that not a single enzyme but the entire membrane-bound nucleotide metabolism is altered in psoriatic keratinocytes, causing a disturbance of the membrane-bound energy utilization, similar to findings in proliferating tumour cells.

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“…Two lines of research grew simultaneously. The first was devoted to find out intrinsic keratinocyte abnormalities: extensive biochemical studies performed in the seventies demonstrated several defects of the psoriatic keratinocyte, most of them concerning the ‘cellular second messengers’, the role of which in cellular physiology had just been discovered [2, 3, 4]. At the same time, the second line of research was interested in immune disturbances associated with the disease: we and others demonstrated abnormal humoral and cellular immune responses [5, 6, 7, 8, 9]and strong association of psoriasis with histocompatibility antigens [10, 11].…”

Section: Introductionmentioning

confidence: 99%

Immunopathogenesis of Psoriasis: News in an Old Concept

Guilhou

1998

Dermatology

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Twenty years ago, a concept of psoriasis pathogenesis was proposed in which epidermal proliferation of psoriatic lesions was the consequence of immunological abnormalities. This concept has subsequently been supported by the remarkable efficacy of immunosuppressive drugs. Moreover, recent experimental data indicate that activated psoriatic lymphocytes are capable of inducing keratinocyte proliferation. However, we have still to explain the mechanism by which lymphocytes act on keratinocytes and to find out what antigenic material could be responsible for their activation.

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Defects and deficiency of adenyl cyclase in psoriatic skin

Cited by 22 publications

References 0 publications

On the lack of response to catecholamine stimulation by the adenyl cyclase system in psoriatic lesions*

On the lack of response to catecholamine stimulation by the adenyl cyclase system in psoriatic lesions*

Ultrastructural localization and differentiation of membrane-bound ATP utilizing enzymes including adenyl cyclase in normal and psoriatic epidermis*

Immunopathogenesis of Psoriasis: News in an Old Concept

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