Beta-adrenergic stimulation induces intracellular Ca++ increase in human epidermal keratinocytes.
J Invest Dermatol
; 96(2): 234-7, 1991 Feb.
Article
em En
| MEDLINE
| ID: mdl-1671406
ABSTRACT
Intracellular Ca++ ([Ca++]i) is one of the most important second messengers of extracellular signals that induce cellular responses. In epidermal keratinocytes, both extracellular and intracellular Ca++ are reported to be important to cell differentiation and proliferation. Several mechanisms that increase [Ca++]i have been elicited in various tissues; however, in epidermal keratinocytes they remain unknown. Thus, we investigated the [Ca++]i modulation in cultured human epidermal keratinocytes and the stimulation that increases the concentration. The [Ca++]i concentration of keratinocytes was increased immediately and transiently by epinephrine. Methoxamine hydrochloride and clonidine (alpha-1- and 2-adrenergic agonists) did not induce an increase in [Ca++]i. The beta-antagonist, propranolol, inhibited the [Ca++]i increase induced by epinephrine and salbutamol (a beta-2-agonist). These results reveal that the beta-adrenergic stimulation induces an immediate and transient [Ca++]i increase in human keratinocytes. Beta-adrenergic stimulation is known to induce adenylate cyclase activation, which results in cyclic AMP accumulation through stimulatory guanosine 5-triphosphate (GTP) binding proteins in the keratinocytes. Also, epinephrine is reported to inhibit cultured epidermal cell proliferation. The effect of epinephrine has been demonstrated by cyclic AMP accumulation; however, beta-adrenergic stimulation revealed a [Ca++]i increase in keratinocytes in our study. One of epinephrine's regulatory effects on epidermal cell proliferation is assumed to occur through the [Ca++]i increase as well.
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Base de dados:
MEDLINE
Assunto principal:
Epinefrina
/
Queratinócitos
/
Cálcio
/
Metoxamina
Limite:
Humans
/
Male
/
Newborn
Idioma:
En
Revista:
J Invest Dermatol
Ano de publicação:
1991
Tipo de documento:
Article
País de afiliação:
Japão