title: Tumor necrosis factor-alpha attenuates thyroid hormone-induced apoptosis in vascular endothelial cell line XLgoo established from Xenopus tadpole tails.
abstract: Amphibian metamorphosis induced by T(3) involves programmed cell death and the differentiation of various types of cells in degenerated and reconstructed tissues. However, the signaling pathway that directs the T(3)-dependent cell-fate determinations remains unclear. TNF-alpha is a pleiotropic cytokine that affects diverse cellular responses. Engagement of TNF-alpha with its receptor (TNFR1) causes intracellular apoptotic and/or survival signaling. To investigate TNF signaling functions during anuran metamorphosis, we first identified Xenopus laevis orthologs of TNF (xTNF)-alpha and its receptor. We found that xTNF-alpha activated nuclear factor-kappaB in X. laevis A6 cells through the Fas-associated death domain and receptor-interacting protein 1. Interestingly, xTNF-alpha mRNA in blood cells showed prominent expression at prometamorphosis during metamorphosis. Next, to elucidate the apoptotic and/or survival signaling induced by xTNF-alpha in an in vitro model of metamorphosis, we established a vascular endothelial cell line, XLgoo, from X. laevis tadpole tail. XLgoo cells formed actin stress fibers and elongated in response to xTNF-alpha. T(3) induced apoptosis in these cells, but the addition of xTNF-alpha blocked the T(3)-induced apoptosis. In addition, treatment of the cells with T(3) for 2 d induced the expression of thyroid hormone receptor-beta and caspase-3, and this thyroid hormone receptor-beta induction was drastically repressed by xTNF-alpha. Furthermore, in organ culture of the tail, xTNF-alpha significantly attenuated the tail degeneration induced by T(3). These findings suggested that xTNF-alpha could protect vascular endothelial cells from apoptotic cell death induced by T(3) during metamorphosis and thereby participate in the regulation of cell fate.
authors.affiliation: Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, Sagamihara, Japan.
authors.forename: Shuuji
authors.initials: S
authors.lastname: Mawaribuchi
authors.forename: Kei
authors.initials: K
authors.lastname: Tamura
authors.forename: Saori
authors.initials: S
authors.lastname: Okano
authors.forename: Shutaro
authors.initials: S
authors.lastname: Takayama
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yaoita
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Shiba
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Takamatsu
authors.forename: Michihiko
authors.initials: M
authors.lastname: Ito
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D006801:Humans; D007814:Larva / Q000166:cytology; D008969:Molecular Sequence Data; D016328:NF-kappa B / Q000378:metabolism; D011485:Protein Binding; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017386:Sequence Homology, Amino Acid; D013623:Tail / Q000166:cytology; D013963:Thyroid Hormones / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D014982:Xenopus laevis
chemical_list: D053200:Fas-Associated Death Domain Protein; D016328:NF-kappa B; D018124:Receptors, Tumor Necrosis Factor; D013963:Thyroid Hormones; D014409:Tumor Necrosis Factor-alpha