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Article ; Online: Chronic replication stress invokes mitochondria dysfunction via impaired parkin activity.

Kawabata, Tsuyoshi / Sekiya, Reiko / Goto, Shinji / Li, Tao-Sheng

2024 Volume 14, Issue 1, Page(s) 7877

Abstract: Replication stress is a major contributor to tumorigenesis because it provides a source of chromosomal rearrangements via recombination events. PARK2, which encodes parkin, a regulator of mitochondrial homeostasis, is located on one of the common fragile ...

Abstract	Replication stress is a major contributor to tumorigenesis because it provides a source of chromosomal rearrangements via recombination events. PARK2, which encodes parkin, a regulator of mitochondrial homeostasis, is located on one of the common fragile sites that are prone to rearrangement by replication stress, indicating that replication stress may potentially impact mitochondrial homeostasis. Here, we show that chronic low-dose replication stress causes a fixed reduction in parkin expression, which is associated with mitochondrial dysfunction, indicated by an increase in mtROS. Consistent with the major role of parkin in mitophagy, reduction in parkin protein expression was associated with a slight decrease in mitophagy and changes in mitochondrial morphology. In contrast, cells expressing ectopic PARK2 gene does not show mtROS increases and changes in mitochondrial morphology even after exposure to chronic replication stress, suggesting that intrinsic fragility at PARK2 loci associated with parkin reduction is responsible for mitochondrial dysfunction caused by chronic replication stress. As endogenous replication stress and mitochondrial dysfunction are both involved in multiple pathophysiology, our data support the therapeutic development of recovery of parkin expression in human healthcare.
MeSH term(s)	Humans ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Mitophagy/genetics ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism
Chemical Substances	parkin protein (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-58656-w
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Article: Autophagosome biogenesis and human health.

Kawabata, Tsuyoshi / Yoshimori, Tamotsu

Cell discovery

2020 Volume 6, Issue 1, Page(s) 33

Abstract: Autophagy degrades the cytoplasmic contents engulfed by autophagosomes. Besides providing energy and building blocks during starvation via random degradation, autophagy selectively targets cytotoxic components to prevent a wide range of diseases. This ... ...

Abstract	Autophagy degrades the cytoplasmic contents engulfed by autophagosomes. Besides providing energy and building blocks during starvation via random degradation, autophagy selectively targets cytotoxic components to prevent a wide range of diseases. This preventive activity of autophagy is supported by many studies using animal models and reports identifying several mutations in autophagy-related genes that are associated with human genetic disorders, which have been published in the past decade. Here, we summarize the molecular mechanisms of autophagosome biogenesis involving the proteins responsible for these genetic disorders, demonstrating a role for autophagy in human health. These findings will help elucidate the underlying mechanisms of autophagy-related diseases and develop future medications.
Language	English
Publishing date	2020-06-02
Publishing country	England
Document type	Journal Article ; Review
ISSN	2056-5968
ISSN	2056-5968
DOI	10.1038/s41421-020-0166-y
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Article: Enhanced Expression of ABCB1 and Nrf2 in CD133-Positive Cancer Stem Cells Associates with Doxorubicin Resistance.

Goto, Shinji / Kawabata, Tsuyoshi / Li, Tao-Sheng

Stem cells international

2020 Volume 2020, Page(s) 8868849

Abstract: The precise mechanism about drug resistance of cancer stem cells (CSCs) has not yet been completely understood. Based on the expression of CD44 and CD133, two well-recognized cell surface markers for CSC identification, we tried to separate HCT8 ... ...

Abstract	The precise mechanism about drug resistance of cancer stem cells (CSCs) has not yet been completely understood. Based on the expression of CD44 and CD133, two well-recognized cell surface markers for CSC identification, we tried to separate HCT8 colorectal cancer cells into different subpopulations and then investigated how the expression of CD44 and CD133 associated with doxorubicin (DXR) resistance. Interestingly, DXR resistance was observed in CD44
Language	English
Publishing date	2020-08-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573856-2
ISSN	1687-9678 ; 1687-966X
ISSN (online)	1687-9678
ISSN	1687-966X
DOI	10.1155/2020/8868849
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Article ; Online: The mechanisms and roles of selective autophagy in mammals.

Vargas, Jose Norberto S / Hamasaki, Maho / Kawabata, Tsuyoshi / Youle, Richard J / Yoshimori, Tamotsu

Nature reviews. Molecular cell biology

2022 Volume 24, Issue 3, Page(s) 167–185

Abstract: Autophagy is a process that targets various intracellular elements for degradation. Autophagy can be non-selective - associated with the indiscriminate engulfment of cytosolic components - occurring in response to nutrient starvation and is commonly ... ...

Abstract	Autophagy is a process that targets various intracellular elements for degradation. Autophagy can be non-selective - associated with the indiscriminate engulfment of cytosolic components - occurring in response to nutrient starvation and is commonly referred to as bulk autophagy. By contrast, selective autophagy degrades specific targets, such as damaged organelles (mitophagy, lysophagy, ER-phagy, ribophagy), aggregated proteins (aggrephagy) or invading bacteria (xenophagy), thereby being importantly involved in cellular quality control. Hence, not surprisingly, aberrant selective autophagy has been associated with various human pathologies, prominently including neurodegeneration and infection. In recent years, considerable progress has been made in understanding mechanisms governing selective cargo engulfment in mammals, including the identification of ubiquitin-dependent selective autophagy receptors such as p62, NBR1, OPTN and NDP52, which can bind cargo and ubiquitin simultaneously to initiate pathways leading to autophagy initiation and membrane recruitment. This progress opens the prospects for enhancing selective autophagy pathways to boost cellular quality control capabilities and alleviate pathology.
MeSH term(s)	Animals ; Humans ; Macroautophagy ; Proteins/metabolism ; Autophagy ; Ubiquitin/metabolism ; Mammals/metabolism
Chemical Substances	Proteins ; Ubiquitin
Language	English
Publishing date	2022-10-27
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/s41580-022-00542-2
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Zs.A 5446: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 26: Show issues

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Article: Nicaraven induces programmed cell death by distinct mechanisms according to the expression levels of Bcl-2 and poly (ADP-ribose) glycohydrolase in cancer cells.

Abdelghany, Lina / Kawabata, Tsuyoshi / Goto, Shinji / Jingu, Keiichi / Li, Tao-Sheng

Translational oncology

2022 Volume 26, Page(s) 101548

Abstract: The PARP-1 expression level and poly (ADP-ribosyl)ation activity in cancer markedly affect the therapeutic outcome. Nicaraven, a free radical scavenger has been found to inhibit PARP, but the effect on cancer cells is still unclear. In this study, we ... ...

Abstract	The PARP-1 expression level and poly (ADP-ribosyl)ation activity in cancer markedly affect the therapeutic outcome. Nicaraven, a free radical scavenger has been found to inhibit PARP, but the effect on cancer cells is still unclear. In this study, we investigated the potential role and molecular mechanism of nicaraven on cancer cells. Using U937 lymphoma cells and HCT-8 colorectal cancer cells, we found that nicaraven moderately reduced the cell viability of both cells in a dose-dependent manner. Interestingly, nicaraven significantly induced apoptosis of U937 cells that are dominantly expressing Bcl-2 but induced PAR-dependent cell death (parthanatos) of HCT-8 cells that are highly expressing poly (ADP-ribose) glycohydrolase (PARG). Based on our data, nicaraven seems to induce programmed cell death through distinct mechanisms, according to the expression levels of Bcl-2 and PARG in cancer cells.
Language	English
Publishing date	2022-10-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233
ISSN	1936-5233
DOI	10.1016/j.tranon.2022.101548
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Article ; Online: Beyond starvation: An update on the autophagic machinery and its functions.

Kawabata, Tsuyoshi / Yoshimori, Tamotsu

Journal of molecular and cellular cardiology

2016 Volume 95, Page(s) 2–10

Abstract: Autophagy was originally identified as a cytoprotective system that provides emergency backup energy and basic building blocks under starvation condition by digesting self components. Recent advances in the field unveiled that this system also protects ... ...

Abstract	Autophagy was originally identified as a cytoprotective system that provides emergency backup energy and basic building blocks under starvation condition by digesting self components. Recent advances in the field unveiled that this system also protects cells against multiple types of stress, as well as invasion by pathogens. Consistent with these findings, autophagy has been redefined as a safeguard system that plays a vital role in human pathology, and this realization has led to exponential progress in autophagy research. In this review, we introduce the basic mechanisms of canonical autophagy and also discuss selective autophagy, a set of pathways that target specific cellular components for digestion; in particular, we focus on lysophagy, a recently identified mechanism required for lysosomal homeostasis.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy ; Disease Resistance ; Energy Metabolism ; Heart/physiology ; Homeostasis ; Humans ; Intracellular Space ; Lysosomes/metabolism ; Myocardium/metabolism
Language	English
Publishing date	2016-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2015.12.005
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Zs.A 426: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
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Article: Dipyridamole induces the phosphorylation of CREB to promote cancer cell proliferation.

Abdelghany, Lina / El-Mahdy, Nageh / Kawabata, Tsuyoshi / Goto, Shinji / Li, Tao-Sheng

Oncology letters

2021 Volume 21, Issue 4, Page(s) 251

Abstract: Dipyridamole, a traditional anti-platelet drug, has been reported to inhibit the proliferation of cancer cells. The present study aimed to investigate the possibility of dipyridamole as an adjuvant of chemotherapy by enhancing the cytotoxicity of an anti- ...

Abstract	Dipyridamole, a traditional anti-platelet drug, has been reported to inhibit the proliferation of cancer cells. The present study aimed to investigate the possibility of dipyridamole as an adjuvant of chemotherapy by enhancing the cytotoxicity of an anti-cancer drug. The cytotoxicity of colorectal cancer cells (HCT-8), CD133
Language	English
Publishing date	2021-02-03
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2021.12512
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Article ; Online: Loss of RUBCN/rubicon in adipocytes mediates the upregulation of autophagy to promote the fasting response.

Yamamuro, Tadashi / Nakamura, Shuhei / Yanagawa, Kyosuke / Tokumura, Ayaka / Kawabata, Tsuyoshi / Fukuhara, Atsunori / Teranishi, Hirofumi / Hamasaki, Maho / Shimomura, Iichiro / Yoshimori, Tamotsu

Autophagy

2022 Volume 18, Issue 11, Page(s) 2686–2696

Abstract: Upon fasting, adipocytes release their lipids that accumulate in the liver, thus promoting hepatic steatosis and ketone body production. However, the mechanisms underlying this process are not fully understood. In this study, we found that fasting caused ...

Abstract	Upon fasting, adipocytes release their lipids that accumulate in the liver, thus promoting hepatic steatosis and ketone body production. However, the mechanisms underlying this process are not fully understood. In this study, we found that fasting caused a substantial decrease in the adipose levels of RUBCN/rubicon, a negative regulator of macroautophagy/autophagy, along with an increase in autophagy. Adipose-specific
MeSH term(s)	Mice ; Animals ; Autophagy/genetics ; Fasting ; Up-Regulation/genetics ; Adipocytes/metabolism ; Adipogenesis ; Mice, Knockout ; Fatty Liver/metabolism ; Carrier Proteins/metabolism ; PPAR gamma/genetics ; Intracellular Signaling Peptides and Proteins/metabolism
Chemical Substances	Carrier Proteins ; PPAR gamma ; Intracellular Signaling Peptides and Proteins
Language	English
Publishing date	2022-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2047341
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Zs.A 6741: Show issues

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Article ; Online: Biphasic effect of mechanical stress on lymphocyte activation.

Yassouf, Mhd Yousuf / Zhang, Xu / Huang, Zisheng / Zhai, Da / Sekiya, Reiko / Kawabata, Tsuyoshi / Li, Tao-Sheng

Journal of cellular physiology

2021 Volume 237, Issue 2, Page(s) 1521–1531

Abstract: Mechanical forces can modulate the immune response, mostly described as promoting the activation of immune cells, but the role and mechanism of pathological levels of mechanical stress in lymphocyte activation have not been focused on before. By an ex ... ...

Abstract	Mechanical forces can modulate the immune response, mostly described as promoting the activation of immune cells, but the role and mechanism of pathological levels of mechanical stress in lymphocyte activation have not been focused on before. By an ex vivo experimental approach, we observed that mechanical stressing of murine spleen lymphocytes with 50 mmHg for 3 h induced the nuclear localization of NFAT1, increased C-Jun, and increased the expression of early activation marker CD69 in resting CD8+ cells. Interestingly, 50 mmHg mechanical stressing induced the nuclear localization of NFAT1; but conversely decreased C-Jun and inhibited the expression of CD69 in lymphocytes under lipopolysaccharide or phorbol 12-myristate 13-acetate/ionomycin stimulation. Additionally, we observed similar changes trends when comparing RNA-seq data of hypertensive and normotensive COVID-19 patients. Our results indicate a biphasic effect of mechanical stress on lymphocyte activation, which provides insight into the variety of immune responses in pathologies involving elevated mechanical stress.
MeSH term(s)	Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; Biomarkers/metabolism ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; COVID-19/complications ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Comorbidity ; Gene Expression Regulation/drug effects ; Humans ; Hypertension/complications ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Ion Channels/metabolism ; Lectins, C-Type/metabolism ; Lipopolysaccharides/pharmacology ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Male ; Mice, Inbred C57BL ; NFATC Transcription Factors/metabolism ; Protein Transport/drug effects ; Proto-Oncogene Proteins c-jun/metabolism ; Signal Transduction/drug effects ; Stress, Mechanical ; Tetradecanoylphorbol Acetate/pharmacology ; Mice
Chemical Substances	Antigens, CD ; Antigens, Differentiation, T-Lymphocyte ; Biomarkers ; CD69 antigen ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Ion Channels ; Lectins, C-Type ; Lipopolysaccharides ; NFATC Transcription Factors ; Piezo1 protein, mouse ; Proto-Oncogene Proteins c-jun ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2021-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.30623
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Uc I Zs.212: Show issues

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Article ; Online: Rubicon regulates A2E-induced autophagy impairment in the retinal pigment epithelium implicated in the pathology of age-related macular degeneration.

Ando, Satoru / Hashida, Noriyasu / Yamashita, Daisuke / Kawabata, Tsuyoshi / Asao, Kazunobu / Kawasaki, Satoshi / Sakurai, Kazushi / Yoshimori, Tamotsu / Nishida, Kohji

Biochemical and biophysical research communications

2021 Volume 551, Page(s) 148–154

Abstract: Waste product deposition and light stress in the retinal pigment epithelium (RPE) are crucial factors in the pathogenesis of various retinal degenerative diseases, including age-related macular degeneration (AMD), a leading cause of vision loss in ... ...

Abstract	Waste product deposition and light stress in the retinal pigment epithelium (RPE) are crucial factors in the pathogenesis of various retinal degenerative diseases, including age-related macular degeneration (AMD), a leading cause of vision loss in elderly individuals worldwide. Given that autophagy in the RPE suppresses waste accumulation, determining the molecular mechanism by which autophagy is compromised in degeneration is necessary. Using polarized human RPE sheets, we found that bis-retinoid N-retinyl-N-retinylidene ethanolamine (A2E), a major toxic fluorophore of lipofuscin, causes significant impairment of autophagy and the simultaneous upregulation of Rubicon, a negative regulator of autophagy. Importantly, this impairment was reversed in Rubicon-specific siRNA-treated RPE sheets. In a retinal functional analysis using electroretinograms (ERGs), mice with the RPE-specific deletion of Rubicon showed no significant differences from control cre-expressing mice but presented partially but significantly enhanced amplitudes compared with Atg7 knockout mice. We also found that an inflammatory reaction in the retina in response to chronic blue light irradiation was alleviated in mice with the RPE-specific deletion of Rubicon. In summary, we propose that upregulating basal autophagy by targeting Rubicon is beneficial for protecting the RPE from functional damage with ageing and the inflammatory reaction caused by light-induced cellular stress.
MeSH term(s)	Aging/metabolism ; Animals ; Autophagy/drug effects ; Autophagy-Related Protein 7/metabolism ; Electroretinography ; Female ; Inflammation/metabolism ; Intracellular Signaling Peptides and Proteins/deficiency ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Lipofuscin/metabolism ; Macular Degeneration/chemically induced ; Macular Degeneration/metabolism ; Macular Degeneration/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Phagocytosis ; Retinal Pigment Epithelium/drug effects ; Retinal Pigment Epithelium/metabolism ; Retinal Pigment Epithelium/pathology ; Stress, Physiological/radiation effects
Chemical Substances	Atg7 protein, mouse ; Intracellular Signaling Peptides and Proteins ; Lipofuscin ; Rubcn protein, mouse ; Autophagy-Related Protein 7 (EC 6.2.1.45)
Language	English
Publishing date	2021-03-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.02.148
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