Karen Peynshaert

Karen Peynshaert


Karen Peynshaert
Laboratory for General Biochemistry and Physical Pharmacy
Ghent University
Harelbekestraat 72
9000 Gent
Tel: 0032 9 2648047 (secretary)
Tel: 0032 9 264 8049 (direct)
Fax: 0032 9 2648189
E-mail: karen.peynshaert@UGent.be


Having obtained a Bachelor degree in Pharmaceutical Sciences at Ghent University (2010), she continued her study to graduate as a Master of Science in Drug Development. In 2012 she started her PhD in the lab of General Biochemistry and Physical Pharmacy, which mainly focuses on nanoparticle-cell interactions and their potential use as anti-cancer agent.

Summary of Research Project(s)

The use of nanomaterials (NMs) for technological and biomedical applications is vastly increasing. However, their potential toxicity remains largely unknown, which restricts their application. One of the questions yet to be resolved is whether NMs are able to affect autophagy, an essential cellular process for the removal and recycling of unwanted or excessive cytoplasmic material. Currently, various NMs have been described to affect autophagy suggesting this may be a general response towards nanoparticle internalization. This phenomenon could have a great impact on the level of toxicity since autophagy disruption has been associated with various diseases. Alternatively, it could also have great therapeutic implications as autophagy modulation is suggested as a therapeutic strategy for e.g. cancer. As the extensive variety of nanoparticle characteristics (e.g. size, coating) hardens a clear toxicological analysis there is a great need for a systematic screening of widely differing organic and inorganic NMs on their potential to induce or inhibit autophagy.

Using a stepwise approach the optimal NM concentrations to study autophagy will be determined by evaluating the uptake and toxicity of the respective particles in a single cell type. Next, NM-mediated induction or inhibition of autophagy will be assessed by visualization of autophagic compartments and quantification of important autophagy markers. Since NM-induced autophagy likely results in nanomaterial degradation and loss of functionality it will be evaluated if autophagy inhibitors can aid the cell to better tolerate the intracellular presence of NMs with the aim to improve cell labeling and drug delivery. Finally, to test if this process can be exploited as a novel anti-cancer therapy approach, the most potent autophagy-inducing NMs will be screened on cell-specificity by comparing their effects between cancerous and non-cancerous cell types.

In summary, this project aims to examine the link between NMs and autophagy to enrich our understanding of nanomaterial-mediated toxicity. This will allow to ameliorate cell labeling and drug delivery and to evaluate the potential intrinsic toxicity of nanoparticles towards cancerous cells as a novel way of combating cancer.