title: Testosterone induced Ca2+ influx in bone marrow-derived macrophages via surface binding sites.
abstract: The biological activity of testosterone is thought to occur predominantly through binding to the androgen receptor (AR), a member of the nuclear receptor superfamily that functions as a ligand-activated transcription factor. Here, we found that testosterone could induce a rapid rise in the intracellular free Ca2+ concentration ([Ca2+]i) of Fura-2 loaded bone marrow-derived macrophages (BMMs), which was found to be predominantly due to the influx of extracellular Ca2+ through Ni2+-blockable Ca2+ channels in the plasma membrane. However, these effects of testosterone could not be associated with the classical intracellular AR in BMMs, since AR was not detectable using different experimental techniques. Instead, it was found that testosterone could bind to the surface of BMMs by the use of an impermeable testosterone-BSA-FITC, and Ca2+ influx could also be induced by testosterone conjugated to BSA. Our data indicated a novel mode of direct action of testosterone on BMMs, which was not mediated through the classical AR response, but through the binding sites of testosterone on cell surfaces.
authors.affiliation: Medical School, Shanghai Jiaotong University, Huashanlu, Shanghai, People's Republic of China.
authors.forename: L
authors.initials: L
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Zhao
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: Q
authors.initials: Q
authors.lastname: Li
authors.forename: Z
authors.initials: Z
authors.lastname: Wang
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: Z
authors.initials: Z
authors.lastname: Qiao
mesh_terms: D000726:Androgen Antagonists / Q000494:pharmacology; D000818:Animals; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D003534:Cyproterone / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009532:Nickel / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011944:Receptors, Androgen / Q000235:genetics / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology*
chemical_list: D000726:Androgen Antagonists; D002121:Calcium Channel Blockers; D012333:RNA, Messenger; D011944:Receptors, Androgen; D011956:Receptors, Cell Surface; D013739:Testosterone; D009532:Nickel; D003534:Cyproterone; D002118:Calcium