Paraskevi Heldin - my privileged life as scientist
My scientific life started in 1981, when I started as a graduate student in the laboratory of the eminent professor Lorentz Engström, at the Department of Medical and Physiological Chemistry, studying regulatory phosphorylation of proteins. After my dissertation in 1987, I started to work on hyaluronan biology, as a postdoctoral fellow in the laboratory of professor Torvard Laurent, who worked on the same department. Under Torvard´s enlightened leadership, I became dedicated to the hyaluronan field and particularly to the investigation of the effect of over-expression of hyaluronan in inflammation, cancer and infection.
As was known in the 1980-ies, an overproduction of hyaluronan occurred in blood and tissues under rapid tissue remodeling and infection, where a plethora of growth factors and cytokines are released. At that time, there was a growing interest both in clinical work on hyaluronan, and in basic research to elucidate the molecular mechanisms underlying its excess production during disease. In 1983, CD44, which first was described as the receptor leading to the extravasation of inflamed lymphocytes into inflammatory foci, was interestingly found to be the principal cell surface receptor for hyaluronan. This finding united immunology and extracellular matrix research, and it was possible to understand why one of the physiological functions of hyaluronan was to capture circulating cells, such as lymphocytes and neutrophils, and lead them to inflamed sites.
My subsequent career involved employment as Head of the Matrix Biology Group at the Ludwig Institute for Cancer Research, Uppsala, where world leading research on growth factor signaling was performed. In this inspiring and productive environment, our studies ontargeting of hyaluronan-CD44 signalling in cancer and infection revealed a correlation between tumor progression and growth-factor-mediated hyaluronan synthesis and CD44 over-activity.
In 2017, I became a guest professor at the Department of Medical Biochemistry and Microbiology (IMBIM) and continued our research on hyaluronan-CD44 signaling. In this nice environment, we demonstrated that perturbation of hyaluronan signaling contributes to the progression of diseases, such as aggressive breast cancer, glioblastoma, Dengue virus infection and COVID-19 infection. I formally retired in 2022, but am still working on the elucidation of the underlying mechanisms of CD44 signaling and on the development of ways to inhibit hyaluronan-CD44 signaling.