Liliane Michalik received her PhD from the University Louis Pasteur of Strasbourg in 1993, for work on microtubule-associated proteins in the group of Jean-François Launay, INSERM. In 1994, she joined the group of Walter Wahli at UNIL for her post-doctoral training, during which she initiated a research project aimed at elucidating the roles of the nuclear hormone receptors PPARs in skin homeostasis and repair. Between 1996 and 2002, she persued her research in the same field as Maître Assistant, then Maître d’Enseignement et de Recherche at UNIL. She arrived at the Center for Integrative Genomics in 2003 as Maître d'Enseignement et de Recherche, and is MER-privat docent since 2008.
skin repair, UV induced skin cancer, angiogenesis, peroxisome proliferator-activated receptors.
INTERVIEWRESEARCH REPORT 2015-2016
Research summary
Cells in our body must adapt to a constantly changing environment. They continually receive a whole repertoire of cues that our genome translates into cell responses by changing gene expression. To maintain appropriate cell responses, and thereby to maintain our body integrity, the control of gene expression is crucial, as misregulated gene expression programs can cause a broad range of diseases, including cancers.
Our overall goal is to understand how our cells integrate environmental cues and how they respond by adapting gene transcription. In this purpose, we study how the skin, our largest interface with the environment, responds to insults like mechanical injuries, allergens or sunlight Ultra Violet (UV) rays (a major environmental cue and a complete carcinogen). Notably, we explore how the nuclear hormone receptors PPARs control gene expression and skin cell responses to these environmental insults.
PPARs are ligand activated transcription factors that sense cues and transform them into transcriptional responses. As nuclear hormone receptors, they are activated by natural endogenous agonists, but can also be regulated by synthetic agonists or antagonists, what makes them very attractive drugable targets. We study PPAR-dependent regulations of skin responses to insults and of UV-induced skin cancers using genetically modified mice, organ and cell culture models, as well as genomic approaches.
Representative publications
Identification of a novel PPARβ/δ/miR-21-3p axis in UV-induced skin inflammation.
Degueurce G., D'Errico I., Pich C., Ibberson M., Schütz F., Montagner A., Sgandurra M., Mury L., Jafari P., Boda A. et al., 2016. EMBO Molecular Medicine, 8 (8) pp. 919-936. Peer-reviewed.
[URN] [DOI] [WoS] [Pmid] [serval:BIB_EC0CAB165489]
Endothelial, but not smooth muscle, peroxisome proliferator-activated receptor β/δ regulates vascular permeability and anaphylaxis.
Wawrzyniak M., Pich C., Gross B., Schütz F., Fleury S., Quemener S., Sgandurra M., Bouchaert E., Moret C., Mury L. et al., 2015. Journal of Allergy and Clinical Immunology, 135 (6) pp. 1625-1635.e5. Peer-reviewed.
[DOI] [WoS] [Pmid] [serval:BIB_1ED6EDEE8520]
Src is activated by the nuclear receptor peroxisome proliferator-activated receptor β/δ in ultraviolet radiation-induced skin cancer.
Montagner A., Delgado M.B., Tallichet-Blanc C., Chan J.S., Sng M.K., Mottaz H., Degueurce G., Lippi Y., Moret C., Baruchet M. et al., 2014. EMBO Molecular Medicine, 6 (1) pp. 80-98.
[URN] [DOI] [WoS] [Pmid] [serval:BIB_61D2EDA76529]
PPARs at the crossroads of lipid signaling and inflammation.
Wahli W., Michalik L., 2012. Trends in Endocrinology and Metabolism, 23 (7) pp. 351-363.
[DOI] [WoS] [Pmid] [serval:BIB_EA74394CACCD]
The nuclear hormone receptor peroxisome proliferator-activated receptor beta/delta potentiates cell chemotactism, polarization, and migration.
Tan N.S., Icre G., Montagner A., Bordier-ten-Heggeler B., Wahli W., Michalik L., 2007. Molecular and Cellular Biology, 27 (20) pp. 7161-7175. Peer-reviewed.
[DOI] [WoS] [Pmid] [serval:BIB_A57EC9DCD756]
