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Article: Case Report: Transthyretin Glu54Leu-a rare mutation with predominant cardiac phenotype.

Gospodinova, Mariana / Zhelyazkova, Sashka / Chamova, Teodora / Asenov, Ognyan / Pavlova, Zornitsa / Todorov, Tihomir / Mikova, Dilyana / Palashev, Yordan / Gruev, Ivan / Kundurdjiev, Atanas / Todorova, Albena / Tournev, Ivailo

Frontiers in cardiovascular medicine

2023 Volume 10, Page(s) 1228410

Abstract: We report two unrelated Bulgarian families with hereditary transthyretin (ATTR) amyloidosis due to a rare p.Glu74Leu (Glu54Leu) pathogenic variant found in seven individuals-three of them symptomatic. Only one family with the same variant and with a ... ...

Abstract	We report two unrelated Bulgarian families with hereditary transthyretin (ATTR) amyloidosis due to a rare p.Glu74Leu (Glu54Leu) pathogenic variant found in seven individuals-three of them symptomatic. Only one family with the same variant and with a Swedish origin has been clinically described so far. Our patients are characterized by predominant cardiac involvement, very much similar to the Swedish patients. Although the initial complaint was bilateral carpal tunnel syndrome, advanced amyloid cardiomyopathy was found in two symptomatic carriers at diagnosis with heart failure manifestations. The neurological involvement was considered as mild, with mainly sensory signs and symptoms being present. We followed a non-biopsy algorithm to confirm the diagnosis. Tafamidis 61 mg has been initiated as the only approved disease modifying treatment for ATTR cardiomyopathy. Clinical stability in the absence of adverse events has been observed at follow up.
Language	English
Publishing date	2023-10-31
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2023.1228410
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Article ; Online: hESC-derived immune suppressive dendritic cells induce immune tolerance of parental hESC-derived allografts.

Todorova, Dilyana / Zhang, Yue / Chen, Qu / Liu, Jingfeng / He, Jingjin / Fu, Xuemei / Xu, Yang

EBioMedicine

2020 Volume 62, Page(s) 103120

Abstract: Background: With their inherent capability of unlimited self-renewal and unique potential to differentiate into functional cells of the three germ layers, human embryonic stem cells (hESCs) hold great potential in regenerative medicine. A major ... ...

Abstract	Background: With their inherent capability of unlimited self-renewal and unique potential to differentiate into functional cells of the three germ layers, human embryonic stem cells (hESCs) hold great potential in regenerative medicine. A major challenge in the application of hESC-based cell therapy is the allogeneic immune rejection of hESC-derived allografts. Methods: We derived dendritic cell-like cells (DCLs) from wild type and CTLA4-Ig/PD-L1 knock-in hESCs, denoted WT DCLs and CP DCLs. The expression of DC-related genes and surface molecules was evaluated, as well as their DCL capacity to stimulate allogeneic T cells and induce regulatory T (Treg) cells in vitro. Using an immune system humanized mouse model, we investigated whether the adoptive transfer of CP DCLs can induce long-term immune tolerance of parental hESC-derived smooth muscle and cardiomyocyte allografts. Findings: CP DCLs can maintain immune suppressive properties after robust inflammatory stimulation and induce Treg cells. While CP DCLs survive transiently in vivo, they induce long-term immune tolerance of parental hESC-derived allografts. Interpretation: This strategy does not cause systemic immune suppression but induces immune tolerance specific for DCL-specific HLAs, and thus it presents a safe and effective approach to induce immune tolerance of allografts derived from any clinically approved hESC line. Funding: NSFC, leading talents of Guangdong Province Program (No. 00201516), Key R&D Program of Guangdong Province (2019B020235003), Science and Technology Innovation Committee of Shenzhen Municipality (JCYJ20180504170301309), National High-tech R&D Program (863 Program No. 2015AA020310), Shenzhen "Sanming" Project of Medicine (SZSM201602102), Development and Reform Commission of Shenzhen Municipality (S2016004730009), CIRM (DISC2-10559).
MeSH term(s)	Adoptive Transfer ; Allografts/immunology ; Animals ; Biomarkers ; Cell Communication ; Cell Line ; Cells, Cultured ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Graft Rejection/immunology ; Graft Survival/immunology ; Human Embryonic Stem Cells/metabolism ; Humans ; Immune Tolerance ; Immunomodulation ; Immunophenotyping ; Mice ; Myocytes, Cardiac/metabolism ; Myocytes, Smooth Muscle/metabolism
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-11-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2020.103120
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Article ; Online: hESC-derived immune suppressive dendritic cells induce immune tolerance of parental hESC-derived allografts

Dilyana Todorova / Yue Zhang / Qu Chen / Jingfeng Liu / Jingjin He / Xuemei Fu / Yang Xu

EBioMedicine, Vol 62, Iss , Pp 103120- (2020)

2020

Abstract	Background: With their inherent capability of unlimited self-renewal and unique potential to differentiate into functional cells of the three germ layers, human embryonic stem cells (hESCs) hold great potential in regenerative medicine. A major challenge in the application of hESC-based cell therapy is the allogeneic immune rejection of hESC-derived allografts. Methods: We derived dendritic cell-like cells (DCLs) from wild type and CTLA4-Ig/PD-L1 knock-in hESCs, denoted WT DCLs and CP DCLs. The expression of DC-related genes and surface molecules was evaluated, as well as their DCL capacity to stimulate allogeneic T cells and induce regulatory T (Treg) cells in vitro. Using an immune system humanized mouse model, we investigated whether the adoptive transfer of CP DCLs can induce long-term immune tolerance of parental hESC-derived smooth muscle and cardiomyocyte allografts. Findings: CP DCLs can maintain immune suppressive properties after robust inflammatory stimulation and induce Treg cells. While CP DCLs survive transiently in vivo, they induce long-term immune tolerance of parental hESC-derived allografts. Interpretation: This strategy does not cause systemic immune suppression but induces immune tolerance specific for DCL-specific HLAs, and thus it presents a safe and effective approach to induce immune tolerance of allografts derived from any clinically approved hESC line. Funding: NSFC, leading talents of Guangdong Province Program (No. 00201516), Key R&D Program of Guangdong Province (2019B020235003), Science and Technology Innovation Committee of Shenzhen Municipality (JCYJ20180504170301309), National High-tech R&D Program (863 Program No. 2015AA020310), Shenzhen “Sanming” Project of Medicine (SZSM201602102), Development and Reform Commission of Shenzhen Municipality (S2016004730009), CIRM (DISC2–10559).
Keywords	Human embryonic stem cells ; Allogeneic immune rejection ; Immune tolerance ; Dendritic cells ; Regulatory T cells ; Immune system humanized mice ; Medicine ; R ; Medicine (General) ; R5-920
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Brief Report: Immune Microenvironment Determines the Immunogenicity of Induced Pluripotent Stem Cell Derivatives.

Todorova, Dilyana / Kim, Jinchul / Hamzeinejad, Sara / He, Jingjin / Xu, Yang

Stem cells (Dayton, Ohio)

2016 Volume 34, Issue 2, Page(s) 510–515

Abstract: The breakthrough of induced pluripotent stem cells (iPSCs) has raised the possibility that patient-specific iPSCs can provide autologous cells for cell therapy without the concern for immune rejection. However, the immunogenicity of iPSC-derived cells ... ...

Abstract	The breakthrough of induced pluripotent stem cells (iPSCs) has raised the possibility that patient-specific iPSCs can provide autologous cells for cell therapy without the concern for immune rejection. However, the immunogenicity of iPSC-derived cells remains controversial. Using syngeneic C57BL/6 (B6) mouse transplantation model, several studies indicate that B6 iPSC-derived cells exhibit some levels of immunogenicity when transplanted into B6 mice subcutaneously. In contrast, one recent study has concluded that various lineages of B6 iPSC-derived cells exhibit no immunogenicity when transplanted under the kidney capsule of B6 mice. To resolve the controversy concerning this critical issue of iPSC biology, we used the same B6 transplantation model to demonstrate that the immune response toward antigens is dependent on the immune environment of the transplantation site. Immunogenic antigen-expressing B6 embryonic stem cells (ESCs) as well as B6 iPSCs and their terminally differentiated cells survived under the kidney capsule but are immune rejected when transplanted subcutaneously or intramuscularly. The cotransplantation of mature B6 dendritic cells under the kidney capsule leads to immune rejection of B6 iPSC-derived grafts but not B6 ESC-derived grafts, indicating that the lack of detectable immune response to iPSC-derived grafts under the kidney capsule is due to the lack of functional antigen presenting cells.
MeSH term(s)	Animals ; Autografts ; Induced Pluripotent Stem Cells/immunology ; Mice ; Stem Cell Niche/immunology ; Stem Cell Transplantation ; Transplantation Immunology
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.2227
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Article ; Online: Extracellular Vesicles in Angiogenesis.

Todorova, Dilyana / Simoncini, Stéphanie / Lacroix, Romaric / Sabatier, Florence / Dignat-George, Françoise

Circulation research

2017 Volume 120, Issue 10, Page(s) 1658–1673

Abstract: During the past decade, extracellular vesicles (EVs), which include apoptotic bodies, microvesicles, and exosomes, have emerged as important players in cell-to-cell communication in normal physiology and pathological conditions. EVs encapsulate and ... ...

Abstract	During the past decade, extracellular vesicles (EVs), which include apoptotic bodies, microvesicles, and exosomes, have emerged as important players in cell-to-cell communication in normal physiology and pathological conditions. EVs encapsulate and convey various bioactive molecules that are further transmitted to neighboring or more distant cells, where they induce various signaling cascades. The message delivered to the target cells is dependent on EV composition, which, in turn, is determined by the cell of origin and the surrounding microenvironment during EV biogenesis. Among their multifaceted role in the modulation of biological responses, the involvement of EVs in vascular development, growth, and maturation has been widely documented and their potential therapeutic application in regenerative medicine or angiogenesis-related diseases is drawing increasing interest. EVs derived from various cell types have the potential to deliver complex information to endothelial cells and to induce either pro- or antiangiogenic signaling. As dynamic systems, in response to changes in the microenvironment, EVs adapt their cargo composition to fine-tune the process of blood vessel formation. This article reviews the current knowledge on the role of microvesicles and exosomes from various cellular origins in angiogenesis, with a particular emphasis on the underlying mechanisms, and discusses the main challenges and prerequisites for their therapeutic applications.
MeSH term(s)	Biomarkers/blood ; Clinical Trials as Topic/methods ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/transplantation ; Humans ; Neovascularization, Pathologic/blood ; Neovascularization, Pathologic/diagnosis ; Neovascularization, Pathologic/therapy ; Tissue Distribution/physiology
Chemical Substances	Biomarkers
Language	English
Publishing date	2017-05-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.117.309681
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Article ; Online: Extracellular vesicles from T cells overexpress miR-146b-5p in HIV-1 infection and repress endothelial activation.

Balducci, Estelle / Leroyer, Aurélie S / Lacroix, Romaric / Robert, Stéphane / Todorova, Dilyana / Simoncini, Stéphanie / Lyonnet, Luc / Chareyre, Corinne / Zaegel-Faucher, Olivia / Micallef, Joëlle / Poizot-Martin, Isabelle / Roll, Patrice / Dignat-George, Françoise

Scientific reports

2019 Volume 9, Issue 1, Page(s) 10299

Abstract: Human immunodeficiency virus type 1 (HIV-1) infection promotes a generalized activation of host responses that involves not only CD4 T cells, but also cells of the microenvironment, which are not directly infected, such as endothelial cells. The ... ...

Abstract	Human immunodeficiency virus type 1 (HIV-1) infection promotes a generalized activation of host responses that involves not only CD4 T cells, but also cells of the microenvironment, which are not directly infected, such as endothelial cells. The mechanisms triggering HIV-1-associated vascular alterations remain poorly understood. Extracellular vesicles (EVs), implicated in cell-to-cell communication, have been recently described as carriers of microRNAs (miRNAs). Here, we show that miR-146b-5p is upregulated in both CD4 T cells, CD4 T cell-derived EVs and circulating EVs obtained from antiretroviral therapy-naive HIV-1-infected patients. We further demonstrate that EVs from T cell line overexpressing miR-146b-5p mimics (miR-146b-EVs): 1) protect their miRNA cargo from RNase degradation, 2) transfer miR-146b-5p mimics into endothelial cells and 3) reduce endothelial inflammatory responses in vitro and in vivo in the lungs of mice through the downregulation of nuclear factor-κB-responsive molecules. These data advance our understanding on chronic inflammatory responses affecting endothelial homeostasis, in infectious and non-infectious diseases and pave the way for potential new anti-inflammatory strategies.
MeSH term(s)	Adult ; Animals ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/virology ; Case-Control Studies ; Cell Line ; Endothelial Cells/chemistry ; Endothelial Cells/cytology ; Extracellular Vesicles/genetics ; Female ; HIV Infections/genetics ; HIV Infections/immunology ; HIV-1/immunology ; HIV-1/pathogenicity ; Human Umbilical Vein Endothelial Cells ; Humans ; Male ; MicroRNAs/genetics ; Up-Regulation
Chemical Substances	MIRN146 microRNA, human ; MicroRNAs
Language	English
Publishing date	2019-07-16
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/s41598-019-44743-w
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Article ; Online: Wild-Type p53 Promotes Cancer Metabolic Switch by Inducing PUMA-Dependent Suppression of Oxidative Phosphorylation.

Kim, Jinchul / Yu, Lili / Chen, Wancheng / Xu, Yanxia / Wu, Meng / Todorova, Dilyana / Tang, Qingshuang / Feng, Bingbing / Jiang, Lei / He, Jingjin / Chen, Guihua / Fu, Xuemei / Xu, Yang

Cancer cell

2019 Volume 35, Issue 2, Page(s) 191–203.e8

Abstract: The tumor suppressor p53 is somatically mutated in half of all human cancers. Paradoxically, the wild-type p53 (WTp53) is often retained in certain human cancers, such as hepatocarcinoma (HCC). We discovered a physiological and oncogenic role of WTp53 in ...

Abstract	The tumor suppressor p53 is somatically mutated in half of all human cancers. Paradoxically, the wild-type p53 (WTp53) is often retained in certain human cancers, such as hepatocarcinoma (HCC). We discovered a physiological and oncogenic role of WTp53 in suppressing pyruvate-driven oxidative phosphorylation by inducing PUMA. PUMA inhibits mitochondrial pyruvate uptake by disrupting the oligomerization and function of mitochondrial pyruvate carrier (MPC) through PUMA-MPC interaction, which depends on IκB kinase-mediated phosphorylation of PUMA at Ser96/106. High expression levels of PUMA are correlated with decreased mitochondrial pyruvate uptake and increased glycolysis in HCCs and poor prognosis of HCC patients. These findings are instrumental for cancer drug discovery aiming at activating WTp53 or restoring WTp53 activity to p53 mutants.
MeSH term(s)	A549 Cells ; Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Proliferation ; Glycolysis ; HCT116 Cells ; HeLa Cells ; Hep G2 Cells ; Humans ; I-kappa B Kinase/metabolism ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Male ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Mitochondrial Membrane Transport Proteins/metabolism ; Monocarboxylic Acid Transporters/metabolism ; Oxidative Phosphorylation ; Prognosis ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Pyruvic Acid/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; BBC3 protein, human ; MPC1 protein, human ; MPC2 protein, human ; Mitochondrial Membrane Transport Proteins ; Monocarboxylic Acid Transporters ; PUMA protein, mouse ; Proto-Oncogene Proteins ; TP53 protein, human ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins ; Pyruvic Acid (8558G7RUTR) ; I-kappa B Kinase (EC 2.7.11.10) ; IKBKB protein, human (EC 2.7.11.10)
Language	English
Publishing date	2019-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2018.12.012
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Article ; Online: Stemness factor Sall4 is required for DNA damage response in embryonic stem cells.

Xiong, Jianhua / Todorova, Dilyana / Su, Ning-Yuan / Kim, Jinchul / Lee, Pei-Jen / Shen, Zhouxin / Briggs, Steven P / Xu, Yang

The Journal of cell biology

2015 Volume 208, Issue 5, Page(s) 513–520

Abstract: Mouse embryonic stem cells (ESCs) are genetically more stable than somatic cells, thereby preventing the passage of genomic abnormalities to their derivatives including germ cells. The underlying mechanisms, however, remain largely unclear. In this paper, ...

Abstract	Mouse embryonic stem cells (ESCs) are genetically more stable than somatic cells, thereby preventing the passage of genomic abnormalities to their derivatives including germ cells. The underlying mechanisms, however, remain largely unclear. In this paper, we show that the stemness factor Sall4 is required for activating the critical Ataxia Telangiectasia Mutated (ATM)-dependent cellular responses to DNA double-stranded breaks (DSBs) in mouse ESCs and confer their resistance to DSB-induced cytotoxicity. Sall4 is rapidly mobilized to the sites of DSBs after DNA damage. Furthermore, Sall4 interacts with Rad50 and stabilizes the Mre11-Rad50-Nbs1 complex for the efficient recruitment and activation of ATM. Sall4 also interacts with Baf60a, a member of the SWI/SNF (switch/sucrose nonfermentable) ATP-dependent chromatin-remodeling complex, which is responsible for recruiting Sall4 to the site of DNA DSB damage. Our findings provide novel mechanisms to coordinate stemness of ESCs with DNA damage response, ensuring genomic stability during the expansion of ESCs.
MeSH term(s)	ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Breaks, Double-Stranded ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; MRE11 Homologue Protein ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	ATP-Binding Cassette Transporters ; Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; DNA-Binding Proteins ; Mre11a protein, mouse ; Nijmegen breakage syndrome 1 protein, mouse ; Nuclear Proteins ; SWI-SNF-B chromatin-remodeling complex ; Sall4 protein, mouse ; Smarcd1 protein, mouse ; Transcription Factors ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; MRE11 Homologue Protein (EC 3.1.-) ; Rad50 protein, mouse (EC 3.6.-) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2015-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201408106
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Article ; Online: Biogenesis of Pro-senescent Microparticles by Endothelial Colony Forming Cells from Premature Neonates is driven by SIRT1-Dependent Epigenetic Regulation of MKK6.

Simoncini, Stéphanie / Chateau, Anne-Line / Robert, Stéphane / Todorova, Dilyana / Yzydorzick, Catherine / Lacroix, Romaric / Ligi, Isabelle / Louis, Laurence / Bachelier, Richard / Simeoni, Umberto / Magdinier, Frédérique / Dignat-George, Françoise / Sabatier, Florence

Scientific reports

2017 Volume 7, Issue 1, Page(s) 8277

Abstract: Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that ... ...

Abstract	Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that sirtuin-1 (SIRT1) deficiency drives accelerated senescence and dysfunction of endothelial colony-forming cells (ECFC) in PT neonates. Because preterm birth (PT) increases the risk for cardiovascular diseases during neonatal period as well as at adulthood, we hypothesized that SIRT1 deficiency could control the biogenesis of microparticles as part of a senescence-associated secretory phenotype (SASP) of PT-ECFC and investigated the related molecular mechanisms. Compared to control ECFC, PT-ECFC displayed a SASP associated with increased release of endothelial microparticles (EMP), mediating a paracrine induction of senescence in naïve endothelial cells. SIRT1 level inversely correlated with EMP release and drives PT-ECFC vesiculation. Global transcriptomic analysis revealed changes in stress response pathways, specifically the MAPK pathway. We delineate a new epigenetic mechanism by which SIRT1 deficiency regulates MKK6/p38
MeSH term(s)	Cell-Derived Microparticles/metabolism ; Cellular Senescence ; Endothelial Cells/metabolism ; Endothelial Progenitor Cells/metabolism ; Epigenesis, Genetic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Infant, Newborn ; MAP Kinase Kinase 6/genetics ; Models, Biological ; Paracrine Communication ; Premature Birth ; Signal Transduction ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Transcriptome ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 6 (EC 2.7.12.2) ; MAP2K6 protein, human (EC 2.7.12.2) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2017-08-15
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/s41598-017-08883-1
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Article ; Online: Biogenesis of Pro-senescent Microparticles by Endothelial Colony Forming Cells from Premature Neonates is driven by SIRT1-Dependent Epigenetic Regulation of MKK6

Stéphanie Simoncini / Anne-Line Chateau / Stéphane Robert / Dilyana Todorova / Catherine Yzydorzick / Romaric Lacroix / Isabelle Ligi / Laurence Louis / Richard Bachelier / Umberto Simeoni / Frédérique Magdinier / Françoise Dignat-George / Florence Sabatier

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

2017 Volume 16

Abstract: Abstract Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported ...

Abstract	Abstract Senescent cells may exert detrimental effect on microenvironment through the secretion of soluble factors and the release of extracellular vesicles, such as microparticles, key actors in ageing and cardiovascular diseases. We previously reported that sirtuin-1 (SIRT1) deficiency drives accelerated senescence and dysfunction of endothelial colony-forming cells (ECFC) in PT neonates. Because preterm birth (PT) increases the risk for cardiovascular diseases during neonatal period as well as at adulthood, we hypothesized that SIRT1 deficiency could control the biogenesis of microparticles as part of a senescence–associated secretory phenotype (SASP) of PT-ECFC and investigated the related molecular mechanisms. Compared to control ECFC, PT-ECFC displayed a SASP associated with increased release of endothelial microparticles (EMP), mediating a paracrine induction of senescence in naïve endothelial cells. SIRT1 level inversely correlated with EMP release and drives PT-ECFC vesiculation. Global transcriptomic analysis revealed changes in stress response pathways, specifically the MAPK pathway. We delineate a new epigenetic mechanism by which SIRT1 deficiency regulates MKK6/p38MAPK/Hsp27 pathway to promote EMP biogenesis in senescent ECFC. These findings deepen our understanding of the role of ECFC senescence in the disruption of endothelial homeostasis and provide potential new targets towards the control of cardiovascular risk in individuals born preterm.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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