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Title: Thyroid hormone induces PGC-1α during dendritic outgrowth in mouse cerebellar purkinje cells
Authors: Hatsukano, Tetsu
Kurisu, Junko
Fukumitsu, Kansai
Fujishima, Kazuto
Kengaku, Mineko  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-1666-3648 (unconfirmed)
Author's alias: 栗栖, 純子
藤島, 和人
見学, 美根子
Keywords: Purkinje cell
thyroid hormone
PGC-1α
mitochondria
dendritogenesis
hypothyroid
Issue Date: 9-May-2017
Publisher: Frontiers Media SA
Journal title: Frontiers in Cellular Neuroscience
Volume: 11
Thesis number: 133
Abstract: Thyroid hormone 3, 3′, 5-Triiodo-L-thyronine (T3) is essential for proper brain development. Perinatal loss of T3 causes severe growth defects in neurons and glia, including strong inhibition of dendrite formation in Purkinje cells in the cerebellar cortex. Here we show that T3 promotes dendritic outgrowth of Purkinje cells through induction of peroxisome proliferator-activated receptor gamma (PPARγ) co-activator 1α (PGC-1α), a master regulator of mitochondrial biogenesis. PGC-1α expression in Purkinje cells is upregulated during dendritic outgrowth in normal mice, while it is significantly retarded in hypothyroid mice or in cultures depleted of T3. In cultured Purkinje cells, PGC-1α knockdown or molecular perturbation of PGC-1α signaling inhibits enhanced dendritic outgrowth and mitochondrial generation and activation caused by T3 treatment. In contrast, PGC-1α overexpression promotes dendrite extension even in the absence of T3. PGC-1α knockdown also downregulates dendrite formation in Purkinje cells in vivo. Our findings suggest that the growth-promoting activity of T3 is partly mediated by PGC-1α signaling in developing Purkinje cells.
Rights: © 2017 Hatsukano, Kurisu, Fukumitsu, Fujishima and Kengaku. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
URI: http://hdl.handle.net/2433/226300
DOI(Published Version): 10.3389/fncel.2017.00133
PubMed ID: 28536504
Appears in Collections:Journal Articles

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