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Artikel: Piezo inhibition prevents

Griffin, Michelle F / Talbott, Heather E / Guardino, Nicholas J / Guo, Jason L / Spielman, Amanda F / Chen, Kellen / Parker, Jennifer B L / Mascharak, Shamik / Henn, Dominic / Liang, Norah / King, Megan / Cotterell, Asha C / Bauer-Rowe, Khristian E / Abbas, Darren B / Diaz Deleon, Nestor M / Sivaraj, Dharshan / Fahy, Evan J / Downer, Mauricio / Akras, Deena /

Berry, Charlotte / Cook, Jessica / Quarto, Natalina / Klein, Ophir D / Lorenz, H Peter / Gurtner, Geoffrey C / Januszyk, Michael / Wan, Derrick C / Longaker, Michael T

bioRxiv : the preprint server for biology

2023

Abstract: While past studies have suggested that plasticity exists between dermal fibroblasts and adipocytes, it remains unknown whether fat actively contributes to fibrosis in scarring. We show that adipocytes convert to scar-forming fibroblasts in response ... ...

Abstract	While past studies have suggested that plasticity exists between dermal fibroblasts and adipocytes, it remains unknown whether fat actively contributes to fibrosis in scarring. We show that adipocytes convert to scar-forming fibroblasts in response to
Sprache	Englisch
Erscheinungsdatum	2023-04-04
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2023.04.03.535302
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Dietary suppression of MHC class II expression in intestinal epithelial cells enhances intestinal tumorigenesis.

Beyaz, Semir / Chung, Charlie / Mou, Haiwei / Bauer-Rowe, Khristian E / Xifaras, Michael E / Ergin, Ilgin / Dohnalova, Lenka / Biton, Moshe / Shekhar, Karthik / Eskiocak, Onur / Papciak, Katherine / Ozler, Kadir / Almeqdadi, Mohammad / Yueh, Brian / Fein, Miriam / Annamalai, Damodaran / Valle-Encinas, Eider / Erdemir, Aysegul / Dogum, Karoline /

Shah, Vyom / Alici-Garipcan, Aybuke / Meyer, Hannah V / Özata, Deniz M / Elinav, Eran / Kucukural, Alper / Kumar, Pawan / McAleer, Jeremy P / Fox, James G / Thaiss, Christoph A / Regev, Aviv / Roper, Jatin / Orkin, Stuart H / Yilmaz, Ömer H

Cell stem cell

2021 Band 28, Heft 11, Seite(n) 1922–1935.e5

Abstract: Little is known about how interactions of diet, intestinal stem cells (ISCs), and immune cells affect early-stage intestinal tumorigenesis. We show that a high-fat diet (HFD) reduces the expression of the major histocompatibility complex class II (MHC ... ...

Abstract	Little is known about how interactions of diet, intestinal stem cells (ISCs), and immune cells affect early-stage intestinal tumorigenesis. We show that a high-fat diet (HFD) reduces the expression of the major histocompatibility complex class II (MHC class II) genes in intestinal epithelial cells, including ISCs. This decline in epithelial MHC class II expression in a HFD correlates with reduced intestinal microbiome diversity. Microbial community transfer experiments suggest that epithelial MHC class II expression is regulated by intestinal flora. Mechanistically, pattern recognition receptor (PRR) and interferon-gamma (IFNγ) signaling regulates epithelial MHC class II expression. MHC class II-negative (MHC-II-) ISCs exhibit greater tumor-initiating capacity than their MHC class II-positive (MHC-II+) counterparts upon loss of the tumor suppressor Apc coupled with a HFD, suggesting a role for epithelial MHC class II-mediated immune surveillance in suppressing tumorigenesis. ISC-specific genetic ablation of MHC class II increases tumor burden cell autonomously. Thus, HFD perturbs a microbiome-stem cell-immune cell interaction that contributes to tumor initiation in the intestine.
Mesh-Begriff(e)	Carcinogenesis ; Diet, High-Fat ; Epithelial Cells ; Histocompatibility Antigens Class II ; Humans ; Intestines
Chemische Substanzen	Histocompatibility Antigens Class II
Sprache	Englisch
Erscheinungsdatum	2021-09-15
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2021.08.007
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Ketone Body Signaling Mediates Intestinal Stem Cell Homeostasis and Adaptation to Diet

Cheng, Chia-Wei / Biton, Moshe / Haber, Adam L / Gunduz, Nuray / Eng, George / Gaynor, Liam T / Tripathi, Surya / Calibasi-Kocal, Gizem / Rickelt, Steffen / Butty, Vincent L / Moreno-Serrano, Marta / Iqbal, Ameena M / Bauer-Rowe, Khristian E / Imada, Shinya / Ulutas, Mehmet Sefa / Mylonas, Constantine / Whary, Mark T / Levine, Stuart S / Basbinar, Yasemin /

Hynes, Richard O / Mino-Kenudson, Mari / Deshpande, Vikram / Boyer, Laurie A / Fox, James G / Terranova, Christopher / Rai, Kunal / Piwnica-Worms, Helen / Mihaylova, Maria M / Regev, Aviv / Yilmaz, Ömer H

Cell. 2019 Aug. 22, v. 178, no. 5

2019

Abstract: Little is known about how metabolites couple tissue-specific stem cell function with physiology. Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the rate- ... ...

Abstract	Little is known about how metabolites couple tissue-specific stem cell function with physiology. Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the rate-limiting enzyme in the production of ketone bodies, including beta-hydroxybutyrate (βOHB), distinguishes self-renewing Lgr5+ stem cells (ISCs) from differentiated cell types. Hmgcs2 loss depletes βOHB levels in Lgr5+ ISCs and skews their differentiation toward secretory cell fates, which can be rescued by exogenous βOHB and class I histone deacetylase (HDAC) inhibitor treatment. Mechanistically, βOHB acts by inhibiting HDACs to reinforce Notch signaling, instructing ISC self-renewal and lineage decisions. Notably, although a high-fat ketogenic diet elevates ISC function and post-injury regeneration through βOHB-mediated Notch signaling, a glucose-supplemented diet has the opposite effects. These findings reveal how control of βOHB-activated signaling in ISCs by diet helps to fine-tune stem cell adaptation in homeostasis and injury.
Schlagwörter	3-hydroxybutyric acid ; genes ; histone deacetylase ; homeostasis ; hydroxymethylglutaryl-CoA synthase ; ketogenic diet ; ketone bodies ; mammals ; small intestine ; stem cells
Sprache	Englisch
Erscheinungsverlauf	2019-0822
Umfang	p. 1115-1131.e15.
Erscheinungsort	Elsevier Inc.
Dokumenttyp	Artikel
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2019.07.048
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Multiomic analysis reveals conservation of cancer-associated fibroblast phenotypes across species and tissue of origin.

Foster, Deshka S / Januszyk, Michael / Delitto, Daniel / Yost, Kathryn E / Griffin, Michelle / Guo, Jason / Guardino, Nicholas / Delitto, Andrea E / Chinta, Malini / Burcham, Austin R / Nguyen, Alan T / Bauer-Rowe, Khristian E / Titan, Ashley L / Salhotra, Ankit / Jones, R Ellen / da Silva, Oscar / Lindsay, Hunter G / Berry, Charlotte E / Chen, Kellen /

Henn, Dominic / Mascharak, Shamik / Talbott, Heather E / Kim, Alexia / Nosrati, Fatemeh / Sivaraj, Dharshan / Ransom, R Chase / Matthews, Michael / Khan, Anum / Wagh, Dhananjay / Coller, John / Gurtner, Geoffrey C / Wan, Derrick C / Wapnir, Irene L / Chang, Howard Y / Norton, Jeffrey A / Longaker, Michael T

Cancer cell

2022 Band 40, Heft 11, Seite(n) 1392–1406.e7

Abstract: Cancer-associated fibroblasts (CAFs) are integral to the solid tumor microenvironment. CAFs were once thought to be a relatively uniform population of matrix-producing cells, but single-cell RNA sequencing has revealed diverse CAF phenotypes. Here, we ... ...

Abstract	Cancer-associated fibroblasts (CAFs) are integral to the solid tumor microenvironment. CAFs were once thought to be a relatively uniform population of matrix-producing cells, but single-cell RNA sequencing has revealed diverse CAF phenotypes. Here, we further probed CAF heterogeneity with a comprehensive multiomics approach. Using paired, same-cell chromatin accessibility and transcriptome analysis, we provided an integrated analysis of CAF subpopulations over a complex spatial transcriptomic and proteomic landscape to identify three superclusters: steady state-like (SSL), mechanoresponsive (MR), and immunomodulatory (IM) CAFs. These superclusters are recapitulated across multiple tissue types and species. Selective disruption of underlying mechanical force or immune checkpoint inhibition therapy results in shifts in CAF subpopulation distributions and affected tumor growth. As such, the balance among CAF superclusters may have considerable translational implications. Collectively, this research expands our understanding of CAF biology, identifying regulatory pathways in CAF differentiation and elucidating therapeutic targets in a species- and tumor-agnostic manner.
Mesh-Begriff(e)	Humans ; Cancer-Associated Fibroblasts/pathology ; Proteomics ; Tumor Microenvironment/genetics ; Phenotype ; Neoplasms/genetics ; Neoplasms/pathology
Sprache	Englisch
Erscheinungsdatum	2022-10-20
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2022.09.015
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging.

Cell stem cell

2018 Band 22, Heft 5, Seite(n) 769–778.e4

Abstract: Diet has a profound effect on tissue regeneration in diverse organisms, and low caloric states such as intermittent fasting have beneficial effects on organismal health and age-associated loss of tissue function. The role of adult stem and progenitor ... ...

Abstract	Diet has a profound effect on tissue regeneration in diverse organisms, and low caloric states such as intermittent fasting have beneficial effects on organismal health and age-associated loss of tissue function. The role of adult stem and progenitor cells in responding to short-term fasting and whether such responses improve regeneration are not well studied. Here we show that a 24 hr fast augments intestinal stem cell (ISC) function in young and aged mice by inducing a fatty acid oxidation (FAO) program and that pharmacological activation of this program mimics many effects of fasting. Acute genetic disruption of Cpt1a, the rate-limiting enzyme in FAO, abrogates ISC-enhancing effects of fasting, but long-term Cpt1a deletion decreases ISC numbers and function, implicating a role for FAO in ISC maintenance. These findings highlight a role for FAO in mediating pro-regenerative effects of fasting in intestinal biology, and they may represent a viable strategy for enhancing intestinal regeneration.
Mesh-Begriff(e)	Aging ; Animals ; Cells, Cultured ; Fasting/metabolism ; Fatty Acids/metabolism ; Homeostasis ; Intestines/cytology ; Mice ; Mice, Inbred Strains ; Oxidation-Reduction ; Stem Cells/cytology ; Stem Cells/metabolism
Chemische Substanzen	Fatty Acids
Sprache	Englisch
Erscheinungsdatum	2018-05-04
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2018.04.001
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Ketone Body Signaling Mediates Intestinal Stem Cell Homeostasis and Adaptation to Diet.

Cell

2019 Band 178, Heft 5, Seite(n) 1115–1131.e15

Abstract	Little is known about how metabolites couple tissue-specific stem cell function with physiology. Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the rate-limiting enzyme in the production of ketone bodies, including beta-hydroxybutyrate (βOHB), distinguishes self-renewing Lgr5
Mesh-Begriff(e)	3-Hydroxybutyric Acid/blood ; 3-Hydroxybutyric Acid/pharmacology ; Aged, 80 and over ; Animals ; Cell Differentiation/drug effects ; Cell Self Renewal ; Diet, High-Fat ; Female ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Synthase/deficiency ; Hydroxymethylglutaryl-CoA Synthase/genetics ; Hydroxymethylglutaryl-CoA Synthase/metabolism ; Intestines/cytology ; Intestines/pathology ; Ketone Bodies/metabolism ; Male ; Mice ; Mice, Knockout ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Notch/metabolism ; Signal Transduction/drug effects ; Stem Cells/cytology ; Stem Cells/metabolism ; Young Adult
Chemische Substanzen	Histone Deacetylase Inhibitors ; Ketone Bodies ; Lgr5 protein, mouse ; Receptors, G-Protein-Coupled ; Receptors, Notch ; HMGCS2 protein, mouse (EC 2.3.3.10) ; Hydroxymethylglutaryl-CoA Synthase (EC 2.3.3.10) ; 3-Hydroxybutyric Acid (TZP1275679)
Sprache	Englisch
Erscheinungsdatum	2019-09-03
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2019.07.048
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Author Correction: High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

Beyaz, Semir / Mana, Miyeko D / Roper, Jatin / Kedrin, Dmitriy / Saadatpour, Assieh / Hong, Sue-Jean / Bauer-Rowe, Khristian E / Xifaras, Michael E / Akkad, Adam / Arias, Erika / Pinello, Luca / Katz, Yarden / Shinagare, Shweta / Abu-Remaileh, Monther / Mihaylova, Maria M / Lamming, Dudley W / Dogum, Rizkullah / Guo, Guoji / Bell, George W /

Selig, Martin / Nielsen, G Petur / Gupta, Nitin / Ferrone, Cristina R / Deshpande, Vikram / Yuan, Guo-Cheng / Orkin, Stuart H / Sabatini, David M / Yilmaz, Ömer H

Nature

2018 Band 560, Heft 7717, Seite(n) E26

Abstract: In Fig. 4e of this Article, the labels for 'Control' and 'HFD' were reversed ('Control' should have been labelled blue rather than purple, and 'HFD' should have been labelled purple rather than blue). Similarly, in Fig. 4f of this Article, the labels for ...

Abstract	In Fig. 4e of this Article, the labels for 'Control' and 'HFD' were reversed ('Control' should have been labelled blue rather than purple, and 'HFD' should have been labelled purple rather than blue). Similarly, in Fig. 4f of this Article, the labels for 'V' and 'GW' were reversed ('V' should have been labelled blue rather than purple, and 'GW' should have been labelled purple instead of blue). The original figure has been corrected online.
Sprache	Englisch
Erscheinungsdatum	2018-05-17
Erscheinungsland	England
Dokumenttyp	Journal Article ; Published Erratum
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-018-0187-y
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake.

Yilmaz, Ömer H / Katajisto, Pekka / Lamming, Dudley W / Gültekin, Yetis / Bauer-Rowe, Khristian E / Sengupta, Shomit / Birsoy, Kivanc / Dursun, Abdulmetin / Yilmaz, V Onur / Selig, Martin / Nielsen, G Petur / Mino-Kenudson, Mari / Zukerberg, Lawrence R / Bhan, Atul K / Deshpande, Vikram / Sabatini, David M

Nature

2012 Band 486, Heft 7404, Seite(n) 490–495

Abstract: How adult tissue stem and niche cells respond to the nutritional state of an organism is not well understood. Here we find that Paneth cells, a key constituent of the mammalian intestinal stem-cell (ISC) niche, augment stem-cell function in response to ... ...

Abstract	How adult tissue stem and niche cells respond to the nutritional state of an organism is not well understood. Here we find that Paneth cells, a key constituent of the mammalian intestinal stem-cell (ISC) niche, augment stem-cell function in response to calorie restriction. Calorie restriction acts by reducing mechanistic target of rapamycin complex 1 (mTORC1) signalling in Paneth cells, and the ISC-enhancing effects of calorie restriction can be mimicked by rapamycin. Calorie intake regulates mTORC1 in Paneth cells, but not ISCs, and forced activation of mTORC1 in Paneth cells during calorie restriction abolishes the ISC-augmenting effects of the niche. Finally, increased expression of bone stromal antigen 1 (Bst1) in Paneth cells—an ectoenzyme that produces the paracrine factor cyclic ADP ribose—mediates the effects of calorie restriction and rapamycin on ISC function. Our findings establish that mTORC1 non-cell-autonomously regulates stem-cell self-renewal, and highlight a significant role of the mammalian intestinal niche in coupling stem-cell function to organismal physiology.
Mesh-Begriff(e)	ADP-ribosyl Cyclase/metabolism ; Animals ; Antigens, CD/metabolism ; Caloric Restriction ; Cell Count ; Cell Division/drug effects ; Cyclic ADP-Ribose/metabolism ; Energy Intake/physiology ; Female ; GPI-Linked Proteins/agonists ; GPI-Linked Proteins/metabolism ; Intestines/cytology ; Longevity/physiology ; Male ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Multiprotein Complexes ; Paneth Cells/cytology ; Paneth Cells/drug effects ; Paneth Cells/metabolism ; Paracrine Communication ; Proteins/antagonists & inhibitors ; Proteins/metabolism ; Regeneration/drug effects ; Signal Transduction ; Sirolimus/pharmacology ; Stem Cell Niche/drug effects ; Stem Cell Niche/physiology ; Stem Cells/cytology ; Stem Cells/drug effects ; Stem Cells/metabolism ; TOR Serine-Threonine Kinases
Chemische Substanzen	Antigens, CD ; GPI-Linked Proteins ; Multiprotein Complexes ; Proteins ; Cyclic ADP-Ribose (119340-53-3) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; ADP-ribosyl Cyclase (EC 3.2.2.5) ; ADP-ribosyl cyclase 2 (EC 3.2.2.5) ; Sirolimus (W36ZG6FT64)
Sprache	Englisch
Erscheinungsdatum	2012-06-22
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature11163
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

Selig, Martin / Nielsen, G Petur / Gupta, Nitin / Ferrone, Cristina R / Deshpande, Vikram / Yuan, Guo-Cheng / Orkin, Stuart H / Sabatini, David M / Yilmaz, Ömer H

Nature

2016 Band 531, Heft 7592, Seite(n) 53–58

Abstract: Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. ... ...

Abstract	Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-δ) signature in intestinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation of PPAR-δ recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-δ-dependent manner. Notably, HFD- and agonist-activated PPAR-δ signalling endow organoid-initiating capacity to progenitors, and enforced PPAR-δ signalling permits these progenitors to form in vivo tumours after loss of the tumour suppressor Apc. These findings highlight how diet-modulated PPAR-δ activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumours.
Mesh-Begriff(e)	Animals ; Cell Count ; Cell Self Renewal/drug effects ; Cell Transformation, Neoplastic/drug effects ; Colonic Neoplasms/pathology ; Diet, High-Fat/adverse effects ; Female ; Genes, APC ; Humans ; Intestines/pathology ; Male ; Mice ; Obesity/chemically induced ; Obesity/pathology ; Organoids/drug effects ; Organoids/metabolism ; Organoids/pathology ; PPAR delta/metabolism ; Signal Transduction/drug effects ; Stem Cell Niche/drug effects ; Stem Cells/drug effects ; Stem Cells/metabolism ; Stem Cells/pathology ; beta Catenin/metabolism
Chemische Substanzen	PPAR delta ; beta Catenin
Sprache	Englisch
Erscheinungsdatum	2016-03-03
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature17173
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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