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Article: Evidence for

Katsuda, Takeshi / Li, Jinyang / Merrell, Allyson J / Sussman, Jonathan / Matsuzaki, Juntaro / Ochiya, Takahiro / Stanger, Ben Z

bioRxiv : the preprint server for biology

2023

Abstract: Over the last several years, a method has emerged which endows adult hepatocytes ... ...

Abstract	Over the last several years, a method has emerged which endows adult hepatocytes with
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.03.522656
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Article ; Online: A Feedback Loop Controlling Organ Size.

Merrell, Allyson J / Stanger, Ben Z

Developmental cell

2019 Volume 48, Issue 4, Page(s) 425–426

Abstract: To maintain proper organ size, nature has devised trans-organ communication systems-involving both paracrine and circulating regulatory factors-to safeguard homeostasis. In this issue of Developmental Cell, Ji et al. (2019) now describe an enterohepatic ... ...

Abstract	To maintain proper organ size, nature has devised trans-organ communication systems-involving both paracrine and circulating regulatory factors-to safeguard homeostasis. In this issue of Developmental Cell, Ji et al. (2019) now describe an enterohepatic feedback loop that balances tissue size and function in the mammalian liver.
MeSH term(s)	Animals ; Bile Acids and Salts ; Carcinogenesis ; Liver ; Organ Size ; Signal Transduction
Chemical Substances	Bile Acids and Salts
Language	English
Publishing date	2019-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2019.02.008
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Zs.A 5742: 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 76: Show issues

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Article ; Online: Evidence for in vitro extensive proliferation of adult hepatocytes and biliary epithelial cells.

Katsuda, Takeshi / Sussman, Jonathan / Li, Jinyang / Merrell, Allyson J / Vostrejs, William / Secreto, Anthony / Matsuzaki, Juntaro / Ochiya, Takahiro / Stanger, Ben Z

Stem cell reports

2023 Volume 18, Issue 7, Page(s) 1436–1450

Abstract: Over the last several years, a method has emerged that endows adult hepatocytes with in vitro proliferative capacity, producing chemically induced liver progenitors (CLiPs). However, there is a growing controversy regarding the origin of these cells. ... ...

Abstract	Over the last several years, a method has emerged that endows adult hepatocytes with in vitro proliferative capacity, producing chemically induced liver progenitors (CLiPs). However, there is a growing controversy regarding the origin of these cells. Here, we provide lineage tracing-based evidence that adult hepatocytes acquire proliferative capacity in vitro using rat and mouse models. Unexpectedly, we also found that the CLiP method allows biliary epithelial cells to acquire extensive proliferative capacity. Interestingly, after long-term culture, hepatocyte-derived cells (hepCLiPs) and biliary epithelial cell-derived cells (bilCLiPs) become similar in their gene expression patterns, and they both exhibit differentiation capacity to form hepatocyte-like cells. Finally, we provide evidence that hepCLiPs can repopulate injured mouse livers, reinforcing our earlier argument that CLiPs can be a cell source for liver regenerative medicine. This study advances our understanding of the origin of CLiPs and motivates the application of this technique in liver regenerative medicine.
MeSH term(s)	Mice ; Rats ; Animals ; Stem Cells/metabolism ; Hepatocytes ; Liver ; Epithelial Cells/metabolism ; Cell Differentiation ; Cell Proliferation
Language	English
Publishing date	2023-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2023.05.016
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Article ; Online: Cellular reprogramming in vivo initiated by SOX4 pioneer factor activity.

Katsuda, Takeshi / Sussman, Jonathan H / Ito, Kenji / Katznelson, Andrew / Yuan, Salina / Takenaka, Naomi / Li, Jinyang / Merrell, Allyson J / Cure, Hector / Li, Qinglan / Rasool, Reyaz Ur / Asangani, Irfan A / Zaret, Kenneth S / Stanger, Ben Z

Nature communications

2024 Volume 15, Issue 1, Page(s) 1761

Abstract: Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate " ... ...

Abstract	Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate "reprogramming" by opening new chromatin sites for expression that can attract transcription factors from the starting cell's enhancers. Here we report that SOX4 is sufficient to initiate hepatobiliary metaplasia in the adult mouse liver, closely mimicking metaplasia initiated by toxic damage to the liver. In lineage-traced cells, we assessed the timing of SOX4-mediated opening of enhancer chromatin versus enhancer decommissioning. Initially, SOX4 directly binds to and closes hepatocyte regulatory sequences via an overlapping motif with HNF4A, a hepatocyte master regulatory transcription factor. Subsequently, SOX4 exerts pioneer factor activity to open biliary regulatory sequences. The results delineate a hierarchy by which gene networks become reprogrammed under physiological conditions, providing deeper insight into the basis for cell fate transitions in animals.
MeSH term(s)	Animals ; Mice ; Cell Differentiation/genetics ; Cellular Reprogramming/genetics ; Chromatin ; Metaplasia ; Transcription Factors/metabolism
Chemical Substances	Chromatin ; Transcription Factors ; Sox4 protein, mouse
Language	English
Publishing date	2024-02-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45939-z
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Article ; Online: Adult cell plasticity in vivo: de-differentiation and transdifferentiation are back in style.

Merrell, Allyson J / Stanger, Ben Z

Nature reviews. Molecular cell biology

2016 Volume 17, Issue 7, Page(s) 413–425

Abstract: Biologists have long been intrigued by the possibility that cells can change their identity, a phenomenon known as cellular plasticity. The discovery that terminally differentiated cells can be experimentally coaxed to become pluripotent has invigorated ... ...

Abstract	Biologists have long been intrigued by the possibility that cells can change their identity, a phenomenon known as cellular plasticity. The discovery that terminally differentiated cells can be experimentally coaxed to become pluripotent has invigorated the field, and recent studies have demonstrated that changes in cell identity are not limited to the laboratory. Specifically, certain adult cells retain the capacity to de-differentiate or transdifferentiate under physiological conditions, as part of an organ's normal injury response. Recent studies have highlighted the extent to which cell plasticity contributes to tissue homeostasis, findings that have implications for cell-based therapy.
MeSH term(s)	Adult Stem Cells/physiology ; Animals ; Cell Dedifferentiation ; Cell Transdifferentiation ; Cell Transformation, Neoplastic ; Humans ; Neoplasms/pathology ; Regeneration ; Signal Transduction
Language	English
Publishing date	2016-03-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/nrm.2016.24
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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)
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Article: Physiological reprogramming

Katsuda, Takeshi / Sussman, Jonathan / Ito, Kenji / Katznelson, Andrew / Yuan, Salina / Li, Jinyang / Merrell, Allyson J / Takenaka, Naomi / Cure, Hector / Li, Qinglan / Rasool, Reyaz Ur / Asangani, Irfan A / Zaret, Kenneth S / Stanger, Ben Z

bioRxiv : the preprint server for biology

2023

Abstract	Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate "reprogramming" by opening new chromatin sites for expression that can attract transcription factors from the starting cell's enhancers. Here we report that Sox4 is sufficient to initiate hepatobiliary metaplasia in the adult liver. In lineage-traced cells, we assessed the timing of Sox4-mediated opening of enhancer chromatin versus enhancer decommissioning. Initially, Sox4 directly binds to and closes hepatocyte regulatory sequences via a motif it overlaps with Hnf4a, a hepatocyte master regulator. Subsequently, Sox4 exerts pioneer factor activity to open biliary regulatory sequences. The results delineate a hierarchy by which gene networks become reprogrammed under physiological conditions, providing deeper insight into the basis for cell fate transitions in animals.
Language	English
Publishing date	2023-02-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.14.528556
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Article ; Online: Fibroblast-derived

Sefton, Elizabeth M / Gallardo, Mirialys / Tobin, Claire E / Collins, Brittany C / Colasanto, Mary P / Merrell, Allyson J / Kardon, Gabrielle

eLife

2022 Volume 11

Abstract: The diaphragm is a domed muscle between the thorax and abdomen essential for breathing in mammals. Diaphragm development requires the coordinated development of muscle, connective tissue, and nerve, which are derived from different embryonic sources. ... ...

Abstract	The diaphragm is a domed muscle between the thorax and abdomen essential for breathing in mammals. Diaphragm development requires the coordinated development of muscle, connective tissue, and nerve, which are derived from different embryonic sources. Defects in diaphragm development cause the common and often lethal birth defect, congenital diaphragmatic hernias (CDH). HGF/MET signaling is required for diaphragm muscularization, but the source of HGF and the specific functions of this pathway in muscle progenitors and effects on phrenic nerve have not been explicitly tested. Using conditional mutagenesis in mice and pharmacological inhibition of MET, we demonstrate that the pleuroperitoneal folds (PPFs), transient embryonic structures that give rise to the connective tissue in the diaphragm, are the source of HGF critical for diaphragm muscularization. PPF-derived HGF is directly required for recruitment of MET+ muscle progenitors to the diaphragm and indirectly (via its effect on muscle development) required for phrenic nerve primary branching. In addition, HGF is continuously required for maintenance and motility of the pool of progenitors to enable full muscularization. Localization of HGF at the diaphragm's leading edges directs dorsal and ventral expansion of muscle and regulates its overall size and shape. Surprisingly, large muscleless regions in
MeSH term(s)	Animals ; Diaphragm ; Disease Models, Animal ; Fibroblasts/metabolism ; Hernias, Diaphragmatic, Congenital/genetics ; Mammals ; Mice ; Morphogenesis ; Phenyl Ethers/metabolism ; Thorax/metabolism
Chemical Substances	Phenyl Ethers
Language	English
Publishing date	2022-09-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.74592
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Article ; Online: Dissecting phenotypic transitions in metastatic disease via photoconversion-based isolation.

Sela, Yogev / Li, Jinyang / Kuri, Paola / Merrell, Allyson J / Li, Ning / Lengner, Chris / Rompolas, Pantelis / Stanger, Ben Z

eLife

2021 Volume 10

Abstract: Cancer patients often harbor occult metastases, a potential source of relapse that is targetable only through systemic therapy. Studies of this occult fraction have been limited by a lack of tools with which to isolate discrete cells on spatial grounds. ... ...

Abstract	Cancer patients often harbor occult metastases, a potential source of relapse that is targetable only through systemic therapy. Studies of this occult fraction have been limited by a lack of tools with which to isolate discrete cells on spatial grounds. We developed PIC-IT, a photoconversion-based isolation technique allowing efficient recovery of cell clusters of any size - including single-metastatic cells - which are largely inaccessible otherwise. In a murine pancreatic cancer model, transcriptional profiling of spontaneously arising microcolonies revealed phenotypic heterogeneity, functionally reduced propensity to proliferate and enrichment for an inflammatory-response phenotype associated with NF-κB/AP-1 signaling. Pharmacological inhibition of NF-κB depleted microcolonies but had no effect on macrometastases, suggesting microcolonies are particularly dependent on this pathway. PIC-IT thus enables systematic investigation of metastatic heterogeneity. Moreover, the technique can be applied to other biological systems in which isolation and characterization of spatially distinct cell populations is not currently feasible.
MeSH term(s)	Animals ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Light ; Male ; Medical Oncology/methods ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/diagnosis ; Pancreatic Neoplasms/physiopathology ; Phenotype ; Photochemical Processes
Language	English
Publishing date	2021-02-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.63270
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Article ; Online: Dynamic Transcriptional and Epigenetic Changes Drive Cellular Plasticity in the Liver.

Merrell, Allyson J / Peng, Tao / Li, Jinyang / Sun, Kathryn / Li, Bin / Katsuda, Takeshi / Grompe, Markus / Tan, Kai / Stanger, Ben Z

Hepatology (Baltimore, Md.)

2021 Volume 74, Issue 1, Page(s) 444–457

Abstract: Background and aims: Following liver injury, a fraction of hepatocytes adopt features of biliary epithelial cells (BECs) in a process known as biliary reprogramming. The aim of this study was to elucidate the molecular events accompanying this dramatic ... ...

Abstract	Background and aims: Following liver injury, a fraction of hepatocytes adopt features of biliary epithelial cells (BECs) in a process known as biliary reprogramming. The aim of this study was to elucidate the molecular events accompanying this dramatic shift in cellular identity. Approach and results: We applied the techniques of bulk RNA-sequencing (RNA-seq), single-cell RNA-seq, and assay for transposase-accessible chromatin with high-throughput sequencing to define the epigenetic and transcriptional changes associated with biliary reprogramming. In addition, we examined the role of TGF-β signaling by profiling cells undergoing reprogramming in mice with hepatocyte-specific deletion in the downstream TGF-β signaling component mothers against decapentaplegic homolog 4 (Smad4). Biliary reprogramming followed a stereotyped pattern of altered gene expression consisting of robust induction of biliary genes and weaker repression of hepatocyte genes. These changes in gene expression were accompanied by corresponding modifications at the chromatin level. Although some reprogrammed cells had molecular features of "fully differentiated" BECs, most lacked some biliary characteristics and retained some hepatocyte characteristics. Surprisingly, single-cell analysis of Smad4 mutant mice revealed a dramatic increase in reprogramming. Conclusion: Hepatocytes undergo widespread chromatin and transcriptional changes during biliary reprogramming, resulting in epigenetic and gene expression profiles that are similar to, but distinct from, native BECs. Reprogramming involves a progressive accumulation of biliary molecular features without discrete intermediates. Paradoxically, canonical TGF-β signaling through Smad4 appears to constrain biliary reprogramming, indicating that TGF-β can either promote or inhibit biliary differentiation depending on which downstream components of the pathway are engaged. This work has implications for the formation of BECs and bile ducts in the adult liver.
MeSH term(s)	Animals ; Bile Ducts/cytology ; Cell Differentiation/genetics ; Cell Plasticity/genetics ; Epigenesis, Genetic ; Epithelial Cells/physiology ; Hepatocytes/physiology ; Hepatocytes/transplantation ; Humans ; Liver/cytology ; Liver/physiology ; Liver Regeneration/genetics ; Male ; Mice ; Mice, Transgenic ; RNA-Seq ; Single-Cell Analysis ; Smad4 Protein/genetics
Chemical Substances	Smad4 Protein ; Smad4 protein, mouse
Language	English
Publishing date	2021-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.31704
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Article ; Online: Dissecting phenotypic transitions in metastatic disease via photoconversion-based isolation

Yogev Sela / Jinyang Li / Paola Kuri / Allyson J Merrell / Ning Li / Chris Lengner / Pantelis Rompolas / Ben Z Stanger

eLife, Vol

2021 Volume 10

Abstract	Cancer patients often harbor occult metastases, a potential source of relapse that is targetable only through systemic therapy. Studies of this occult fraction have been limited by a lack of tools with which to isolate discrete cells on spatial grounds. We developed PIC-IT, a photoconversion-based isolation technique allowing efficient recovery of cell clusters of any size – including single-metastatic cells – which are largely inaccessible otherwise. In a murine pancreatic cancer model, transcriptional profiling of spontaneously arising microcolonies revealed phenotypic heterogeneity, functionally reduced propensity to proliferate and enrichment for an inflammatory-response phenotype associated with NF-κB/AP-1 signaling. Pharmacological inhibition of NF-κB depleted microcolonies but had no effect on macrometastases, suggesting microcolonies are particularly dependent on this pathway. PIC-IT thus enables systematic investigation of metastatic heterogeneity. Moreover, the technique can be applied to other biological systems in which isolation and characterization of spatially distinct cell populations is not currently feasible.
Keywords	cell isolation ; metastasis ; photoconversion ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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