Direkt zum Inhalt
Leiter:
PD Dr. Daniel Duerschmied
Mitarbeiter:
Daniela Stallmann (BS)
Dr. Thilo Witsch
Dr. Christoph Schmidt-Hofner
PhD student Maximilian Mauler
MD student Janine Guenther
MD student Nadine Herr
MD student Julia Seyfert
MD student Ludwig Dorner
MD student Simon Halter
Kelly Daryll Blanz
Links:
Kooperationen:
Professor Denisa D. Wagner (Harvard Medical School)
Professor Christoph Bode
Assistant Professor Constantin von zur Muhlen
Professor Marco Idzko
Assistant Professor Andreas Zirlik

Blood platelets not only orchestrate hemostasis and (athero-) thrombosis, but have also been recognized as key modulators of immune functions.

Platelets circulate through the body in a quiescent state, ready to interact with the vessel wall after injury or inflammatory challange. They are prepared to rapidly interact with neutrophils, monocytes/macrophages, Iymphocytes, and with endothelial cells to promote the recruitment of immune cells into inflamed tissues, to control cytokine release, and in some cases trap and kill pathogens.

Platelets store a variety of factors in their granules and can release these factors within seconds after stimulation. The multitude of these factors and their functions has only started to be fully understood. One of the secreted factors is serotonin. Some of our research efforts focus on this biogenic amine not (only) because it has been dubbed the "happiness hormone" but because we are convinced that it is an important modulator of many immune functions. Platelets store serotonin at a very high concentration int their dense granules, from where they can release it in severed, atherosclerotic, or inflamed vessels. Diego Walther and Michael Bader discovered in Berlin that serotonin supports the hemostatic function of platelets by binding to small GTPases and called this mechanism "serotonylation".

We found that isolated serotonin receptor stimulation greatly decreases platelet adhesion because glycoprotein Ibα becomes shed from the surface. Platelets are therefore unable to incorporate into growing arterial thrombi after serotonergic stimulation. Interestingly, this involves the activation of tumor necrosis factor-α converting enzyme (TACE), an enzyme that is also an important player in inflammation.

Recently, we discovered that platelet serotonin also affects the recruitment of immune cells to sites of inflammation. We started to decipher the involved mechanisms because if we understand these processes, we may be able to develop new therapeutic strategies for acute and chronic inflammatory diseases such as atherosclerosis or ischemia/reperfusion injury after myocardial infarction.

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