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Article: [Liver fibrosis:underlying mechanisms and clinical implication].

Inagaki, Yutaka

Nihon Shokakibyo Gakkai zasshi The Japanese journal of gastro-enterology

2019 Volume 117, Issue 1, Page(s) 9–19

MeSH term(s)	Humans ; Liver Cirrhosis
Language	Japanese
Publishing date	2019-12-23
Publishing country	Japan
Document type	Journal Article
ZDB-ID	708695-7
ISSN	1349-7693 ; 0446-6586
ISSN (online)	1349-7693
ISSN	0446-6586
DOI	10.11405/nisshoshi.117.9
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Article ; Online: Liver-specific knockout of B cell lymphoma 6 suppresses progression of non-alcoholic steatohepatitis in mice.

Chikada, Hiromi / Ida, Kinuyo / Nishikawa, Yuji / Inagaki, Yutaka / Kamiya, Akihide

Scientific reports

2020 Volume 10, Issue 1, Page(s) 9704

Abstract: The prevalence of non-alcoholic steatohepatitis (NASH) rapidly increases with metabolic disorders such as dyslipidaemia, high blood pressure, and hyperglycaemia. B cell lymphoma 6 (Bcl6), a transcriptional repressor, is essential for the formation of ... ...

Abstract	The prevalence of non-alcoholic steatohepatitis (NASH) rapidly increases with metabolic disorders such as dyslipidaemia, high blood pressure, and hyperglycaemia. B cell lymphoma 6 (Bcl6), a transcriptional repressor, is essential for the formation of germinal centre B cells. In this study, we analysed the role of Bcl6 in NASH progression-associated pathological changes, such as hepatic lipid accumulation, liver fibrosis, and hepatocarcinogenesis. The roles of Bcl6 in NASH were analysed using liver-specific Bcl6 knockout (Bcl6-LKO) and control wild-type (WT) mice. The murine NASH model was established by feeding the mice with choline-deficient, L-amino-acid-defined, high-fat diet (CDAHFD). Feeding the WT mice with CDAHFD for 7 weeks induced the formation of histopathological features resembling human NASH, such as hepatic lipid accumulation, hepatocellular injury, and fibrosis. These histopathological changes were significantly attenuated in Bcl6-LKO mice. Additionally, feeding the male WT mice with CDAHFD for 38 weeks induced the formation of liver tumours, which was suppressed in Bcl6-LKO mice. These findings indicate that Bcl6 is involved in the progression of NASH and NASH-derived tumours.
MeSH term(s)	Animals ; Disease Models, Animal ; Disease Progression ; Female ; Lipid Metabolism ; Liver/chemistry ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Proto-Oncogene Proteins c-bcl-6/physiology ; Real-Time Polymerase Chain Reaction ; Triglycerides/analysis ; Triglycerides/metabolism
Chemical Substances	Proto-Oncogene Proteins c-bcl-6 ; Triglycerides
Language	English
Publishing date	2020-06-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-66539-z
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Article ; Online: Metabolic reprogramming sustains cancer cell survival following extracellular matrix detachment.

Endo, Hitoshi / Owada, Satoshi / Inagaki, Yutaka / Shida, Yukari / Tatemichi, Masayuki

Redox biology

2020 Volume 36, Page(s) 101643

Abstract: Epithelial cells require attachment to a support, such as the extracellular matrix, for survival. During cancer progression and metastasis, cancerous epithelial cells must overcome their dependence on adhesion signals. Dependence on glucose metabolism is ...

Abstract	Epithelial cells require attachment to a support, such as the extracellular matrix, for survival. During cancer progression and metastasis, cancerous epithelial cells must overcome their dependence on adhesion signals. Dependence on glucose metabolism is a hallmark of cancer cells, but the nutrient requirements of cancer cells under anchorage-deficient conditions remain uncharacterized. Here, we report that cancer cells prioritize glutamine-derived tricarboxylic acid cycle energy metabolism over glycolysis to sustain anchorage-independent survival. Moreover, glutamine-dependent metabolic reprogramming is required not only to maintain ATP levels but also to suppress excessive oxidative stress through interaction with cystine. Mechanistically, AMPK, a central regulator of cellular responses to metabolic stress, participates in the induction of the expression of ASCT2, a glutamine transporter, and enhances glutamine consumption. Most interestingly, AMPK activation induces Nrf2 and its target proteins, allowing cancer cells to maintain energy homeostasis and redox status through glutaminolysis. Treatment with an integrin inhibitor was used to mimic the alterations in cell morphology and metabolic reprogramming caused by detachment. Under these conditions, cells were vulnerable to glutamine starvation or glutamine metabolism inhibitors. The observed preference for glutamine over glucose was more pronounced in aggressive cancer cell lines, and treatment with the glutaminase inhibitor, CB839, and cystine transporter inhibitor, sulfasalazine, caused strong cytotoxicity. Our data clearly show that anchorage-independent survival of cancer cells is supported mainly by glutaminolysis via the AMPK-Nrf2 signal axis. The discovery of new vulnerabilities along this route could help slow or prevent cancer progression.
MeSH term(s)	Cell Survival ; Extracellular Matrix/metabolism ; Glutamine/metabolism ; Glycolysis ; Humans ; Neoplasms/genetics
Chemical Substances	Glutamine (0RH81L854J)
Language	English
Publishing date	2020-07-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101643
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Article: [111th Scientific Meeting of the Japanese Society of Internal Medicine: Symposium: 3. Fibrosis of the viscera and its treatment; 1) Reversibility and treatment of liver fibrosis].

Inagaki, Yutaka / Sumiyoshi, Hideaki

Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine

2016 Volume 103, Issue 9, Page(s) 2171–2175

MeSH term(s)	Biopsy ; Disease Progression ; Drug Design ; Humans ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/etiology ; Liver Cirrhosis/pathology ; Liver Cirrhosis/physiopathology
Language	Japanese
Publishing date	2016-07-19
Publishing country	Japan
Document type	Journal Article
ZDB-ID	952816-7
ISSN	1883-2083 ; 0021-5384
ISSN (online)	1883-2083
ISSN	0021-5384
DOI	10.2169/naika.103.2171
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Article ; Online: Kruppel-like factor 15 induces the development of mature hepatocyte-like cells from hepatoblasts.

Anzai, Kazuya / Tsuruya, Kota / Ida, Kinuyo / Kagawa, Tatehiro / Inagaki, Yutaka / Kamiya, Akihide

Scientific reports

2021 Volume 11, Issue 1, Page(s) 18551

Abstract: 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 ... ...

Abstract	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.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Gene Expression Regulation, Developmental ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Liver/cytology ; Liver/embryology ; Liver/metabolism ; Mice, Inbred C57BL ; Mice
Chemical Substances	KLF15 protein, human ; Klf15 protein, mouse ; Kruppel-Like Transcription Factors
Language	English
Publishing date	2021-09-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-97937-6
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Article ; Online: Two distinct Notch signals, Delta-like 4/Notch1 and Jagged-1/Notch2, antagonistically regulate chemical hepatocarcinogenesis in mice.

Nakano, Yasuhiro / Nakao, Sachie / Sueoka, Minako / Kasahara, Daigo / Tanno, Yuri / Sumiyoshi, Hideaki / Itoh, Tohru / Miyajima, Atsushi / Hozumi, Katsuto / Inagaki, Yutaka

Communications biology

2022 Volume 5, Issue 1, Page(s) 85

Abstract: Notch signaling is one of the most common drivers of carcinogenesis in many types of cancers, including hepatocellular carcinoma (HCC); however, it occasionally suppresses tumor progression. Moreover, it is virtually unknown how different sets of Notch ... ...

Abstract	Notch signaling is one of the most common drivers of carcinogenesis in many types of cancers, including hepatocellular carcinoma (HCC); however, it occasionally suppresses tumor progression. Moreover, it is virtually unknown how different sets of Notch ligands and receptors regulate the HCC development. In this study, we demonstrate that the expression of the Notch ligands, Delta-like 4 (Dll4) and Jagged-1 (Jag1), is upregulated during diethylnitrosamine-induced hepatocarcinogenesis. Dll4 is detected in the preneoplastic hepatocytes and HCC cells, but not in the normal hepatocytes, while Jag1 is expressed in the desmin-positive mesenchymal cells. Hepatocyte-specific Dll4 knockout abolishes the Notch1 signaling and suppresses the tumor progression. In contrast, Jag1 deletion induces the ectopic expression of Dll4 in hepatocytes along with the loss of Notch2 signaling, leading to the tumor progression. These results indicate that the two distinct Notch signals, Dll4/Notch1 and Jag1/Notch2, are antagonistic to each other, exerting opposite effects on HCC progression.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Calcium-Binding Proteins/metabolism ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Jagged-1 Protein/genetics ; Jagged-1 Protein/metabolism ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Mice ; Mice, Knockout ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Receptor, Notch2/genetics ; Receptor, Notch2/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Calcium-Binding Proteins ; DLL4 protein, mouse ; Jagged-1 Protein ; Notch1 protein, mouse ; Notch2 protein, mouse ; Receptor, Notch1 ; Receptor, Notch2
Language	English
Publishing date	2022-01-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03013-8
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Article ; Online: Intrinsic Control of Surface Immune and Epithelial Homeostasis by Tissue-Resident Gut Stromal Cells.

Kurashima, Yosuke / Tokuhara, Daisuke / Kamioka, Mariko / Inagaki, Yutaka / Kiyono, Hiroshi

Frontiers in immunology

2019 Volume 10, Page(s) 1281

Abstract: The epithelial layer creates a chemical and physical barrier at the forefront of intestinal mucosa, and immune cells beneath the surface epithelium are poised to react to extrinsic factors, to maintain tissue homeostasis. Importantly, the nexus of ... ...

Abstract	The epithelial layer creates a chemical and physical barrier at the forefront of intestinal mucosa, and immune cells beneath the surface epithelium are poised to react to extrinsic factors, to maintain tissue homeostasis. Importantly, the nexus of epithelial-immune responses at mucosal surfaces is dexterously modulated by intrinsic stromal-mesenchymal cells. First, organogenesis of lymphoid tissues, including Peyer's patches, requires dynamic interplay between lymphoid cells and stromal cells, which have become known as "lymphoid organizers." Second, correct spatiotemporal interaction between these cell populations is essential to generate the infrastructure for gut immune responses. Moreover, immune cells at the intestinal barrier are functionally modulated by stromal cells; one such example is the stromal cell-mediated differentiation of innate immune cells, including innate lymphoid cells and mast cells. Ultimately, mucosal stromal cells orchestrate the destinations of epithelial and immune cells to maintain intestinal immune homeostasis.
MeSH term(s)	Animals ; Epithelial Cells/immunology ; Homeostasis/immunology ; Humans ; Immunity, Innate/immunology ; Intestinal Mucosa/immunology ; Lymphocytes/immunology ; Lymphoid Tissue/immunology ; Mast Cells/immunology ; Stromal Cells/immunology
Language	English
Publishing date	2019-06-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.01281
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Article: Stem and progenitor cell systems in liver development and regeneration.

Kamiya, Akihide / Inagaki, Yutaka

Hepatology research : the official journal of the Japan Society of Hepatology

2014 Volume 45, Issue 1, Page(s) 29–37

Abstract: The liver comprises two stem/progenitor cell systems: fetal and adult liver stem/progenitor cells. Fetal hepatic progenitor cells, derived from foregut endoderm, differentiate into mature hepatocytes and cholangiocytes during liver development. Adult ... ...

Abstract	The liver comprises two stem/progenitor cell systems: fetal and adult liver stem/progenitor cells. Fetal hepatic progenitor cells, derived from foregut endoderm, differentiate into mature hepatocytes and cholangiocytes during liver development. Adult hepatic progenitor cells contribute to regeneration after severe and chronic liver injuries. However, the characteristics of these somatic hepatic stem/progenitor cells remain unknown. Culture systems that can be used to analyze these cells were recently established and hepatic stem/progenitor cell-specific surface markers including delta-like 1 homolog (DLK), cluster of differentiation (CD) 13, CD133, and LIV2 were identified. Cells purified using antibodies against these markers proliferate for an extended period and differentiate into mature cells both in vitro and in vivo. Methods to force the differentiation of human embryonic stem and induced pluripotent stem (iPS) cells into hepatic progenitor cells have been recently established. We demonstrated that the CD13(+) CD133(+) fraction of human iPS-derived cells contained numerous hepatic progenitor-like cells. These analyses of hepatic stem/progenitor cells derived from somatic tissues and pluripotent stem cells will contribute to the development of new therapies for severe liver diseases.
Language	English
Publishing date	2014-07-18
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1387041-5
ISSN	1386-6346 ; 0928-4346
ISSN	1386-6346 ; 0928-4346
DOI	10.1111/hepr.12349
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Article ; Online: A Deactivation Factor of Fibrogenic Hepatic Stellate Cells Induces Regression of Liver Fibrosis in Mice.

Nakano, Yasuhiro / Kamiya, Akihide / Sumiyoshi, Hideaki / Tsuruya, Kota / Kagawa, Tatehiro / Inagaki, Yutaka

Hepatology (Baltimore, Md.)

2020 Volume 71, Issue 4, Page(s) 1437–1452

Abstract: Background and aims: Hepatic stellate cells (HSCs), a key player in the progression of liver fibrosis, are activated by various inflammatory stimuli and converted to myofibroblast-like cells with excessive collagen production. Despite many attempts to ... ...

Abstract	Background and aims: Hepatic stellate cells (HSCs), a key player in the progression of liver fibrosis, are activated by various inflammatory stimuli and converted to myofibroblast-like cells with excessive collagen production. Despite many attempts to suppress activation of HSCs or inhibit collagen production in activated HSCs, their clinical applications have not been established yet. Recently, the deactivation of HSCs has been reported as a mechanism underlying the reversibility of experimental liver fibrosis. In the present study, we sought for deactivation factors of HSCs that induce regression of established liver fibrosis. Approach and results: We identified transcription factor 21 (Tcf21) as one of the transcription factors whose expression was up-regulated in parallel to the differentiation of fetal HSCs. Expression of Tcf21 in HSCs remarkably decreased during culture-induced activation in vitro and in murine and human fibrotic liver tissue in vivo. This reduced Tcf21 expression was recovered during the spontaneous regression of murine liver fibrosis. Tcf21 was also examined for its effects by adeno-associated virus serotype 6-mediated Tcf21 gene transfer into cultured activated HSCs and mice with carbon tetrachloride- or methionine-choline deficient diet-induced liver fibrosis. Overexpression of Tcf21 in activated HSCs not only suppressed fibrogenic gene expression but also restored cells, at least in part, to a quiescent phenotype both in vitro and in vivo. These phenotypic changes of HSCs were accompanied by the regression of steatohepatitis and fibrosis and improved hepatic architecture and function. Conclusions: Tcf21 has been identified as a deactivation factor of fibrogenic HSCs, providing insight into a treatment strategy for the otherwise intractable liver fibrosis.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/physiology ; Gene Expression Regulation ; Gene Transfer Techniques ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Mice ; Mice, Inbred C57BL
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Tcf21 protein, mouse
Language	English
Publishing date	2020-03-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.30965
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Article ; Online: Glucose starvation induces LKB1-AMPK-mediated MMP-9 expression in cancer cells.

Endo, Hitoshi / Owada, Satoshi / Inagaki, Yutaka / Shida, Yukari / Tatemichi, Masayuki

Scientific reports

2018 Volume 8, Issue 1, Page(s) 10122

Abstract: Cancer cells utilise the glycolytic pathway to support their rapid growth and proliferation. Since cells in most solid tumours are subjected to severe microenvironmental stresses including low nutrient and oxygen availability, such cancer cells must ... ...

Abstract	Cancer cells utilise the glycolytic pathway to support their rapid growth and proliferation. Since cells in most solid tumours are subjected to severe microenvironmental stresses including low nutrient and oxygen availability, such cancer cells must develop mechanisms to overcome these unfavourable growth conditions by metabolic adaptation. Although the liver kinase B1 (LKB1)-adenosine monophosphate-activated kinase (AMPK) signalling pathway plays a pivotal role in maintaining energy homeostasis under conditions of metabolic stress, the role of LKB1-AMPK signalling in aiding cancer cell survival and in malignant tumours has not yet been fully elucidated. We show that glucose starvation promotes cancer cell invasiveness and migration through LKB1-AMPK-regulated MMP-9 expression. Most intriguingly, triggering the LKB1-AMPK signalling pathway by glucose starvation-induced oxidative stress facilitates selective autophagy, which in turn enhances Keap1 degradation and the subsequent activation of Nrf2. Following this, Nrf2 regulates the transactivation of MMP-9 via Nrf2 binding sites in the promoter region of the MMP-9 gene. These mechanisms also contribute to the suppression of excessive oxidative stress under glucose starvation, and protect against cell death. Our data clearly shows that LKB1-AMPK signalling not only maintains energy and oxidative stress homeostasis, but could also promote cancer progression during metabolic stress conditions by MMP-9 induction.
MeSH term(s)	Autophagy ; Cell Movement ; Cell Proliferation ; Glucose/deficiency ; Glucose/metabolism ; HeLa Cells ; Hep G2 Cells ; Humans ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; NF-E2-Related Factor 2/metabolism ; Neoplasms/metabolism ; Oxidative Stress ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction
Chemical Substances	NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Protein Kinases (EC 2.7.-) ; AMP-activated protein kinase kinase (EC 2.7.1.-) ; STK11 protein, human (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; MMP9 protein, human (EC 3.4.24.35) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-07-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-28074-w
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