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  1. Article: Microparticles as intercellular carriers of the microRNA signal: insights for novel diagnostic and therapeutic approaches.

    Mause, Sebastian F

    Thrombosis and haemostasis

    2016  Volume 115, Issue 2, Page(s) 236

    MeSH term(s) Cell Communication ; Cell-Derived Microparticles ; Humans ; MicroRNAs
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2016-01
    Publishing country Germany
    Document type Comment ; Journal Article
    ZDB-ID 518294-3
    ISSN 0340-6245
    ISSN 0340-6245
    DOI 10.1160/TH16-01-0013
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  2. Article ; Online: Intravenous iron supplementation in heart failure patients induces temporary endothelial dysfunction with release of endothelial microvesicles.

    Mause, Sebastian F / Berger, Martin / Lim, Hwee Ying / Vogt, Felix / Brandenburg, Vincent / Stöhr, Robert

    Frontiers in immunology

    2023  Volume 13, Page(s) 1092704

    Abstract: Background: Intravenous iron supplementation is an established therapy for patients with heart failure (HF) and concomitant iron deficiency reducing the risk of HF hospitalization. However, concerns persist regarding potential adverse vascular effects, ... ...

    Abstract Background: Intravenous iron supplementation is an established therapy for patients with heart failure (HF) and concomitant iron deficiency reducing the risk of HF hospitalization. However, concerns persist regarding potential adverse vascular effects, since iron may induce oxidative stress, inflammation, and apoptosis of endothelial cells. To assess endothelial health following ferric carboxymaltose (FCM) administration, we analyzed the profile of circulating endothelial microvesicles (EMVs) and endothelial progenitor cells (EPCs) in a cohort of 23 HF patients using flow cytometry.
    Results: Compared to healthy subjects, baseline levels of CD31+/CD41- EMVs were higher and EMVs featured a more apoptotic phenotype in HF patients. Following FCM administration, EMV levels showed a rapid but transient increase and displayed an altered phenotype profile with dominant augmentation of EMVs expressing inducible markers CD62E and CD54, indicating endothelial inflammatory activation and injury. Levels of circulating vasoregenerative CD45lowCD34+KDR+ EPCs were lower in HF patients and FCM application resulted in an early decrease of EPCs followed by substantial mobilization into the circulation after one week. Levels of EMVs and EPCs returned to baseline values within two and four weeks, respectively. HF patients with additional chronic kidney disease showed an elevated EMV/EPC ratio and diminished EPC mobilization, suggesting impaired vascular repair capacity. Providing a mechanistic link,
    Conclusion: Intravenous iron supplementation with FCM in HF patients induces a biphasic response with initial increased release of CD62E+ and CD54+ enriched EMVs and subsequent mobilization of EPCs, indicating endothelial dysfunction upon FCM and suggesting consecutive engagement of a defense program aimed to reconstitute vascular health.
    MeSH term(s) Humans ; Iron ; Iron Deficiencies ; Endothelial Progenitor Cells ; Heart Failure/drug therapy ; Dietary Supplements
    Chemical Substances Iron (E1UOL152H7) ; ferric carboxymaltose (6897GXD6OE)
    Language English
    Publishing date 2023-01-24
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1092704
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Platelet microparticles: reinforcing the hegemony of platelets in atherothrombosis.

    Mause, Sebastian F

    Thrombosis and haemostasis

    2013  Volume 109, Issue 1, Page(s) 5–6

    MeSH term(s) Cell-Derived Microparticles/physiology ; Humans ; Plaque, Atherosclerotic/blood ; Plaque, Atherosclerotic/complications ; Thrombosis/blood ; Thrombosis/etiology
    Language English
    Publishing date 2013-01
    Publishing country Germany
    Document type Comment ; Editorial
    ZDB-ID 518294-3
    ISSN 0340-6245
    ISSN 0340-6245
    DOI 10.1160/TH12-11-0817
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article: Microparticles as intercellular carriers of the microRNA signal: insights for novel diagnostic and therapeutic approaches

    Mause, Sebastian F.

    Thrombosis and Haemostasis

    2016  Volume 115, Issue 02, Page(s) 236–236

    Language English
    Publishing date 2016-03-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/th16-01-0013
    Database Thieme publisher's database

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: Engagement of the CXCL12-CXCR4 Axis in the Interaction of Endothelial Progenitor Cell and Smooth Muscle Cell to Promote Phenotype Control and Guard Vascular Homeostasis.

    Mause, Sebastian F / Ritzel, Elisabeth / Deck, Annika / Vogt, Felix / Liehn, Elisa A

    International journal of molecular sciences

    2022  Volume 23, Issue 2

    Abstract: Endothelial progenitor cells (EPCs) are involved in vascular repair and modulate properties of smooth muscle cells (SMCs) relevant for their contribution to neointima formation following injury. Considering the relevant role of the CXCL12-CXCR4 axis in ... ...

    Abstract Endothelial progenitor cells (EPCs) are involved in vascular repair and modulate properties of smooth muscle cells (SMCs) relevant for their contribution to neointima formation following injury. Considering the relevant role of the CXCL12-CXCR4 axis in vascular homeostasis and the potential of EPCs and SMCs to release CXCL12 and express CXCR4, we analyzed the engagement of the CXCL12-CXCR4 axis in various modes of EPC-SMC interaction relevant for injury- and lipid-induced atherosclerosis. We now demonstrate that the expression and release of CXCL12 is synergistically increased in a CXCR4-dependent mechanism following EPC-SMC interaction during co-cultivation or in response to recombinant CXCL12, thus establishing an amplifying feedback loop Additionally, mechanical injury of SMCs induces increased release of CXCL12, resulting in enhanced CXCR4-dependent recruitment of EPCs to SMCs. The CXCL12-CXCR4 axis is crucially engaged in the EPC-triggered augmentation of SMC migration and the attenuation of SMC apoptosis but not in the EPC-mediated increase in SMC proliferation. Compared to EPCs alone, the alliance of EPC-SMC is superior in promoting the CXCR4-dependent proliferation and migration of endothelial cells. When direct cell-cell contact is established, EPCs protect the contractile phenotype of SMCs via CXCL12-CXCR4 and reverse cholesterol-induced transdifferentiation toward a synthetic, macrophage-like phenotype. In conclusion we show that the interaction of EPCs and SMCs unleashes a CXCL12-CXCR4-based autoregulatory feedback loop promoting regenerative processes and mediating SMC phenotype control to potentially guard vascular homeostasis.
    MeSH term(s) Atherosclerosis/etiology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Biomarkers ; Blood Vessels/metabolism ; Cell Movement ; Cells, Cultured ; Chemokine CXCL12/genetics ; Chemokine CXCL12/metabolism ; Endothelial Progenitor Cells/metabolism ; Gene Expression ; Homeostasis ; Humans ; Myocytes, Smooth Muscle/metabolism ; Neointima/genetics ; Neointima/metabolism ; Phenotype ; Protein Binding ; Receptors, CXCR4/genetics ; Receptors, CXCR4/metabolism ; Signal Transduction
    Chemical Substances Biomarkers ; CXCL12 protein, human ; CXCR4 protein, human ; Chemokine CXCL12 ; Receptors, CXCR4
    Language English
    Publishing date 2022-01-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23020867
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: miR155 Deficiency Reduces Myofibroblast Density but Fails to Improve Cardiac Function after Myocardial Infarction in Dyslipidemic Mouse Model.

    Schumacher, David / Curaj, Adelina / Simsekyilmaz, Sakine / Schober, Andreas / Liehn, Elisa A / Mause, Sebastian F

    International journal of molecular sciences

    2021  Volume 22, Issue 11

    Abstract: Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac ... ...

    Abstract Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role of miR155 in cardiac remodeling and dysfunction following myocardial infarction in a dyslipidemic mouse model. Myocardial infarction was induced in dyslipidemic apolipoprotein E-deficient (ApoE
    MeSH term(s) Animals ; Disease Models, Animal ; Echocardiography/methods ; Fibrosis/genetics ; Fibrosis/metabolism ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Ventricles/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; MicroRNAs/genetics ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; Myofibroblasts/metabolism ; Stroke Volume/genetics ; Ventricular Function, Left/genetics ; Ventricular Remodeling/genetics
    Chemical Substances MicroRNAs ; Mirn155 microRNA, mouse
    Language English
    Publishing date 2021-05-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22115480
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Endothelial Progenitor Cells Modulate the Phenotype of Smooth Muscle Cells and Increase Their Neointimal Accumulation Following Vascular Injury.

    Mause, Sebastian F / Ritzel, Elisabeth / Deck, Annika / Vogt, Felix / Liehn, Elisa A

    Thrombosis and haemostasis

    2021  Volume 122, Issue 3, Page(s) 456–469

    Abstract: Background:  Smooth muscle cells (SMCs) are the main driver of neointima formation and restenosis following vascular injury. In animal models, endothelial progenitor cells (EPCs) accelerate endothelial regeneration and reduce neointima formation after ... ...

    Abstract Background:  Smooth muscle cells (SMCs) are the main driver of neointima formation and restenosis following vascular injury. In animal models, endothelial progenitor cells (EPCs) accelerate endothelial regeneration and reduce neointima formation after arterial injury; however, EPC-capture stents do not reduce target vessel failure compared with conventional stents. Here we examined the influence of EPCs on features of SMCs pivotal for their impact on injury-induced neointima formation including proliferation, migration, and phenotype switch.
    Methods and results:  EPCs, their conditioned medium, and EPC-derived microparticles induced proliferation of SMCs while limiting their apoptosis. In transwell membrane experiments and scratch assays, EPCs stimulated migration of SMCs and accelerated their recovery from scratch-induced injury. Treatment of SMCs with an EPC-derived conditioned medium or microparticles triggered transformation of SMCs toward a synthetic phenotype. However, co-cultivation of EPCs and SMCs enabling direct cell-cell contacts preserved their original phenotype and protected from the transformative effect of SMC cholesterol loading. Adhesion of EPCs to SMCs was stimulated by SMC injury and reduced by blocking CXCR2 and CCR5. Interaction of EPCs with SMCs modulated their secretory products and synergistically increased the release of selected chemokines. Following carotid wire injury in athymic mice, injection of EPCs resulted not only in reduced neointima formation but also in altered cellular composition of the neointima with augmented accumulation of SMCs.
    Conclusion:  EPCs stimulate proliferation and migration of SMCs and increase their neointimal accumulation following vascular injury. Furthermore, EPCs context-dependently modify the SMC phenotype with protection from the transformative effect of cholesterol when a direct cell-cell contact is established.
    MeSH term(s) Adaptation, Physiological/physiology ; Animals ; Apoptosis ; Arteries/injuries ; Arteries/metabolism ; Cell Movement/physiology ; Cell Proliferation/physiology ; Cells, Cultured ; Disease Models, Animal ; Endothelial Progenitor Cells/pathology ; Endothelial Progenitor Cells/physiology ; Mice ; Myocytes, Smooth Muscle ; Neointima/etiology ; Neointima/metabolism ; Neointima/pathology ; Neointima/prevention & control ; Receptors, CCR5/metabolism ; Receptors, Interleukin-8B/metabolism ; Regeneration/physiology ; Signal Transduction/physiology ; Vascular System Injuries/metabolism ; Vascular System Injuries/pathology
    Chemical Substances CCR5 protein, mouse ; Cxcr2 protein, mouse ; Receptors, CCR5 ; Receptors, Interleukin-8B
    Language English
    Publishing date 2021-07-02
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1055/s-0041-1731663
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 433: Show issues

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  8. Article ; Online: Engagement of the CXCL12–CXCR4 Axis in the Interaction of Endothelial Progenitor Cell and Smooth Muscle Cell to Promote Phenotype Control and Guard Vascular Homeostasis

    Sebastian F. Mause / Elisabeth Ritzel / Annika Deck / Felix Vogt / Elisa A. Liehn

    International Journal of Molecular Sciences, Vol 23, Iss 867, p

    2022  Volume 867

    Abstract: Endothelial progenitor cells (EPCs) are involved in vascular repair and modulate properties of smooth muscle cells (SMCs) relevant for their contribution to neointima formation following injury. Considering the relevant role of the CXCL12–CXCR4 axis in ... ...

    Abstract Endothelial progenitor cells (EPCs) are involved in vascular repair and modulate properties of smooth muscle cells (SMCs) relevant for their contribution to neointima formation following injury. Considering the relevant role of the CXCL12–CXCR4 axis in vascular homeostasis and the potential of EPCs and SMCs to release CXCL12 and express CXCR4, we analyzed the engagement of the CXCL12–CXCR4 axis in various modes of EPC–SMC interaction relevant for injury- and lipid-induced atherosclerosis. We now demonstrate that the expression and release of CXCL12 is synergistically increased in a CXCR4-dependent mechanism following EPC–SMC interaction during co-cultivation or in response to recombinant CXCL12, thus establishing an amplifying feedback loop Additionally, mechanical injury of SMCs induces increased release of CXCL12, resulting in enhanced CXCR4-dependent recruitment of EPCs to SMCs. The CXCL12–CXCR4 axis is crucially engaged in the EPC-triggered augmentation of SMC migration and the attenuation of SMC apoptosis but not in the EPC-mediated increase in SMC proliferation. Compared to EPCs alone, the alliance of EPC–SMC is superior in promoting the CXCR4-dependent proliferation and migration of endothelial cells. When direct cell–cell contact is established, EPCs protect the contractile phenotype of SMCs via CXCL12–CXCR4 and reverse cholesterol-induced transdifferentiation toward a synthetic, macrophage-like phenotype. In conclusion we show that the interaction of EPCs and SMCs unleashes a CXCL12–CXCR4-based autoregulatory feedback loop promoting regenerative processes and mediating SMC phenotype control to potentially guard vascular homeostasis.
    Keywords endothelial progenitor cells ; smooth muscle cells ; CXCR4 ; chemokine ; atherosclerosis ; vascular injury ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: Platelet microparticles: reinforcing the hegemony of platelets in atherothrombosis

    Mause, Sebastian F.

    Thrombosis and Haemostasis

    2013  Volume 109, Issue 01, Page(s) 5–6

    Language English
    Publishing date 2013-01-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH12-11-0817
    Database Thieme publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
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    Zs.MO 433: Show issues

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  10. Article ; Online: miR155 Deficiency Reduces Myofibroblast Density but Fails to Improve Cardiac Function after Myocardial Infarction in Dyslipidemic Mouse Model

    David Schumacher / Adelina Curaj / Sakine Simsekyilmaz / Andreas Schober / Elisa A. Liehn / Sebastian F. Mause

    International Journal of Molecular Sciences, Vol 22, Iss 5480, p

    2021  Volume 5480

    Abstract: Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac ... ...

    Abstract Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role of miR155 in cardiac remodeling and dysfunction following myocardial infarction in a dyslipidemic mouse model. Myocardial infarction was induced in dyslipidemic apolipoprotein E-deficient (ApoE −/− ) mice with and without additional miR155 knockout by ligation of the LAD. Four weeks later, echocardiography was performed to assess left ventricular (LV) dimensions and function, and mice were subsequently sacrificed for histological analysis. Echocardiography revealed no difference in LV ejection fractions, LV mass and LV volumes between ApoE −/− and ApoE −/− /miR155 −/− mice. Histology confirmed comparable infarction size and unaltered neoangiogenesis in the myocardial scar. Notably, myofibroblast density was significantly decreased in ApoE −/− /miR155 −/− mice compared to the control, but no difference was observed for total collagen deposition. Our findings reveal that genetic depletion of miR155 in a dyslipidemic mouse model of myocardial infarction does not reduce infarction size and consecutive heart failure but does decrease myofibroblast density in the post-ischemic scar.
    Keywords microRNA ; cardiovascular disease ; myocardial infarction ; heart failure ; dyslipidemia ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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