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Article: HIGD1A-mediated dormancy and tumor survival.

Ameri, Kurosh / Maltepe, Emin

Molecular & cellular oncology

2015 Volume 2, Issue 4, Page(s) e1030537

Abstract: Solid tumors contain regions of anoxia that are also glucose deprived. How cancer cells survive such extreme conditions remains unclear. Here, we discuss our recent findings that regulation of hypoxia inducible gene domain family member 1 A (HIGD1A) via ... ...

Abstract	Solid tumors contain regions of anoxia that are also glucose deprived. How cancer cells survive such extreme conditions remains unclear. Here, we discuss our recent findings that regulation of hypoxia inducible gene domain family member 1 A (HIGD1A) via epigenetic mechanisms during glucose starvation modulates oxygen consumption and reactive oxygen species production to enable tumor cell survival through the activation of dormancy mechanisms.
Language	English
Publishing date	2015-04-14
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2015.1030537
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Article ; Online: Three-Dimensional Bioprinting: Emerging Technology in Cardiovascular Medicine.

Ameri, Kurosh / Samurkashian, Raffi / Yeghiazarians, Yerem

Circulation

2017 Volume 135, Issue 14, Page(s) 1281–1283

MeSH term(s)	Animals ; Biomedical Research/instrumentation ; Biomedical Research/methods ; Bioprinting/instrumentation ; Bioprinting/methods ; Blood Vessel Prosthesis ; Computer-Aided Design ; Diffusion of Innovation ; Heart Valve Prosthesis ; Humans ; Lab-On-A-Chip Devices ; Models, Anatomic ; Models, Cardiovascular ; Patient-Specific Modeling ; Printing, Three-Dimensional/instrumentation ; Prosthesis Design
Language	English
Publishing date	2017-03-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.116.024945
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Article ; Online: Interleukin-15 modulates the response of cortical neurons to ischemia.

Nguyen, Vien / Ameri, Kurosh / Huynh, Kevin / Fredkin, Maxwell / Grona, Reinier / Larpthaveesarp, Amara / Gonzalez, Fernando / Yeghiazarians, Yerem

Molecular and cellular neurosciences

2021 Volume 115, Page(s) 103658

Abstract: Objective: Stroke is a major cause of death and disability in the United States. Current acute stroke therapy consists of clot-dissolving drugs, catheter-based interventions and physical rehabilitation. To date, there are no therapies that directly ... ...

Abstract	Objective: Stroke is a major cause of death and disability in the United States. Current acute stroke therapy consists of clot-dissolving drugs, catheter-based interventions and physical rehabilitation. To date, there are no therapies that directly enhance neuronal survival after a stroke. Previous work from our lab demonstrated that Interleukin-15 (IL-15) peptide could rescue cardiomyocytes subjected to hypoxia. We sought to extend these findings to cortical neurons since IL-15 has been implicated to have an important role in neuronal homeostasis. Methods: We have evaluated the effect of IL-15 peptide on primary cortical neurons derived from embryonic rats in vitro under conditions of anoxia and glucose deprivation, and in vivo following middle cerebral artery occlusion. Results: IL-15 administration rescued neuronal cells subjected to anoxia coupled with glucose deprivation (AGD), as well as with reoxygenation. A hallmark of stroke is the ischemic microenvironment and associated oxidative stress, which results in DNA damage and ER stress, both of which contribute to neuronal cell damage and death. The expression of anoxia, ER stress, and DNA damage factors/markers was evaluated via western blot and correlated with the cellular survival effects of IL-15 in vitro. In addition, IL-15 effect of alleviating ER stress and increasing cell survival was also observed in vivo. Interpretation: Our data indicate, for the first time, that administration of the pleiotropic factor IL-15 reduces neuronal cell death during AGD, which correlates with modulation of multiple cellular stress pathways.
MeSH term(s)	Animals ; Brain Ischemia/drug therapy ; Cell Survival ; Cells, Cultured ; Glucose ; Infarction, Middle Cerebral Artery ; Interleukin-15 ; Neurons ; Rats ; Stroke
Chemical Substances	Interleukin-15 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-07-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2021.103658
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Article ; Online: Administration of Interleukin-15 Peptide Improves Cardiac Function in a Mouse Model of Myocardial Infarction.

Ameri, Kurosh / Bayardorj, Dulguun / Samurkashian, Raffi / Fredkin, Maxwell / Fuh, Eric / Nguyen, Vien / Yeghiazarians, Yerem

Journal of cardiovascular pharmacology

2019 Volume 75, Issue 1, Page(s) 98–102

Abstract: Interleukin-15 is a pleotropic factor, capable of modulating metabolism, survival, proliferation, and differentiation in many different cell types. The rationale behind this study relates to previous work demonstrating that IL-15 is a major factor ... ...

Abstract	Interleukin-15 is a pleotropic factor, capable of modulating metabolism, survival, proliferation, and differentiation in many different cell types. The rationale behind this study relates to previous work demonstrating that IL-15 is a major factor present in stem cell extracts, which protects cardiomyocytes subjected to hypoxic stress in vitro. The objective of this current study was to assess whether administration of IL-15 peptide will also show protective effects in vivo. The data indicate that administration of IL-15 reduces cell death, increases vascularity, decreases scar size, and significantly improves left ventricular ejection fraction in a mouse model of myocardial infarction.
MeSH term(s)	Animals ; Cardiovascular Agents/pharmacology ; Cell Death/drug effects ; Cells, Cultured ; Disease Models, Animal ; Human Umbilical Vein Endothelial Cells/drug effects ; Humans ; Interleukin-15/pharmacology ; Male ; Mice, Inbred C57BL ; Myocardial Infarction/drug therapy ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; Neovascularization, Physiologic/drug effects ; Recovery of Function ; Stroke Volume/drug effects ; Ventricular Function, Left/drug effects
Chemical Substances	Cardiovascular Agents ; Interleukin-15
Language	English
Publishing date	2019-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000000764
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Article ; Online: TGF-β1/CD105 signaling controls vascular network formation within growth factor sequestering hyaluronic acid hydrogels.

Browne, Shane / Jha, Amit K / Ameri, Kurosh / Marcus, Sivan G / Yeghiazarians, Yerem / Healy, Kevin E

PloS one

2018 Volume 13, Issue 3, Page(s) e0194679

Abstract: Cell-based strategies for the treatment of ischemic diseases are at the forefront of tissue engineering and regenerative medicine. Cell therapies purportedly can play a key role in the neovascularization of ischemic tissue; however, low survival and poor ...

Abstract	Cell-based strategies for the treatment of ischemic diseases are at the forefront of tissue engineering and regenerative medicine. Cell therapies purportedly can play a key role in the neovascularization of ischemic tissue; however, low survival and poor cell engraftment with the host vasculature following implantation limits their potential to treat ischemic diseases. To overcome these limitations, we previously developed a growth factor sequestering hyaluronic acid (HyA)-based hydrogel that enhanced transplanted mouse cardiosphere-derived cell survival and formation of vasculature that anastomosed with host vessels. In this work, we examined the mechanism by which HyA hydrogels presenting transforming growth factor beta-1 (TGF-β1) promoted proliferation of more clinically relevant human cardiosphere-derived cells (hCDC), and their formation of vascular-like networks in vitro. We observed hCDC proliferation and enhanced formation of vascular-like networks occurred in the presence of TGF-β1. Furthermore, production of nitric oxide (NO), VEGF, and a host of angiogenic factors were increased in the presence of TGF-β1. This response was dependent on the co-activity of CD105 (Endoglin) with the TGF-βR2 receptor, demonstrating its role in the process of angiogenic differentiation and vascular organization of hCDC. These results demonstrated that hCDC form vascular-like networks in vitro, and that the induction of vascular networks by hCDC within growth factor sequestering HyA hydrogels was mediated by TGF-β1/CD105 signaling.
MeSH term(s)	Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cell- and Tissue-Based Therapy/instrumentation ; Cell- and Tissue-Based Therapy/methods ; Cells, Cultured ; Drug Compounding/methods ; Endoglin/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/physiology ; Humans ; Hyaluronic Acid/chemistry ; Hydrogels/chemistry ; Hydrogels/metabolism ; Myocardium/cytology ; Myocardium/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/physiology ; Neovascularization, Physiologic/drug effects ; Neovascularization, Physiologic/physiology ; Signal Transduction/drug effects ; Spheroids, Cellular/cytology ; Spheroids, Cellular/drug effects ; Spheroids, Cellular/metabolism ; Tissue Scaffolds/chemistry ; Transforming Growth Factor beta1/metabolism ; Transforming Growth Factor beta1/pharmacology
Chemical Substances	Endoglin ; Hydrogels ; Transforming Growth Factor beta1 ; Hyaluronic Acid (9004-61-9)
Language	English
Publishing date	2018-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0194679
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Article ; Online: Sonic Hedgehog Agonist Protects Against Complex Neonatal Cerebellar Injury.

Nguyen, Vien / Sabeur, Khalida / Maltepe, Emin / Ameri, Kurosh / Bayraktar, Omer / Rowitch, David H

Cerebellum (London, England)

2017 Volume 17, Issue 2, Page(s) 213–227

Abstract: The cerebellum undergoes rapid growth during the third trimester and is vulnerable to injury and deficient growth in infants born prematurely. Factors associated with preterm cerebellar hypoplasia include chronic lung disease and postnatal glucocorticoid ...

Abstract	The cerebellum undergoes rapid growth during the third trimester and is vulnerable to injury and deficient growth in infants born prematurely. Factors associated with preterm cerebellar hypoplasia include chronic lung disease and postnatal glucocorticoid administration. We modeled chronic hypoxemia and glucocorticoid administration in neonatal mice to study whole cerebellar and cell type-specific effects of dual exposure. Chronic neonatal hypoxia resulted in permanent cerebellar hypoplasia. This was compounded by administration of prednisolone as shown by greater volume loss and Purkinje cell death. In the setting of hypoxia and prednisolone, administration of a small molecule Smoothened-Hedgehog agonist (SAG) preserved cerebellar volume and protected against Purkinje cell death. Such protective effects were observed even when SAG was given as a one-time dose after dual insult. To model complex injury and determine cell type-specific roles for the hypoxia inducible factor (HIF) pathway, we performed conditional knockout of von Hippel Lindau (VHL) to hyperactivate HIF1α in cerebellar granule neuron precursors (CGNP) or Purkinje cells. Surprisingly, HIF activation in either cell type resulted in no cerebellar deficit. However, in mice administered prednisolone, HIF overactivation in CGNPs resulted in significant cerebellar hypoplasia, whereas HIF overactivation in Purkinje cells caused cell death. Together, these findings indicate that HIF primes both cell types for injury via glucocorticoids, and that hypoxia/HIF + postnatal glucocorticoid administration act on distinct cellular pathways to cause cerebellar injury. They further suggest that SAG is neuroprotective in the setting of complex neonatal cerebellar injury.
MeSH term(s)	Amino Acids, Dicarboxylic/pharmacology ; Animals ; Animals, Newborn ; Anti-Inflammatory Agents/therapeutic use ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Calcium-Binding Proteins/metabolism ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Cells, Cultured ; Cerebellum/abnormalities ; Cerebellum/drug effects ; Cyclohexylamines/therapeutic use ; Developmental Disabilities/etiology ; Disease Models, Animal ; Gene Expression Regulation, Developmental/drug effects ; Gene Expression Regulation, Developmental/genetics ; Glucocorticoids/pharmacology ; Hedgehog Proteins/agonists ; Hedgehog Proteins/metabolism ; Hypoxia, Brain/complications ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microfilament Proteins/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nervous System Malformations/etiology ; Neuroprotective Agents/therapeutic use ; Prednisolone/therapeutic use ; Purkinje Cells/drug effects ; Purkinje Cells/metabolism ; Thiophenes/therapeutic use ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism ; Zinc Finger Protein GLI1/genetics ; Zinc Finger Protein GLI1/metabolism
Chemical Substances	Aif1 protein, mouse ; Amino Acids, Dicarboxylic ; Anti-Inflammatory Agents ; Atoh1 protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Calcium-Binding Proteins ; Cyclohexylamines ; Glucocorticoids ; Hedgehog Proteins ; Microfilament Proteins ; Nerve Tissue Proteins ; Neuroprotective Agents ; Purkinje cell protein L7 ; SAG compound ; Shh protein, mouse ; Thiophenes ; Zinc Finger Protein GLI1 ; Prednisolone (9PHQ9Y1OLM) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; VHL protein, mouse (EC 6.3.2.-) ; oxalylglycine (VVW38EB8YS)
Language	English
Publishing date	2017-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	2112586-7
ISSN	1473-4230 ; 1473-4222
ISSN (online)	1473-4230
ISSN	1473-4222
DOI	10.1007/s12311-017-0895-0
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Article ; Online: TGF-β1/CD105 signaling controls vascular network formation within growth factor sequestering hyaluronic acid hydrogels.

Shane Browne / Amit K Jha / Kurosh Ameri / Sivan G Marcus / Yerem Yeghiazarians / Kevin E Healy

PLoS ONE, Vol 13, Iss 3, p e

2018 Volume 0194679

Abstract	Cell-based strategies for the treatment of ischemic diseases are at the forefront of tissue engineering and regenerative medicine. Cell therapies purportedly can play a key role in the neovascularization of ischemic tissue; however, low survival and poor cell engraftment with the host vasculature following implantation limits their potential to treat ischemic diseases. To overcome these limitations, we previously developed a growth factor sequestering hyaluronic acid (HyA)-based hydrogel that enhanced transplanted mouse cardiosphere-derived cell survival and formation of vasculature that anastomosed with host vessels. In this work, we examined the mechanism by which HyA hydrogels presenting transforming growth factor beta-1 (TGF-β1) promoted proliferation of more clinically relevant human cardiosphere-derived cells (hCDC), and their formation of vascular-like networks in vitro. We observed hCDC proliferation and enhanced formation of vascular-like networks occurred in the presence of TGF-β1. Furthermore, production of nitric oxide (NO), VEGF, and a host of angiogenic factors were increased in the presence of TGF-β1. This response was dependent on the co-activity of CD105 (Endoglin) with the TGF-βR2 receptor, demonstrating its role in the process of angiogenic differentiation and vascular organization of hCDC. These results demonstrated that hCDC form vascular-like networks in vitro, and that the induction of vascular networks by hCDC within growth factor sequestering HyA hydrogels was mediated by TGF-β1/CD105 signaling.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Activating transcription factor 4.

Ameri, Kurosh / Harris, Adrian L

The international journal of biochemistry & cell biology

2008 Volume 40, Issue 1, Page(s) 14–21

Abstract: Activating transcription factor 4 (ATF4) belongs to the ATF/CREB (activating transcription factor/cyclic AMP response element binding protein) family of basic region-leucine zipper (bZip) transcription factors, which have the consensus binding site cAMP ... ...

Abstract	Activating transcription factor 4 (ATF4) belongs to the ATF/CREB (activating transcription factor/cyclic AMP response element binding protein) family of basic region-leucine zipper (bZip) transcription factors, which have the consensus binding site cAMP responsive element (CRE). ATF4 has numerous dimerization partners. ATF4 is induced by stress signals including anoxia/hypoxia, endoplasmic reticulum stress, amino acid deprivation, and oxidative stress. ATF4 expression is regulated transcriptionally, translationally via the PERK pathway of eIF2alpha phosphorylation, and posttranslationally by phosphorylation, which targets ATF4 to proteasomal degradation. ATF4 regulates the expression of genes involved in oxidative stress, amino acid synthesis, differentiation, metastasis and angiogenesis. Transgenic studies have demonstrated ATF4 to be involved in hematopoiesis, lens and skeletal development, fertility, proliferation, differentiation, and long-term memory. ATF4 expression is upregulated in cancer. Since ATF4 is induced by tumour microenvironmental factors, and regulates processes relevant to cancer progression, it might serve as a potential therapeutic target in cancer.
MeSH term(s)	Activating Transcription Factor 4/chemistry ; Activating Transcription Factor 4/genetics ; Activating Transcription Factor 4/metabolism ; Animals ; Animals, Genetically Modified ; Cell Differentiation ; Gene Expression Regulation ; Hematopoiesis/physiology ; Humans ; Hypoxia/metabolism ; Mice ; Oxidative Stress/physiology ; Transcription, Genetic
Chemical Substances	Activating Transcription Factor 4 (145891-90-3)
Language	English
Publishing date	2008
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2007.01.020
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Zs.A 431: Show issues

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Article ; Online: HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth.

Ameri, Kurosh / Jahangiri, Arman / Rajah, Anthony M / Tormos, Kathryn V / Nagarajan, Ravi / Pekmezci, Melike / Nguyen, Vien / Wheeler, Matthew L / Murphy, Michael P / Sanders, Timothy A / Jeffrey, Stefanie S / Yeghiazarians, Yerem / Rinaudo, Paolo F / Costello, Joseph F / Aghi, Manish K / Maltepe, Emin

Cell reports

2015 Volume 10, Issue 6, Page(s) 891–899

Abstract: Hypoxia-inducible gene domain family member 1A (HIGD1A) is a survival factor induced by hypoxia-inducible factor 1 (HIF-1). HIF-1 regulates many responses to oxygen deprivation, but viable cells within hypoxic perinecrotic solid tumor regions frequently ... ...

Abstract	Hypoxia-inducible gene domain family member 1A (HIGD1A) is a survival factor induced by hypoxia-inducible factor 1 (HIF-1). HIF-1 regulates many responses to oxygen deprivation, but viable cells within hypoxic perinecrotic solid tumor regions frequently lack HIF-1α. HIGD1A is induced in these HIF-deficient extreme environments and interacts with the mitochondrial electron transport chain to repress oxygen consumption, enhance AMPK activity, and lower cellular ROS levels. Importantly, HIGD1A decreases tumor growth but promotes tumor cell survival in vivo. The human Higd1a gene is located on chromosome 3p22.1, where many tumor suppressor genes reside. Consistent with this, the Higd1a gene promoter is differentially methylated in human cancers, preventing its hypoxic induction. However, when hypoxic tumor cells are confronted with glucose deprivation, DNA methyltransferase activity is inhibited, enabling HIGD1A expression, metabolic adaptation, and possible dormancy induction. Our findings therefore reveal important new roles for this family of mitochondrial proteins in cancer biology.
Language	English
Publishing date	2015-02-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2015.01.020
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Article ; Online: Use of a mouse in vitro fertilization model to understand the developmental origins of health and disease hypothesis.

Feuer, Sky K / Liu, Xiaowei / Donjacour, Annemarie / Lin, Wingka / Simbulan, Rhodel K / Giritharan, Gnanaratnam / Piane, Luisa Delle / Kolahi, Kevin / Ameri, Kurosh / Maltepe, Emin / Rinaudo, Paolo F

Endocrinology

2014 Volume 155, Issue 5, Page(s) 1956–1969

Abstract: The Developmental Origins of Health and Disease hypothesis holds that alterations to homeostasis during critical periods of development can predispose individuals to adult-onset chronic diseases such as diabetes and metabolic syndrome. It remains ... ...

Abstract	The Developmental Origins of Health and Disease hypothesis holds that alterations to homeostasis during critical periods of development can predispose individuals to adult-onset chronic diseases such as diabetes and metabolic syndrome. It remains controversial whether preimplantation embryo manipulation, clinically used to treat patients with infertility, disturbs homeostasis and affects long-term growth and metabolism. To address this controversy, we have assessed the effects of in vitro fertilization (IVF) on postnatal physiology in mice. We demonstrate that IVF and embryo culture, even under conditions considered optimal for mouse embryo culture, alter postnatal growth trajectory, fat accumulation, and glucose metabolism in adult mice. Unbiased metabolic profiling in serum and microarray analysis of pancreatic islets and insulin sensitive tissues (liver, skeletal muscle, and adipose tissue) revealed broad changes in metabolic homeostasis, characterized by systemic oxidative stress and mitochondrial dysfunction. Adopting a candidate approach, we identify thioredoxin-interacting protein (TXNIP), a key molecule involved in integrating cellular nutritional and oxidative states with metabolic response, as a marker for preimplantation stress and demonstrate tissue-specific epigenetic and transcriptional TXNIP misregulation in selected adult tissues. Importantly, dysregulation of TXNIP expression is associated with enrichment for H4 acetylation at the Txnip promoter that persists from the blastocyst stage through adulthood in adipose tissue. Our data support the vulnerability of preimplantation embryos to environmental disturbance and demonstrate that conception by IVF can reprogram metabolic homeostasis through metabolic, transcriptional, and epigenetic mechanisms with lasting effects for adult growth and fitness. This study has wide clinical relevance and underscores the importance of continued follow-up of IVF-conceived offspring.
MeSH term(s)	Acetylation ; Adipose Tissue/embryology ; Adipose Tissue/growth & development ; Adipose Tissue/metabolism ; Animals ; Biomarkers/blood ; Biomarkers/metabolism ; Carrier Proteins/biosynthesis ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Disease Susceptibility ; Ectogenesis ; Embryo Transfer/adverse effects ; Epigenesis, Genetic ; Female ; Fertilization in Vitro/adverse effects ; Histones/metabolism ; Male ; Metabolic Diseases/blood ; Metabolic Diseases/etiology ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Mice ; Mice, Inbred C57BL ; Obesity/blood ; Obesity/etiology ; Obesity/metabolism ; Obesity/pathology ; Oxidative Stress ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Thioredoxins/biosynthesis ; Thioredoxins/genetics ; Thioredoxins/metabolism ; Transcription, Genetic ; Up-Regulation
Chemical Substances	Biomarkers ; Carrier Proteins ; Histones ; Txnip protein, mouse ; Thioredoxins (52500-60-4)
Language	English
Publishing date	2014-03-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2013-2081
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