Catecholamine effects on human melanoma cells evoked by alpha(1)-adrenoceptors
Data
2004-08-01
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The biological effects of catecholamines in mammalian pigment cells are poorly understood. Our previous results showed the presence of alpha(1)-adrenoceptors in SK-Mel 23 human melanoma cells. the aims of this work were to (1) characterize catecholamine effects on proliferation, tyrosinase activity and expression, (2) identify the alpha(1)-adrenoceptor subtypes, and (3) verify whether chronic norepinephrine (NE) treatment modified the types and/or pharmacological characteristics of adrenoceptors present in SK-Mel 23 human melanoma cells. Cells treated with the alpha(1)-adrenergic agonist, phenylephrine (PHE, 10(-5) or 10(-4) M), for 24-72 h, exhibited decreased cell proliferation and enhanced tyrosinase activity, but unaltered tyrosinase expression as compared with the control. the proliferation and tyrosinase activity responses were inhibited by the alpha(1)-adrenergic antagonist prazosin, suggesting they were evoked by alpha(1)-adrenoceptors. the presence of actinomycin D, a transcription inhibitor, did not diminish PHE-induced effects. RT-PCR assays, followed by cloning and sequencing, demonstrated the presence of alpha(1A)- and alpha(1B)-adrenoceptor subtypes. NE-treated cells (24 or 72 h) were used in competition assays, and showed no significant change in the competition curves of alpha(1)-adrenoceptors as compared with control curves. Other adrenoceptor subtypes were not identified in these cells, and NE pretreatment did not induce their expression. in conclusion, the activation of SK-Mel 23 human melanoma alpha(1)-adrenoceptors elicit biological effects, such as proliferation decrease and tyrosinase activity increase. Desensitization or expression of other adrenoceptor subtypes after chronic NE treatment were not observed.
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Archives of Dermatological Research. New York: Springer, v. 296, n. 3, p. 112-119, 2004.