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Effects of beta adrenergic agents and prostaglandin E 1 on erythroid colony (CFU‐E) growth and cyclic AMP formation in friend erythroleukemic cells
Author(s) -
Beckman Barbara,
Mirand Edwin,
Fisher James W.
Publication year - 1980
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041050218
Subject(s) - adenylate kinase , cyclase , endocrinology , medicine , spleen , stimulation , prostaglandin , agonist , prostaglandin e2 , chemistry , bone marrow , biology , receptor
The formation of erythroid colonies from bone marrow and spleen cells infected with the polycythemic strain of the Friend virus (FV‐P) was characterized in an in vitro methyl cellulose colony‐forming system in response to prostaglandin E 1 and the beta‐2 adrenergic agonist, albuterol. Both drugs markedly inhibited the formation of CFU‐E colonies of FV‐P‐infected bone marrow and spleen in the absence or presence of erythropoietin. The albuterolmediated inhibition of CFU‐E colonies (FV‐P‐infected) was selectively blocked by butoxamine, a beta‐2 antagonist. Adenylate cyclase (AC) activity was also determined in FV‐P spleen membrane preparations in response to albuterol and PGE 1 . Both agents stimulated enzyme activity, and butoxamine blocked the stimulation seen with albuterol. The ability of albuterol and PGE 1 to stimulate AC activity in the FV‐P‐infected cells suggests that the effects of these agents on CFU‐E formation may be mediated by specific beta‐2 adrenergic and PG receptors through the adenylate cyclase‐cyclic AMP system.