Alice Assinger

Medical University of Vienna
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Austria

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Articles (20)

Age-Dependent Surface Receptor Expression Patterns in Immature Versus Mature Platelets in Mouse Models of Regenerative Thrombocytopenia

Aging is a multifaceted process that unfolds at both the individual and cellular levels, resulting in changes in platelet count and platelet reactivity. These alterations are influenced by shifts in platelet production, as well as by various environmental factors that affect circulating platelets. Aging also triggers functional changes in platelets, including a reduction in RNA content and protein production capacity. Older individuals and RNA-rich immature platelets often exhibit hyperactivity, contributing significantly to pathologic conditions such as cardiovascular diseases, sepsis, and thrombosis. However, the impact of aging on surface receptor expression of circulating platelets, particularly whether these effects vary between immature and mature platelets, remains largely unexplored. Thus, we investigated the expression of certain surface and activation receptors on platelets from young and old mice as well as on immature and mature platelets from mouse models of regenerative thrombocytopenia by flow cytometry. Our findings indicate that aged mice show an upregulated expression of the platelet endothelial cell adhesion molecule-1 (CD31), tetraspanin-29 (CD9), and Toll-like receptor 2 (TLR2) compared to their younger counterparts. Interestingly, when comparing immature and mature platelets in both young and old mice, no differences were observed in mature platelets. However, immature platelets from young mice displayed higher surface expression compared to immature platelets from old mice. Additionally, in mouse models of regenerative thrombocytopenia, the majority of receptors were upregulated in immature platelets. These results suggest that distinct surface receptor expressions are increased on platelets from old mice and immature platelets, which may partially explain their heightened activity and contribute to an increased thrombotic risk.

Year:

2023

Collaborators (26)

Maiju Myllys

Leibniz-Institut für Arbeitsforschung an der TU Dortmund

GERMANY

Corina T. Madreiter-Sokolowski

Associate Professor

Medical University of Graz

AUSTRIA

Melanie Korbelius

Medical University of Graz

AUSTRIA

Stefan Heber

Medical University of Vienna

AUSTRIA

Johan Heemskerk

Emeritus Prof. of Cell Biochemistry of Thrombosis and Haemostasis

University of Maastricht

NETHERLANDS

Jochen M Schwenk

KTH Royal Institute of Technology

SWEDEN

Karoline Kollmann

University of Veterinary Medicine Vienna

AUSTRIA

José Manuel Soria Fernández

Principal Investigator. Head of Group

Hospital de la Santa Creu i Sant Pau

SPAIN

Elizabeth Habermann

Professor of Health Services Research

Mayo Clinic

UNITED STATES

Christian Hengstenberg

Head of Department

Medical University of Vienna

AUSTRIA

Patrick Starlinger

Medical University of Vienna

AUSTRIA

Wolfgang Graier

Head

Medical University of Graz

AUSTRIA

Marion Mussbacher

Assistant Professor

Graz University of Technology

AUSTRIA

Andreas Bernhard Diendorfer

Head of Computational Biology

-

AUSTRIA

Philip Dusart

KTH Royal Institute of Technology

SWEDEN

Cristina Coman

Universität Wien

AUSTRIA

Jacob Odeberg

KTH Royal Institute of Technology

SWEDEN

Robert Ahrends

Prof.

Universität Wien

AUSTRIA

Axel Schlagenhauf

Head of Research Group

Medical University of Graz

AUSTRIA

Nina Troppmair

Universität Wien

AUSTRIA

Minna Kaikkonen

Professor of Cardiovascular Genomics

University of Eastern Finland

FINLAND

Hubert Hackl

Assistant Professor

Medical University of Innsbruck

AUSTRIA

Dagmar Kratky

Professor of Biochemistry

Medical University of Graz

AUSTRIA

Sarah Beck

Institute for Research in Biomedicine

GERMANY

Lynn M. Butler

UiT The Arctic University of Norway

NORWAY

Thomas Züllig

University of Graz

AUSTRIA
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