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Title: Pivotal roles of Kupffer cells in the progression and regression of DDC-induced chronic cholangiopathy
Authors: Jemail, Leila
Miyao, Masashi  kyouindb  KAKEN_id
Kotani, Hirokazu  kyouindb  KAKEN_id
Kawai, Chihiro
Minami, Hirozo
Abiru, Hitoshi
Tamaki, Keiji  kyouindb  KAKEN_id
Author's alias: 宮尾, 昌
小谷, 泰一
南, 博蔵
川合, 千裕
阿比留, 仁
玉木, 敬二
Issue Date: 23-Apr-2018
Publisher: Nature Publishing Group
Journal title: Scientific Reports
Volume: 8
Thesis number: 6415
Abstract: Kupffer cells (KCs) are key players in maintaining tissue homeostasis and are involved in various liver diseases. However, the roles of KCs in the pathogenesis of cholangiopathy are largely unknown. We aimed to investigate the precise roles of KCs in both the progression and regression phases of the 3, 5-diethoxycarbonyl-1, 4-dihydrocollidine (DDC)-induced cholangiopathy model. In the early phase of DDC-induced cholangiopathy, the number of KCs significantly increased over time. Moreover, KCs were associated with abnormal phenotypic changes in other liver cells, such as hepatocytes, biliary epithelial cells, liver sinusoidal endothelial cells, and hepatic stellate cells. In contrast, KC depletion by clodronate administration suppressed the progression of the disease, and maintained the phenotypes of other cells. In the regression phase, the numbers of KCs significantly decreased, and the cells redifferentiated to their quiescent state. In contrast, KC depletion delayed the recovery of cells by maintaining other liver cells in an active state. These findings suggest that KCs play detrimental roles in the progression phase; however, they are beneficial in the regression phase by mediating interactions between other liver cells. Our data provide new insights into the roles of KCs in the pathogenesis of cholangiopathy.
Rights: © The Author(s) 2018. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/233964
DOI(Published Version): 10.1038/s41598-018-24825-x
PubMed ID: 29686325
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