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4 results on '"Eric Kalo"'

1. Generation of hepatocyte- and endocrine pancreatic-like cells from human induced endodermal progenitor cells.

Author

Rangarajan Sambathkumar, Renate Akkerman, Sumitava Dastidar, Philip Roelandt, Manoj Kumar, Manmohan Bajaj, Ana Rita Mestre Rosa, Nicky Helsen, Veerle Vanslembrouck, Eric Kalo, Satish Khurana, Jos Laureys, Conny Gysemans, Marijke M Faas, Paul de Vos, and Catherine M Verfaillie

Subjects
Medicine, Science
Abstract

Multipotent Adult Progenitor Cells (MAPCs) are one potential stem cell source to generate functional hepatocytes or β-cells. However, human MAPCs have less plasticity than pluripotent stem cells (PSCs), as their ability to generate endodermal cells is not robust. Here we studied the role of 14 transcription factors (TFs) in reprogramming MAPCs to induced endodermal progenitor cells (iENDO cells), defined as cells that can be long-term expanded and differentiated to both hepatocyte- and endocrine pancreatic-like cells. We demonstrated that 14 TF-iENDO cells can be expanded for at least 20 passages, differentiate spontaneously to hepatocyte-, endocrine pancreatic-, gut tube-like cells as well as endodermal tumor formation when grafted in immunodeficient mice. Furthermore, iENDO cells can be differentiated in vitro into hepatocyte- and endocrine pancreatic-like cells. However, the pluripotency TF OCT4, which is not silenced in iENDO cells, may contribute to the incomplete differentiation to mature cells in vitro and to endodermal tumor formation in vivo. Nevertheless, the studies presented here provide evidence that reprogramming of adult stem cells to an endodermal intermediate progenitor, which can be expanded and differentiate to multiple endodermal cell types, might be a valid alternative for the use of PSCs for creation of endodermal cell types.

Published
2018
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2. Targeting Gut–Liver Axis for Treatment of Liver Fibrosis and Portal Hypertension

Author

Golo Ahlenstiel, Eric Kalo, and Scott A. Read

Subjects
Medicine (General), Cirrhosis, biology, business.industry, cirrhosis, portal hypertension, chronic liver disease, General Medicine, Gut flora, biology.organism_classification, medicine.disease, Bioinformatics, Chronic liver disease, Pathogenesis, Liver disease, R5-920, Drug development, gut–liver axis, microbiota, medicine, Portal hypertension, business, Hepatic fibrosis, liver fibrosis
Abstract

Antifibrotic therapies for the treatment of liver fibrosis represent an unconquered area of drug development. The significant involvement of the gut microbiota as a driving force in a multitude of liver disease, be it pathogenesis or fibrotic progression, suggest that targeting the gut–liver axis, relevant signaling pathways, and/or manipulation of the gut’s commensal microbial composition and its metabolites may offer opportunities for biomarker discovery, novel therapies and personalized medicine development. Here, we review potential links between bacterial translocation and deficits of host-microbiome compartmentalization and liver fibrosis that occur in settings of advanced chronic liver disease. We discuss established and emerging therapeutic strategies, translated from our current knowledge of the gut–liver axis, targeted at restoring intestinal eubiosis, ameliorating hepatic fibrosis and rising portal hypertension that characterize and define the course of decompensated cirrhosis.

Published
2021

3. A variant in FTO gene shows association with histological ulceration in cutaneous melanoma

Author

Canan Güvenç, Vivien Marasigan, Diether Lambrechts, Joost van den Oord, Marjan Garmyn, and Eric Kalo

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Skin Neoplasms, Histology, Adolescent, Genotype, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Genome-wide association study, Dermatology, Biology, Polymorphism, Single Nucleotide, FTO gene, Pathology and Forensic Medicine, Young Adult, Belgium, medicine, Humans, Melanoma, Ulcer, Aged, Neoplasm Staging, Genetic association, Aged, 80 and over, Middle Aged, medicine.disease, Case-Control Studies, Cutaneous melanoma, Female, Genome-Wide Association Study
Published
2019

4. Epigenetic Induction of Definitive and Pancreatic Endoderm Cell Fate in Human Fibroblasts

Author

Eric Kalo, Rob Van Rossom, Paul de Vos, Marijke M. Faas, Rangarajan Sambathkumar, Catherine M. Verfaillie, Reproductive Origins of Adult Health and Disease (ROAHD), Translational Immunology Groningen (TRIGR), and Man, Biomaterials and Microbes (MBM)

Subjects
0301 basic medicine, CHROMATIN, INSULIN-SECRETING CELLS, VIVO, that histone deacetylase inhibitor (HDACi) Trichostatin A (TSA) combined with a chromatin remodeling medium (CRM), treatment with DNA methyltransferase inhibitor (DNMTi), Upon removal of TSA-CRM, role epigenetic modification in transdifferentiation of one somatic cell into another. However, full reprogramming of fibroblasts to beta-cells will require combination of this approach with TF overexpression and/or culture of the partially reprogrammed cells under beta-cell specific conditions, induced expression of a number of definitive endoderm and early and late pancreatic marker genes. When CRM was omitted, no further increase, Histone deacetylase inhibitor, Transdifferentiation, pancreatic endoderm, Cell biology, medicine.anatomical_structure, DIFFERENTIATION, embryonic structures, Reprogramming can occur by the introduction of key transcription factors (TFs) as well as by epigenetic changes. We demonstrated, Endoderm, Reprogramming, PLURIPOTENT STEM-CELLS, medicine.drug, Research Article, lcsh:Internal medicine, animal structures, Article Subject, medicine.drug_class, the endoderm/pancreatic gene expression profile returned to baseline. Our findings underscore the, Interestingly, Biology, SMALL MOLECULES, Chromatin remodeling, 03 medical and health sciences, BETA-CELLS, medicine, Epigenetics, endoderm/pancreatic marker genes were not induced. Furthermore, TRICHOSTATIN, lcsh:RC31-1245, Molecular Biology, and when 5AZA was combined with TSA, and endocrine markers was seen over levels induced with TSA alone, Cell Biology, IN-VITRO, Molecular biology, CONVERSION, 030104 developmental biology, Trichostatin A, TSA-CRM did not affect expression of pluripotency and hepatocyte genes but induced some mesoderm transcripts, 5-azacytidine (5AZA) CRM did not affect gene expression changes, sense organs, in gene expression of endoderm, Definitive endoderm
Abstract

Reprogramming can occur by the introduction of key transcription factors (TFs) as well as by epigenetic changes. We demonstrated that histone deacetylase inhibitor (HDACi) Trichostatin A (TSA) combined with a chromatin remodeling medium (CRM) induced expression of a number of definitive endoderm and early and late pancreatic marker genes. When CRM was omitted, endoderm/pancreatic marker genes were not induced. Furthermore, treatment with DNA methyltransferase inhibitor (DNMTi) 5-azacytidine (5AZA) CRM did not affect gene expression changes, and when 5AZA was combined with TSA, no further increase in gene expression of endoderm, pancreatic endoderm, and endocrine markers was seen over levels induced with TSA alone. Interestingly, TSA-CRM did not affect expression of pluripotency and hepatocyte genes but induced some mesoderm transcripts. Upon removal of TSA-CRM, the endoderm/pancreatic gene expression profile returned to baseline. Our findings underscore the role epigenetic modification in transdifferentiation of one somatic cell into another. However, full reprogramming of fibroblasts to β-cells will require combination of this approach with TF overexpression and/or culture of the partially reprogrammed cells under -cell specific conditions. Rangarajan Sambathkumar and Eric Kalo contributed equally as co-first authors in this work (R. Sambathkumar and E. Kalo et al.). ispartof: Stem Cells International vol:2016 pages:1-8 ispartof: location:United States status: published

Published
2016

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