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Detail

Selma Osmanagic-Myers
Dr. Selma Osmanagic-Myers

Center for Pathobiochemistry and Genetics (Institute of Medical Chemistry and Pathobiochemistry)
Position: Research Associate (Postdoc)

ORCID: 0000-0002-3834-1332
T +43 1 40160-38008
selma.osmanagic-myers@meduniwien.ac.at

Further Information

Keywords

Aging; Aging, Premature; Atherosclerosis; Bone Diseases; Cardiovascular Diseases; Endothelial Cells

Research interests

In modern societies with increasingly older populations, age is becoming a major risk factor for atherosclerosis and cardiovascular disease. However, the underlying molecular mechanisms especially with regard to aging of the innermost blood vessel layer, the endothelium, are still not fully understood. Our major focus is the impact of cellular aging (senescence) on endothelial dysfunction and development of chronic diseases, particularly, atherosclerosis, cardiovascular disease but also osteoporosis. We aim to provide deeper insight into the mechanism of senescence development in endothelial cells and explore the effects of senescence-associated secretory phenotype (SASP) in order to work on developing interventions that can manipulate and counteract these processes. Our ultimate goal is to “unwrinkle” the aged blood vessels and promote healthy aging.

Techniques, methods & infrastructure

We use mouse and human endothelial cell cultures from different origins, mesenchymal and hematopoietic stem cells and progeria mouse models of premature aging. Using pharmacological and genetic manipulations combined with flow assays that resemble physiological environment of endothelial cells we analyze senescence pathways in endothelial cells  in order to find ways to restore “juvenile” healthy cell states.

 

Grants

  • The contribution of endothelial senescence to age-related cardiovascular disease in progeria (2019)
    Source of Funding: FWF (Austrian Science Fund), P 32595-B, stand-alone grant
    Principal Investigator

Selected publications

  1. Osmanagic-Myers, S. & Foisner, R., 2019. The structural and gene expression hypotheses in laminopathic diseases—not so different after all K. G. Kozminski, ed. Molecular Biology of the Cell, 30(15), pp.1786–1790. Available at: http://dx.doi.org/10.1091/mbc.E18-10-0672.
  2. Osmanagic-Myers, S. et al., 2018. Endothelial progerin expression causes cardiovascular pathology through an impaired mechanoresponse. Journal of Clinical Investigation, 129(2), pp.531–545. Available at: http://dx.doi.org/10.1172/JCI121297.
  3. Osmanagic‐Myers, S. & Rezniczek, G.A., 2018. Arteriovenous specification: BMPER and TWSG 1 determine endothelial cell fate via activation of synergistic BMP and Notch signaling. The FEBS Journal, 285(8), pp.1399–1402. Available at: http://dx.doi.org/10.1111/febs.14439.
  4. Osmanagic-Myers, S. et al., 2015. Plectin reinforces vascular integrity by mediating crosstalk between the vimentin and the actin networks. Journal of Cell Science, 128(22), pp.4138–4150. Available at: http://dx.doi.org/10.1242/jcs.172056.
  5. Osmanagic-Myers, S., Dechat, T. & Foisner, R., 2015. Lamins at the crossroads of mechanosignaling. Genes & Development, 29(3), pp.225–237. Available at: http://dx.doi.org/10.1101/gad.255968.114.