Transition of blood cells from larva to adult

Abstract

Event Abstract Back to Event Transition of blood cells from larva to adult Michihiko Ito1*, Kei Tamura1, Shuuji Mawaribuchi1 and Nobuhiko Takamatsu1 1 Kitasato University, School of Science, Japan The members of tumor necrosis factor (TNF) superfamily including TRAIL and TNF-alpha induce intracellular signaling upon engagement of their receptors, leading to apoptosis, cell survival or pro-inflammatory responses. We examined how Xenopus orthlogues of TRAIL and TNF-α (xTRAIL1 and xTNF-alpha) could be involved in metamorphosis. The transcripts for xTRAIL and its receptors, xDR-Ms were highly expressed in the tadpole liver and red blood cells (RBCs), respectively. Intriguingly, xTRAIL1 induced apoptosis in larval RBCs, but had little effect on adult RBCs in vitro. Importantly, it enhanced the transition of the RBCs, and a dominant-negative form of the xTRAIL1 receptor attenuated it, when injected into tadpoles. Moreover, we also found that adult RBCs treated with staurosporine, a protein kinase C (PKC) inhibitor, were sensitized to xTRAIL1. These results suggest that xTRAIL1 can cause apoptosis, probably mediated through xDR-Ms, in larval RBCs, but may not kill adult RBCs, presumably owing to PKC activation, as part of the mechanism for RBC switching. xTNF-alpha mRNA in blood cells showed prominent expression at prometamorphosis during metamorphosis. Interestingly, TNF-alpha attenuated thyroid hormone (TH)-induced apoptosis in Xenopus tadpole tail-derived vascular endothelial XLgoo cells, which endogenously expressed its receptor, xTNFRI. Furthermore, in organ culture of the tail, xTNF-alpha significantly attenuated the tail degeneration induced by TH. These findings suggested that survival signal mediated through xTNF-alpha could protect endothelial cells from apoptotic cell death induced by TH during metamorphosis and thereby participate in the regulation of cell fate. Keywords: death receptor, metamorphosis, red blood cell, Tail, Thyroid hormone, TNF, TRAIL, xDR-M Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Invited Symposium Topic: Developmental endocrinology Citation: Ito M, Tamura K, Mawaribuchi S and Takamatsu N (2011). Transition of blood cells from larva to adult. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00145 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 23 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Prof. Michihiko Ito, Kitasato University, School of Science, Sagamihara, Kanagawa, 228-8555, Japan, ito@sci.kitasato-u.ac.jp Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Michihiko Ito Kei Tamura Shuuji Mawaribuchi Nobuhiko Takamatsu Google Michihiko Ito Kei Tamura Shuuji Mawaribuchi Nobuhiko Takamatsu Google Scholar Michihiko Ito Kei Tamura Shuuji Mawaribuchi Nobuhiko Takamatsu PubMed Michihiko Ito Kei Tamura Shuuji Mawaribuchi Nobuhiko Takamatsu Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.