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Article ; Online: Tissue-Resident PDGFRα

Santini, Maria Paola / Malide, Daniela / Hoffman, Gabriel / Pandey, Gaurav / D'Escamard, Valentina / Nomura-Kitabayashi, Aya / Rovira, Ilsa / Kataoka, Hiroshi / Ochando, Jordi / Harvey, Richard P / Finkel, Toren / Kovacic, Jason C

Cell reports

2020 Volume 30, Issue 2, Page(s) 555–570.e7

Abstract: ... ...

Abstract	PDGFRα
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Cells, Cultured ; Female ; Fibrosis/metabolism ; Fibrosis/pathology ; Human Umbilical Vein Endothelial Cells ; Humans ; Male ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cells/pathology ; Mice ; Mice, Nude ; Mice, Transgenic ; Muscle, Skeletal/cytology ; Muscle, Skeletal/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/metabolism
Chemical Substances	Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1)
Language	English
Publishing date	2020-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.12.045
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Article ; Online: The HDAC9-associated risk locus promotes coronary artery disease by governing TWIST1.

Ma, Lijiang / Bryce, Nicole S / Turner, Adam W / Di Narzo, Antonio F / Rahman, Karishma / Xu, Yang / Ermel, Raili / Sukhavasi, Katyayani / d'Escamard, Valentina / Chandel, Nirupama / V'Gangula, Bhargavi / Wolhuter, Kathryn / Kadian-Dodov, Daniella / Franzen, Oscar / Ruusalepp, Arno / Hao, Ke / Miller, Clint L / Björkegren, Johan L M / Kovacic, Jason C

PLoS genetics

2022 Volume 18, Issue 6, Page(s) e1010261

Abstract: Genome wide association studies (GWAS) have identified thousands of single nucleotide polymorphisms (SNPs) associated with the risk of common disorders. However, since the large majority of these risk SNPs reside outside gene-coding regions, GWAS ... ...

Abstract	Genome wide association studies (GWAS) have identified thousands of single nucleotide polymorphisms (SNPs) associated with the risk of common disorders. However, since the large majority of these risk SNPs reside outside gene-coding regions, GWAS generally provide no information about causal mechanisms regarding the specific gene(s) that are affected or the tissue(s) in which these candidate gene(s) exert their effect. The 'gold standard' method for understanding causal genes and their mechanisms of action are laborious basic science studies often involving sophisticated knockin or knockout mouse lines, however, these types of studies are impractical as a high-throughput means to understand the many risk variants that cause complex diseases like coronary artery disease (CAD). As a solution, we developed a streamlined, data-driven informatics pipeline to gain mechanistic insights on complex genetic loci. The pipeline begins by understanding the SNPs in a given locus in terms of their relative location and linkage disequilibrium relationships, and then identifies nearby expression quantitative trait loci (eQTLs) to determine their relative independence and the likely tissues that mediate their disease-causal effects. The pipeline then seeks to understand associations with other disease-relevant genes, disease sub-phenotypes, potential causality (Mendelian randomization), and the regulatory and functional involvement of these genes in gene regulatory co-expression networks (GRNs). Here, we applied this pipeline to understand a cluster of SNPs associated with CAD within and immediately adjacent to the gene encoding HDAC9. Our pipeline demonstrated, and validated, that this locus is causal for CAD by modulation of TWIST1 expression levels in the arterial wall, and by also governing a GRN related to metabolic function in skeletal muscle. Our results reconciled numerous prior studies, and also provided clear evidence that this locus does not govern HDAC9 expression, structure or function. This pipeline should be considered as a powerful and efficient way to understand GWAS risk loci in a manner that better reflects the highly complex nature of genetic risk associated with common disorders.
MeSH term(s)	Animals ; Coronary Artery Disease/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study/methods ; Histone Deacetylases/metabolism ; Linkage Disequilibrium ; Mice ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci/genetics ; Repressor Proteins/metabolism ; Twist-Related Protein 1/metabolism
Chemical Substances	Repressor Proteins ; Twist-Related Protein 1 ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2022-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010261
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Article ; Online: Coronary artery manifestations of fibromuscular dysplasia.

Michelis, Katherine C / Olin, Jeffrey W / Kadian-Dodov, Daniella / d'Escamard, Valentina / Kovacic, Jason C

Journal of the American College of Cardiology

2014 Volume 64, Issue 10, Page(s) 1033–1046

Abstract: Fibromuscular dysplasia (FMD) involving the coronary arteries is an uncommon but important condition that can present as acute coronary syndrome, left ventricular dysfunction, or potentially sudden cardiac death. Although the classic angiographic "string ...

Abstract	Fibromuscular dysplasia (FMD) involving the coronary arteries is an uncommon but important condition that can present as acute coronary syndrome, left ventricular dysfunction, or potentially sudden cardiac death. Although the classic angiographic "string of beads" that may be observed in renal artery FMD does not occur in coronary arteries, potential manifestations include spontaneous coronary artery dissection, distal tapering or long, smooth narrowing that may represent dissection, intramural hematoma, spasm, or tortuosity. Importantly, FMD must be identified in at least one other noncoronary arterial territory to attribute any coronary findings to FMD. Although there is limited evidence to guide treatment, many lesions heal spontaneously; thus, a conservative approach is generally preferred. The etiology is poorly understood, but there are ongoing efforts to better characterize FMD and define its genetic and molecular basis. This report reviews the clinical course of FMD involving the coronary arteries and provides guidance for diagnosis and treatment strategies.
MeSH term(s)	Acute Coronary Syndrome/etiology ; Acute Coronary Syndrome/mortality ; Acute Coronary Syndrome/physiopathology ; Adult ; Cause of Death ; Coronary Angiography/methods ; Coronary Stenosis/diagnostic imaging ; Coronary Stenosis/etiology ; Coronary Stenosis/mortality ; Coronary Vessels/diagnostic imaging ; Coronary Vessels/pathology ; Death, Sudden, Cardiac/etiology ; Disease Progression ; Female ; Fibromuscular Dysplasia/complications ; Fibromuscular Dysplasia/diagnosis ; Fibromuscular Dysplasia/mortality ; Humans ; Male ; Middle Aged ; Myocardial Infarction/etiology ; Myocardial Infarction/mortality ; Myocardial Infarction/physiopathology ; Survival Analysis ; Ventricular Dysfunction, Left/etiology ; Ventricular Dysfunction, Left/mortality ; Ventricular Dysfunction, Left/physiopathology
Language	English
Publishing date	2014-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2014.07.014
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Article ; Online: Histone deacetylase 9 promotes endothelial-mesenchymal transition and an unfavorable atherosclerotic plaque phenotype.

The Journal of clinical investigation

2021 Volume 131, Issue 15

Abstract: Endothelial-mesenchymal transition (EndMT) is associated with various cardiovascular diseases and in particular with atherosclerosis and plaque instability. However, the molecular pathways that govern EndMT are poorly defined. Specifically, the role of ... ...

Abstract	Endothelial-mesenchymal transition (EndMT) is associated with various cardiovascular diseases and in particular with atherosclerosis and plaque instability. However, the molecular pathways that govern EndMT are poorly defined. Specifically, the role of epigenetic factors and histone deacetylases (HDACs) in controlling EndMT and the atherosclerotic plaque phenotype remains unclear. Here, we identified histone deacetylation, specifically that mediated by HDAC9 (a class IIa HDAC), as playing an important role in both EndMT and atherosclerosis. Using in vitro models, we found class IIa HDAC inhibition sustained the expression of endothelial proteins and mitigated the increase in mesenchymal proteins, effectively blocking EndMT. Similarly, ex vivo genetic knockout of Hdac9 in endothelial cells prevented EndMT and preserved a more endothelial-like phenotype. In vivo, atherosclerosis-prone mice with endothelial-specific Hdac9 knockout showed reduced EndMT and significantly reduced plaque area. Furthermore, these mice displayed a more favorable plaque phenotype, with reduced plaque lipid content and increased fibrous cap thickness. Together, these findings indicate that HDAC9 contributes to vascular pathology by promoting EndMT. Our study provides evidence for a pathological link among EndMT, HDAC9, and atherosclerosis and suggests that targeting of HDAC9 may be beneficial for plaque stabilization or slowing the progression of atherosclerotic disease.
MeSH term(s)	Animals ; Atherosclerosis/enzymology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Endothelium/enzymology ; Endothelium/pathology ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Mice ; Mice, Knockout, ApoE ; Plaque, Atherosclerotic/enzymology ; Plaque, Atherosclerotic/genetics ; Plaque, Atherosclerotic/pathology ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
Chemical Substances	Repressor Proteins ; Hdac9 protein, mouse (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2021-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI131178
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Article ; Online: Integrative Prioritization of Causal Genes for Coronary Artery Disease.

Hao, Ke / Ermel, Raili / Sukhavasi, Katyayani / Cheng, Haoxiang / Ma, Lijiang / Li, Ling / Amadori, Letizia / Koplev, Simon / Franzén, Oscar / d'Escamard, Valentina / Chandel, Nirupama / Wolhuter, Kathryn / Bryce, Nicole S / Venkata, Vamsidhar R M / Miller, Clint L / Ruusalepp, Arno / Schunkert, Heribert / Björkegren, Johan L M / Kovacic, Jason C

Circulation. Genomic and precision medicine

2021 Volume 15, Issue 1, Page(s) e003365

Abstract: Background: Hundreds of candidate genes have been associated with coronary artery disease (CAD) through genome-wide association studies. However, a systematic way to understand the causal mechanism(s) of these genes, and a means to prioritize them for ... ...

Abstract	Background: Hundreds of candidate genes have been associated with coronary artery disease (CAD) through genome-wide association studies. However, a systematic way to understand the causal mechanism(s) of these genes, and a means to prioritize them for further study, has been lacking. This represents a major roadblock for developing novel disease- and gene-specific therapies for patients with CAD. Recently, powerful integrative genomics analyses pipelines have emerged to identify and prioritize candidate causal genes by integrating tissue/cell-specific gene expression data with genome-wide association study data sets. Methods: We aimed to develop a comprehensive integrative genomics analyses pipeline for CAD and to provide a prioritized list of causal CAD genes. To this end, we leveraged several complimentary informatics approaches to integrate summary statistics from CAD genome-wide association studies (from UK Biobank and CARDIoGRAMplusC4D) with transcriptomic and expression quantitative trait loci data from 9 cardiometabolic tissue/cell types in the STARNET study (Stockholm-Tartu Atherosclerosis Reverse Network Engineering Task). Results: We identified 162 unique candidate causal CAD genes, which exerted their effect from between one and up to 7 disease-relevant tissues/cell types, including the arterial wall, blood, liver, skeletal muscle, adipose, foam cells, and macrophages. When their causal effect was ranked, the top candidate causal CAD genes were Conclusions: We identified and prioritized candidate causal CAD genes, also localizing their tissue(s) of causal effect. These results should serve as a resource and facilitate targeted studies to identify the functional impact of top causal CAD genes.
MeSH term(s)	Atherosclerosis/genetics ; Coronary Artery Disease/genetics ; Coronary Artery Disease/metabolism ; Gene Regulatory Networks ; Genome-Wide Association Study/methods ; Genomics/methods ; Humans ; Quantitative Trait Loci
Language	English
Publishing date	2021-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2574-8300
ISSN (online)	2574-8300
DOI	10.1161/CIRCGEN.121.003365
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Article ; Online: Genome-wide association meta-analysis of spontaneous coronary artery dissection identifies risk variants and genes related to artery integrity and tissue-mediated coagulation.

Adlam, David / Berrandou, Takiy-Eddine / Georges, Adrien / Nelson, Christopher P / Giannoulatou, Eleni / Henry, Joséphine / Ma, Lijiang / Blencowe, Montgomery / Turley, Tamiel N / Yang, Min-Lee / Chopade, Sandesh / Finan, Chris / Braund, Peter S / Sadeg-Sayoud, Ines / Iismaa, Siiri E / Kosel, Matthew L / Zhou, Xiang / Hamby, Stephen E / Cheng, Jenny /

Liu, Lu / Tarr, Ingrid / Muller, David W M / d'Escamard, Valentina / King, Annette / Brunham, Liam R / Baranowska-Clarke, Ania A / Debette, Stéphanie / Amouyel, Philippe / Olin, Jeffrey W / Patil, Snehal / Hesselson, Stephanie E / Junday, Keerat / Kanoni, Stavroula / Aragam, Krishna G / Butterworth, Adam S / Tweet, Marysia S / Gulati, Rajiv / Combaret, Nicolas / Kadian-Dodov, Daniella / Kalman, Jonathan M / Fatkin, Diane / Hingorani, Aroon D / Saw, Jacqueline / Webb, Tom R / Hayes, Sharonne N / Yang, Xia / Ganesh, Santhi K / Olson, Timothy M / Kovacic, Jason C / Graham, Robert M / Samani, Nilesh J / Bouatia-Naji, Nabila

Nature genetics

2023 Volume 55, Issue 6, Page(s) 964–972

Abstract: Spontaneous coronary artery dissection (SCAD) is an understudied cause of myocardial infarction primarily affecting women. It is not known to what extent SCAD is genetically distinct from other cardiovascular diseases, including atherosclerotic coronary ... ...

Abstract	Spontaneous coronary artery dissection (SCAD) is an understudied cause of myocardial infarction primarily affecting women. It is not known to what extent SCAD is genetically distinct from other cardiovascular diseases, including atherosclerotic coronary artery disease (CAD). Here we present a genome-wide association meta-analysis (1,917 cases and 9,292 controls) identifying 16 risk loci for SCAD. Integrative functional annotations prioritized genes that are likely to be regulated in vascular smooth muscle cells and artery fibroblasts and implicated in extracellular matrix biology. One locus containing the tissue factor gene F3, which is involved in blood coagulation cascade initiation, appears to be specific for SCAD risk. Several associated variants have diametrically opposite associations with CAD, suggesting that shared biological processes contribute to both diseases, but through different mechanisms. We also infer a causal role for high blood pressure in SCAD. Our findings provide novel pathophysiological insights involving arterial integrity and tissue-mediated coagulation in SCAD and set the stage for future specific therapeutics and preventions.
MeSH term(s)	Humans ; Female ; Genome-Wide Association Study ; Vascular Diseases/genetics ; Coronary Artery Disease/genetics ; Myocardial Infarction
Language	English
Publishing date	2023-05-29
Publishing country	United States
Document type	Meta-Analysis ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-023-01410-1
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Zs.A 3613: 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 46: Show issues

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Article ; Online: A plasma proteogenomic signature for fibromuscular dysplasia.

Olin, Jeffrey W / Di Narzo, Antonio F / d'Escamard, Valentina / Kadian-Dodov, Daniella / Cheng, Haoxiang / Georges, Adrien / King, Annette / Thomas, Allison / Barwari, Temo / Michelis, Katherine C / Bouchareb, Rihab / Bander, Emir / Anyanwu, Anelechi / Stelzer, Paul / Filsoufi, Farzan / Florman, Sander / Civelek, Mete / Debette, Stephanie / Jeunemaitre, Xavier /

Björkegren, Johan L M / Mayr, Manuel / Bouatia-Naji, Nabila / Hao, Ke / Kovacic, Jason C

Cardiovascular research

2019 Volume 116, Issue 1, Page(s) 63–77

Abstract: Aims: Fibromuscular dysplasia (FMD) is a poorly understood disease that predominantly affects women during middle-life, with features that include stenosis, aneurysm, and dissection of medium-large arteries. Recently, plasma proteomics has emerged as an ...

Abstract	Aims: Fibromuscular dysplasia (FMD) is a poorly understood disease that predominantly affects women during middle-life, with features that include stenosis, aneurysm, and dissection of medium-large arteries. Recently, plasma proteomics has emerged as an important means to understand cardiovascular diseases. Our objectives were: (i) to characterize plasma proteins and determine if any exhibit differential abundance in FMD subjects vs. matched healthy controls and (ii) to leverage these protein data to conduct systems analyses to provide biologic insights on FMD, and explore if this could be developed into a blood-based FMD test. Methods and results: Females with 'multifocal' FMD and matched healthy controls underwent clinical phenotyping, dermal biopsy, and blood draw. Using dual-capture proximity extension assay and nuclear magnetic resonance-spectroscopy, we evaluated plasma levels of 981 proteins and 31 lipid sub-classes, respectively. In a discovery cohort (Ncases = 90, Ncontrols = 100), we identified 105 proteins and 16 lipid sub-classes (predominantly triglycerides and fatty acids) with differential plasma abundance in FMD cases vs. controls. In an independent cohort (Ncases = 23, Ncontrols = 28), we successfully validated 37 plasma proteins and 10 lipid sub-classes with differential abundance. Among these, 5/37 proteins exhibited genetic control and Bayesian analyses identified 3 of these as potential upstream drivers of FMD. In a 3rd cohort (Ncases = 506, Ncontrols = 876) the genetic locus of one of these upstream disease drivers, CD2-associated protein (CD2AP), was independently validated as being associated with risk of having FMD (odds ratios = 1.36; P = 0.0003). Immune-fluorescence staining identified that CD2AP is expressed by the endothelium of medium-large arteries. Finally, machine learning trained on the discovery cohort was used to develop a test for FMD. When independently applied to the validation cohort, the test showed a c-statistic of 0.73 and sensitivity of 78.3%. Conclusion: FMD exhibits a plasma proteogenomic and lipid signature that includes potential causative disease drivers, and which holds promise for developing a blood-based test for this disease.
MeSH term(s)	Adaptor Proteins, Signal Transducing/blood ; Adaptor Proteins, Signal Transducing/genetics ; Adult ; Aged ; Blood Proteins/genetics ; Case-Control Studies ; Cytoskeletal Proteins/blood ; Cytoskeletal Proteins/genetics ; Female ; Fibromuscular Dysplasia/blood ; Fibromuscular Dysplasia/diagnosis ; Fibromuscular Dysplasia/genetics ; Genetic Markers ; Genetic Predisposition to Disease ; High-Throughput Screening Assays ; Humans ; Lipids/blood ; Machine Learning ; Middle Aged ; Phenotype ; Predictive Value of Tests ; Proof of Concept Study ; Proteogenomics ; Reproducibility of Results ; Systems Biology ; Young Adult
Chemical Substances	Adaptor Proteins, Signal Transducing ; Blood Proteins ; CD2-associated protein ; Cytoskeletal Proteins ; Genetic Markers ; Lipids
Language	English
Publishing date	2019-09-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Validation Study
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvz219
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Zs.A 565: Show issues

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Article ; Online: Author Correction: Genetic investigation of fibromuscular dysplasia identifies risk loci and shared genetics with common cardiovascular diseases.

Georges, Adrien / Yang, Min-Lee / Berrandou, Takiy-Eddine / Bakker, Mark K / Dikilitas, Ozan / Kiando, Soto Romuald / Ma, Lijiang / Satterfield, Benjamin A / Sengupta, Sebanti / Yu, Mengyao / Deleuze, Jean-François / Dupré, Delia / Hunker, Kristina L / Kyryachenko, Sergiy / Liu, Lu / Sayoud-Sadeg, Ines / Amar, Laurence / Brummett, Chad M / Coleman, Dawn M /

d'Escamard, Valentina / de Leeuw, Peter / Fendrikova-Mahlay, Natalia / Kadian-Dodov, Daniella / Li, Jun Z / Lorthioir, Aurélien / Pappaccogli, Marco / Prejbisz, Aleksander / Smigielski, Witold / Stanley, James C / Zawistowski, Matthew / Zhou, Xiang / Zöllner, Sebastian / Amouyel, Philippe / De Buyzere, Marc L / Debette, Stéphanie / Dobrowolski, Piotr / Drygas, Wojciech / Gornik, Heather L / Olin, Jeffrey W / Piwonski, Jerzy / Rietzschel, Ernst R / Ruigrok, Ynte M / Vikkula, Miikka / Warchol Celinska, Ewa / Januszewicz, Andrzej / Kullo, Iftikhar J / Azizi, Michel / Jeunemaitre, Xavier / Persu, Alexandre / Kovacic, Jason C / Ganesh, Santhi K / Bouatia-Naji, Nabila

Nature communications

2022 Volume 13, Issue 1, Page(s) 2251

Language	English
Publishing date	2022-04-20
Publishing country	England
Document type	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-29921-1
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Article ; Online: CD90 Identifies Adventitial Mesenchymal Progenitor Cells in Adult Human Medium- and Large-Sized Arteries.

Michelis, Katherine C / Nomura-Kitabayashi, Aya / Lecce, Laura / Franzén, Oscar / Koplev, Simon / Xu, Yang / Santini, Maria Paola / D'Escamard, Valentina / Lee, Jonathan T L / Fuster, Valentin / Hajjar, Roger / Reddy, Ramachandra C / Chikwe, Joanna / Stelzer, Paul / Filsoufi, Farzan / Stewart, Allan / Anyanwu, Anelechi / Björkegren, Johan L M / Kovacic, Jason C

Stem cell reports

2018 Volume 11, Issue 1, Page(s) 242–257

Abstract: Mesenchymal stem cells (MSCs) reportedly exist in a vascular niche occupying the outer adventitial layer. However, these cells have not been well characterized in vivo in medium- and large-sized arteries in humans, and their potential pathological role ... ...

Abstract	Mesenchymal stem cells (MSCs) reportedly exist in a vascular niche occupying the outer adventitial layer. However, these cells have not been well characterized in vivo in medium- and large-sized arteries in humans, and their potential pathological role is unknown. To address this, healthy and diseased arterial tissues were obtained as surplus surgical specimens and freshly processed. We identified that CD90 marks a rare adventitial population that co-expresses MSC markers including PDGFRα, CD44, CD73, and CD105. However, unlike CD90, these additional markers were widely expressed by other cells. Human adventitial CD90+ cells fulfilled standard MSC criteria, including plastic adherence, spindle morphology, passage ability, colony formation, and differentiation into adipocytes, osteoblasts, and chondrocytes. Phenotypic and transcriptomic profiling, as well as adoptive transfer experiments, revealed a potential role in vascular disease pathogenesis, with the transcriptomic disease signature of these cells being represented in an aortic regulatory gene network that is operative in atherosclerosis.
MeSH term(s)	Arteries/embryology ; Arteries/metabolism ; Biomarkers ; Cell Differentiation/genetics ; Gene Expression Profiling ; Humans ; Immunophenotyping ; Ischemia/etiology ; Ischemia/metabolism ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Neovascularization, Physiologic/genetics ; Thy-1 Antigens/genetics ; Thy-1 Antigens/metabolism
Chemical Substances	Biomarkers ; Thy-1 Antigens
Language	English
Publishing date	2018-06-28
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.2018.06.001
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Article ; Online: FOXO3-mTOR metabolic cooperation in the regulation of erythroid cell maturation and homeostasis.

Zhang, Xin / Campreciós, Genís / Rimmelé, Pauline / Liang, Raymond / Yalcin, Safak / Mungamuri, Sathish Kumar / Barminko, Jeffrey / D'Escamard, Valentina / Baron, Margaret H / Brugnara, Carlo / Papatsenko, Dmitri / Rivella, Stefano / Ghaffari, Saghi

American journal of hematology

2014 Volume 89, Issue 10, Page(s) 954–963

Abstract: Ineffective erythropoiesis is observed in many erythroid disorders including β-thalassemia and anemia of chronic disease in which increased production of erythroblasts that fail to mature exacerbate the underlying anemias. As loss of the transcription ... ...

Abstract	Ineffective erythropoiesis is observed in many erythroid disorders including β-thalassemia and anemia of chronic disease in which increased production of erythroblasts that fail to mature exacerbate the underlying anemias. As loss of the transcription factor FOXO3 results in erythroblast abnormalities similar to the ones observed in ineffective erythropoiesis, we investigated the underlying mechanisms of the defective Foxo3(-/-) erythroblast cell cycle and maturation. Here we show that loss of Foxo3 results in overactivation of the JAK2/AKT/mTOR signaling pathway in primary bone marrow erythroblasts partly mediated by redox modulation. We further show that hyperactivation of mTOR signaling interferes with cell cycle progression in Foxo3 mutant erythroblasts. Importantly, inhibition of mTOR signaling, in vivo or in vitro enhances significantly Foxo3 mutant erythroid cell maturation. Similarly, in vivo inhibition of mTOR remarkably improves erythroid cell maturation and anemia in a model of β-thalassemia. Finally we show that FOXO3 and mTOR are likely part of a larger metabolic network in erythroblasts as together they control the expression of an array of metabolic genes some of which are implicated in erythroid disorders. These combined findings indicate that a metabolism-mediated regulatory network centered by FOXO3 and mTOR control the balanced production and maturation of erythroid cells. They also highlight physiological interactions between these proteins in regulating erythroblast energy. Our results indicate that alteration in the function of this network might be implicated in the pathogenesis of ineffective erythropoiesis.
MeSH term(s)	Animals ; Disease Models, Animal ; Erythroblasts/metabolism ; Erythroblasts/pathology ; Erythropoiesis ; Forkhead Box Protein O3 ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Homeostasis ; Mice ; Mice, Knockout ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; beta-Thalassemia/genetics ; beta-Thalassemia/metabolism ; beta-Thalassemia/pathology
Chemical Substances	Forkhead Box Protein O3 ; Forkhead Transcription Factors ; FoxO3 protein, mouse ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, mouse (EC 2.7.1.1)
Language	English
Publishing date	2014-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.23786
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1251: Show issues

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