Kruppel-like factor 15 induces the development of mature hepatocyte-like cells from hepatoblasts.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
17 09 2021
Historique:
received: 19 05 2021
accepted: 01 09 2021
entrez: 18 9 2021
pubmed: 19 9 2021
medline: 16 11 2021
Statut: epublish

Résumé

The liver is an important metabolic organ that controls homeostasis in the body. Moreover, it functions as a hematopoietic organ, while its metabolic function is low during development. Hepatocytes, which are parenchymal cells of the liver, acquire various metabolic functions by the maturation of hepatic progenitor cells during the fetal period; however, this molecular mechanism is still unclear. In this study, Kruppel-like factor 15 (KLF15) was identified as a new regulator of hepatic maturation through a comprehensive analysis of the expression of transcriptional regulators in mouse fetal and adult hepatocytes. KLF15 is a transcription factor whose expression in the liver increases from the embryonic stage throughout the developmental process. KLF15 induced the overexpression of liver function genes in mouse embryonic hepatocytes. Furthermore, we found that the expression of KLF15 could also induce the expression of liver function genes in hepatoblasts derived from human induced pluripotent stem cells (iPSCs). Moreover, KLF15 increased the promoter activity of tyrosine aminotransferase, a liver function gene. KLF15 also suppressed the proliferation of hepatoblasts. These results suggest that KLF15 induces hepatic maturation through the transcriptional activation of target genes and cell cycle control.

Identifiants

pubmed: 34535735
doi: 10.1038/s41598-021-97937-6
pii: 10.1038/s41598-021-97937-6
pmc: PMC8448749
doi:

Substances chimiques

KLF15 protein, human 0
Klf15 protein, mouse 0
Kruppel-Like Transcription Factors 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

18551

Informations de copyright

© 2021. The Author(s).

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Auteurs

Kazuya Anzai (K)

Department of Molecular Life Sciences, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.

Kota Tsuruya (K)

Department of Molecular Life Sciences, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.

Kinuyo Ida (K)

Department of Molecular Life Sciences, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Center for Matrix Biology and Medicine, Graduate School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.

Tatehiro Kagawa (T)

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.

Yutaka Inagaki (Y)

Center for Matrix Biology and Medicine, Graduate School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Department of Innovative Medical Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.

Akihide Kamiya (A)

Department of Molecular Life Sciences, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. kamiyaa@tokai-u.jp.
Center for Matrix Biology and Medicine, Graduate School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. kamiyaa@tokai-u.jp.

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Classifications MeSH