Induction of cell expansion of goldfish melanocytoma cells (GMM-1) by epinephrine and dexamethasone requires external calcium.

Authors

  • Yung-Luen Shih,

    1. Graduate Institute of Microbiology and Immunology, National Yang-Ming Medical College, Taipei, Taiwan 11221, Republic of China.
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  • Szecheng J. Lo

    Corresponding author
    1. Graduate Institute of Microbiology and Immunology, National Yang-Ming Medical College, Taipei, Taiwan 11221, Republic of China.
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Graduate Institute of Microbiology and Immunology, National Yang-Ming Medical College, Taipei, Taiwan 11221, Republic of China.

Abstract

Treatment of GMM-1 (a goldfish melanocytoma cell line) cells with epinephrine induced a rapid cell expansion (flattening of cells, extension and broadening of cellular processes) similar to the effect of dexamethasone reported previously (Shih et al., 1990). Studies on the possible involvement of secondary messengers in cell expansion indicated that (i) both 8-bromo-CAMP and forskolin caused cell shrinking (the opposite of cell expansion); (ii) TPA also caused cell shrinking; (iii) phospholipid derivatives, such as 1,2-dioctanoyl-sn-glycerol, lysophosphatidic acid, and arachidonic acid caused cell expansion; and (iv) EGTA (calcium chelator) and nifedipine (calcium channel blocker) inhibited the effect of epinephrine. Together with the previous findings, these observations indicate that epinephrine and dexamethasone may share a common pathway in triggering an external calcium influx to cause cell expansion. The results of the effects of epinephrine agonists and antagonists, together with those of other workers, also show that there are multiple isoforms of adrenoceptor in the goldfish.

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