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Book: NK cells in the liver

Bouwens, Luc

(Medical intelligence unit)

1995

Author's details	Luc Bouwens
Series title	Medical intelligence unit
Keywords	Liver / cytology ; Killer Cells, Natural / physiology ; Leber ; Natürliche Killerzelle
Subject	Hepar ; Lebergewebe ; Leberparenchym ; NK-Zelle
Language	English
Size	156 S. : Ill., graph. Darst.
Publisher	Springer u.a.
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT007251441
ISBN	3-540-59099-4 ; 1-57059-249-7 ; 978-3-540-59099-6 ; 978-1-57059-249-2
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: In vitro comparison of various antioxidants and flavonoids from Rooibos as beta cell protectants against lipotoxicity and oxidative stress-induced cell death.

Moens, Céline / Muller, Christo J F / Bouwens, Luc

PloS one

2022 Volume 17, Issue 5, Page(s) e0268551

Abstract: Oxidative stress and lipotoxicity effects on pancreatic β cells play a major role in the pathogenesis of type 2 diabetes (T2D). Flavonoids and antioxidants are under study for their cytoprotective effects and antidiabetic potential. In this study, we ... ...

Abstract	Oxidative stress and lipotoxicity effects on pancreatic β cells play a major role in the pathogenesis of type 2 diabetes (T2D). Flavonoids and antioxidants are under study for their cytoprotective effects and antidiabetic potential. In this study, we aimed to compare the protective effect of the Rooibos components aspalathin, isoorientin, 3-hydroxyphloretin (3-OH) and green Rooibos extract (GRT) itself, and exendin-4 and N-acetylcysteine (NAC) as reference molecules, against lipotoxicity and oxidative stress. The insulin-producing β cell line INS1E was exposed to hydrogen peroxide or streptozotocin (STZ) to induce oxidative stress, and palmitate to induce lipotoxicity. Cell viability was assessed by a MTS cell viability assay. Antioxidant response and antiapoptotic gene expression was performed by qRT-PCR. Glucose transporter 2 (GLUT 2) transporter inhibition was assessed through 2-NBDG uptake. GRT and the flavonoids aspalathin and 3-hydroxyphloretin offered significant protection against oxidative stress and lipotoxicity. GRT downregulated expression of pro-apoptotic genes Txnip and Ddit3. The flavonoids aspalathin and 3-hydroxyphloretin also downregulated these genes and in addition upregulated expression of antioxidant response genes Hmox1, Nqo1 and Sod1. Isoorientin gave no cytoprotection. Cytoprotection by Rooibos components was significantly higher than by NAC or exendin-4. Rooibos components strongly protect INS1E β cells against diabetogenic stress. Cytoprotection was associated with the upregulation of antioxidant response genes of the NRF2/KEAP1 pathway or suppression of the TXN system. The Rooibos molecules offered better protection against these insults than exendin-4 and NAC, making them interesting candidates as β cell cytoprotectants for therapeutic or nutraceutical applications.
MeSH term(s)	Antioxidants/analysis ; Antioxidants/pharmacology ; Aspalathus ; Cell Death ; Diabetes Mellitus, Type 2/drug therapy ; Exenatide/pharmacology ; Flavonoids/analysis ; Flavonoids/pharmacology ; Insulin-Secreting Cells ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Oxidative Stress ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Protective Agents/pharmacology
Chemical Substances	Antioxidants ; Flavonoids ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Plant Extracts ; Protective Agents ; Exenatide (9P1872D4OL)
Language	English
Publishing date	2022-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0268551
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: In vitro comparison of various antioxidants and flavonoids from Rooibos as beta cell protectants against lipotoxicity and oxidative stress-induced cell death.

Céline Moens / Christo J F Muller / Luc Bouwens

PLoS ONE, Vol 17, Iss 5, p e

2022 Volume 0268551

Abstract	Oxidative stress and lipotoxicity effects on pancreatic β cells play a major role in the pathogenesis of type 2 diabetes (T2D). Flavonoids and antioxidants are under study for their cytoprotective effects and antidiabetic potential. In this study, we aimed to compare the protective effect of the Rooibos components aspalathin, isoorientin, 3-hydroxyphloretin (3-OH) and green Rooibos extract (GRT) itself, and exendin-4 and N-acetylcysteine (NAC) as reference molecules, against lipotoxicity and oxidative stress. The insulin-producing β cell line INS1E was exposed to hydrogen peroxide or streptozotocin (STZ) to induce oxidative stress, and palmitate to induce lipotoxicity. Cell viability was assessed by a MTS cell viability assay. Antioxidant response and antiapoptotic gene expression was performed by qRT-PCR. Glucose transporter 2 (GLUT 2) transporter inhibition was assessed through 2-NBDG uptake. GRT and the flavonoids aspalathin and 3-hydroxyphloretin offered significant protection against oxidative stress and lipotoxicity. GRT downregulated expression of pro-apoptotic genes Txnip and Ddit3. The flavonoids aspalathin and 3-hydroxyphloretin also downregulated these genes and in addition upregulated expression of antioxidant response genes Hmox1, Nqo1 and Sod1. Isoorientin gave no cytoprotection. Cytoprotection by Rooibos components was significantly higher than by NAC or exendin-4. Rooibos components strongly protect INS1E β cells against diabetogenic stress. Cytoprotection was associated with the upregulation of antioxidant response genes of the NRF2/KEAP1 pathway or suppression of the TXN system. The Rooibos molecules offered better protection against these insults than exendin-4 and NAC, making them interesting candidates as β cell cytoprotectants for therapeutic or nutraceutical applications.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SSEA4: a marker leading the way towards curing diabetes?

Bouwens, Luc

Biomarkers in medicine

2012 Volume 6, Issue 6, Page(s) 711–713

MeSH term(s)	Biomarkers/metabolism ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/pathology ; Humans ; Pancreas/metabolism ; Pancreas/pathology ; Stem Cells/metabolism ; Stem Cells/pathology
Chemical Substances	Biomarkers
Language	English
Publishing date	2012-12
Publishing country	England
Document type	Editorial
ZDB-ID	2481014-9
ISSN	1752-0371 ; 1752-0363
ISSN (online)	1752-0371
ISSN	1752-0363
DOI	10.2217/bmm.12.83
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Acinar cells in the neonatal pancreas grow by self-duplication and not by neogenesis from duct cells.

Houbracken, Isabelle / Bouwens, Luc

Scientific reports

2017 Volume 7, Issue 1, Page(s) 12643

Abstract: Pancreatic acinar cells secrete digestive enzymes necessary for nutrient digestion in the intestine. They are considered the initiating cell type of pancreatic cancer and are endowed with differentiation plasticity that has been harnessed to regenerate ... ...

Abstract	Pancreatic acinar cells secrete digestive enzymes necessary for nutrient digestion in the intestine. They are considered the initiating cell type of pancreatic cancer and are endowed with differentiation plasticity that has been harnessed to regenerate endocrine beta cells. However, there is still uncertainty about the mechanisms of acinar cell formation during the dynamic period of early postnatal development. To unravel cellular contributions in the exocrine acinar development we studied two reporter mouse strains to trace the fate of acinar and duct cells during the first 4 weeks of life. In the acinar reporter mice, the labelling index of acinar cells remained unchanged during the neonatal pancreas growth period, evidencing that acinar cells are formed by self-duplication. In line with this, duct cell tracing did not show significant increase in acinar cell labelling, excluding duct-to-acinar cell contribution during neonatal development. Immunohistochemical analysis confirms massive levels of acinar cell proliferation in this early period of life. Further, also increase in acinar cell size contributes to the growth of pancreatic mass.We conclude that the growth of acinar cells during physiological neonatal pancreas development is by self-duplication (and hypertrophy) rather than neogenesis from progenitor cells as was suggested before.
MeSH term(s)	Acinar Cells/cytology ; Animals ; Cell Differentiation/genetics ; Cell Proliferation/genetics ; Endocrine Cells/cytology ; Endocrine Cells/metabolism ; Gene Expression Regulation, Developmental ; Humans ; Mice ; Mitotic Index ; Pancreas/cytology ; Pancreas/growth & development ; Pancreatic Ducts/cytology ; Pancreatic Ducts/growth & development ; Regeneration/genetics ; Stem Cells/cytology ; Stem Cells/metabolism
Language	English
Publishing date	2017-10-03
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/s41598-017-12721-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Adult human pancreatic acinar cells dedifferentiate into an embryonic progenitor-like state in 3D suspension culture.

Baldan, Jonathan / Houbracken, Isabelle / Rooman, Ilse / Bouwens, Luc

Scientific reports

2019 Volume 9, Issue 1, Page(s) 4040

Abstract: Human pancreatic exocrine cells were cultured in 3D suspension and formed pancreatospheres composed of acinar-derived and duct-like cells. We investigated, up to 6 days, the fate of human pancreatic acinar cells using fluorescein-conjugated Ulex ... ...

Abstract	Human pancreatic exocrine cells were cultured in 3D suspension and formed pancreatospheres composed of acinar-derived and duct-like cells. We investigated, up to 6 days, the fate of human pancreatic acinar cells using fluorescein-conjugated Ulex Europaeus Agglutinin 1 lectin, a previously published acinar-specific non-genetic lineage tracing strategy. At day 4, fluorescence-activated cell sort for the intracellularly incorporated FITC-conjugated UEA1 lectin and the duct-specific CA19.9 surface marker, distinguished acinar-derived cells (UEA1
MeSH term(s)	Acinar Cells/cytology ; Acinar Cells/metabolism ; Adult ; Antigens, Tumor-Associated, Carbohydrate/metabolism ; Biomarkers/metabolism ; Cell Lineage ; Cell Plasticity ; Cells, Cultured ; GPI-Linked Proteins/metabolism ; Homeodomain Proteins/metabolism ; Humans ; Pancreas, Exocrine/cytology ; Pancreas, Exocrine/metabolism ; Plant Lectins/chemistry ; SOX9 Transcription Factor/metabolism ; Thromboplastin/metabolism ; Trans-Activators/metabolism
Chemical Substances	Antigens, Tumor-Associated, Carbohydrate ; Biomarkers ; GP2 protein, human ; GPI-Linked Proteins ; Homeodomain Proteins ; Plant Lectins ; SOX9 Transcription Factor ; SOX9 protein, human ; Trans-Activators ; Ulex europaeus lectins ; carbohydrate antigen 199, human ; pancreatic and duodenal homeobox 1 protein ; Thromboplastin (9035-58-9)
Language	English
Publishing date	2019-03-11
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/s41598-019-40481-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Diabetes: β cells at last.

Mfopou, Josué K / Bouwens, Luc

Nature reviews. Endocrinology

2015 Volume 11, Issue 1, Page(s) 5–6

MeSH term(s)	Animals ; Cell Culture Techniques ; Humans ; Insulin-Secreting Cells/cytology
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/nrendo.2014.200
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 6336: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 93: Show issues

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Article: Beta cell regeneration.

Bouwens, Luc

Current diabetes reviews

2008 Volume 2, Issue 1, Page(s) 3–9

Abstract: Beta cell replacement and regeneration therapies seem promising approaches to the treatment of insulin-dependent diabetes. The short supply in beta cells from cadaveric organ donors and the very low replication capacity of human beta cells have spurred ... ...

Abstract	Beta cell replacement and regeneration therapies seem promising approaches to the treatment of insulin-dependent diabetes. The short supply in beta cells from cadaveric organ donors and the very low replication capacity of human beta cells have spurred efforts to find robust ways of (re-)generating beta cells in vitro and in vivo. In the pancreas, both the capacity of regeneration and the mechanism involved can differ significantly depending on the experimental model, as it has also been found in other organs like the liver. Robust expansion of the beta cell mass in adult rodent pancreas doesn't normally occur after partial (50-70%) pancreatectomy nor after beta cell destruction by streptozotocin or alloxan. However, extensive tissue injury and treatment with certain gastrointestinal hormones, like gastrin and growth factors from the EGF-family can stimulate beta cell regeneration. Whereas a slow rate of beta cell mass expansion can result from beta cell replication, more robust regeneration depends largely on neogenesis from precursor cells. Precursor cells can be derived from stem cells or from pancreatic exocrine cells which are known to retain phenotypic plasticity and can transdifferentiate into, amongst others, endocrine cells. Identifying the conditions involved in the regulation of cellular plasticity and regenerative growth may lead to new pharmacological strategies for the treatment of diabetes.
MeSH term(s)	Animals ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/physiology ; Metaplasia/pathology ; Metaplasia/physiopathology ; Regeneration ; Stem Cells/cytology ; Stem Cells/physiology
Language	English
Publishing date	2008-01-02
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ISSN	1573-3998
ISSN	1573-3998
DOI	10.2174/157339906775473644
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Acinar cells in the neonatal pancreas grow by self-duplication and not by neogenesis from duct cells

Isabelle Houbracken / Luc Bouwens

Scientific Reports, Vol 7, Iss 1, Pp 1-

2017 Volume 10

Abstract: Abstract Pancreatic acinar cells secrete digestive enzymes necessary for nutrient digestion in the intestine. They are considered the initiating cell type of pancreatic cancer and are endowed with differentiation plasticity that has been harnessed to ... ...

Abstract	Abstract Pancreatic acinar cells secrete digestive enzymes necessary for nutrient digestion in the intestine. They are considered the initiating cell type of pancreatic cancer and are endowed with differentiation plasticity that has been harnessed to regenerate endocrine beta cells. However, there is still uncertainty about the mechanisms of acinar cell formation during the dynamic period of early postnatal development. To unravel cellular contributions in the exocrine acinar development we studied two reporter mouse strains to trace the fate of acinar and duct cells during the first 4 weeks of life. In the acinar reporter mice, the labelling index of acinar cells remained unchanged during the neonatal pancreas growth period, evidencing that acinar cells are formed by self-duplication. In line with this, duct cell tracing did not show significant increase in acinar cell labelling, excluding duct-to-acinar cell contribution during neonatal development. Immunohistochemical analysis confirms massive levels of acinar cell proliferation in this early period of life. Further, also increase in acinar cell size contributes to the growth of pancreatic mass.We conclude that the growth of acinar cells during physiological neonatal pancreas development is by self-duplication (and hypertrophy) rather than neogenesis from progenitor cells as was suggested before.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2017-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Adult human pancreatic acinar cells dedifferentiate into an embryonic progenitor-like state in 3D suspension culture

Jonathan Baldan / Isabelle Houbracken / Ilse Rooman / Luc Bouwens

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 12

Abstract: Abstract Human pancreatic exocrine cells were cultured in 3D suspension and formed pancreatospheres composed of acinar-derived and duct-like cells. We investigated, up to 6 days, the fate of human pancreatic acinar cells using fluorescein-conjugated Ulex ...

Abstract	Abstract Human pancreatic exocrine cells were cultured in 3D suspension and formed pancreatospheres composed of acinar-derived and duct-like cells. We investigated, up to 6 days, the fate of human pancreatic acinar cells using fluorescein-conjugated Ulex Europaeus Agglutinin 1 lectin, a previously published acinar-specific non-genetic lineage tracing strategy. At day 4, fluorescence-activated cell sort for the intracellularly incorporated FITC-conjugated UEA1 lectin and the duct-specific CA19.9 surface marker, distinguished acinar-derived cells (UEA1 + CA1 9.9 −) from duct-like cells (UEA1 − CA1 9.9 +) and acinar-to-duct-like transdifferentiated cells (UEA1 + CA1 9.9 +). mRNA expression analysis of the acinar-derived (UEA1 + CA19.9 −) and duct-like (UEA1 - CA19.9 +) cell fractions with concomitant immunocytochemical analysis of the pancreatospheres revealed acquisition of an embryonic signature in the UEA1 + CA19.9 − acinar-derived cells characterized by de novo expression of SOX9 and CD142, robust expression of PDX1 and surface expression of GP2. The colocalisation of CD142, a multipotent pancreatic progenitor surface marker, PDX1, SOX9 and GP2 is reminiscent of a cellular state present during human embryonic development. Addition of TGF-beta signalling inhibitor Alk5iII, induced a 28-fold increased KI67-labeling in pancreatospheres, more pronounced in the CD142+GP2+ acinar-derived cells. These findings with human cells underscore the remarkable plasticity of pancreatic exocrine acinar cells, previously described in rodents, and could find applications in the field of regenerative medicine.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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