Thrombocytes (platelets) are normally responsible for closing wounds. In the worst case, they are involved in the development of strokes or heart attacks. The platelets work through a complicated process of signaling pathways, messenger substances, migrations, and receptor binding, which is not yet fully understood.

Thrombocytes are not cells in the strict sense, because they do not have a cell nucleus and are only secretions of megakaryocytes, which are formed in the bone marrow. Nevertheless, their significance is undisputed.

To investigate the functional mechanisms, scientists want to know the properties and function of each individual protein on the surface of the platelets. To study one protein, all others have to be eliminated - no easy task, since platelets themselves do not have the genetic material to be genetically modified. In the past, researchers have therefore always genetically modified rodents and isolated their megakaryocytes.

The scientist has now developed a new method, with which the proportion of rodents can be reduced by about 40 percent. In her research, she used cells from donor blood or urine and re-embryonalized them according to known mechanisms into induced pluripotent stem cells (iPSC). Then, the iPSC were genetically modified using the CRISPR/Cas9 method to the extent that only a single protein was formed on the surface of the platelets.

The procedure reduces animal experiments on rodents because gene experiments that do not lead to the desired result can be identified in advance and sorted out as useless.

Otherwise, the genetically modified cell cultures can also be used to test substances and thus replace animal experiments.

The prize is endowed with 25,000 euros.

Source:
https://twitter.com/bmel
https://www.bmel.de/SharedDocs/Pressemitteilungen/DE/2020/238-tierschutzforschungspreis.html

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Witte A, Rohlfing AK, Dannenmann B, Dicenta V, Nasri M, Kolb K, Sudmann J, Castor T, Rath D, Borst O, Skokowa J, Gawaz M. (2020). The chemokine CXCL14 mediates platelet function and migration via direct interaction with CXCR4. Cardiovasc Res. 2020 Apr 1:cvaa080. doi: 10.1093/cvr/cvaa080. Epub ahead of print. PMID: 32239134.