Title: Wim DECLERCQ
Subtitle:
Author:

Declercq team

Research Field:

Team leader: Prof. Dr. Wim Declercq

Tel: +32 9 33 13 721 - Fax: +32 9 221 76 73
Email: Wim.Declercq.spam.detractor@irc.vib-UGentspam.corruptor.be

Research topic

The skin constitutes the first protective barrier of the organism, protecting it against water loss and external physical, chemical, and biological insults such as wounding, UVB radiation, and microorganisms. The skin exists of an outer squamous epithelium, the epidermis, and an inner connective tissue, the dermis. The barrier is mainly constituted by the epidermis, which is continuously rejuvenated due to keratinocyte proliferation. Imbalances in the delicate physiological turn-over of proliferating or differentiating keratinocytes can result in the disturbance of the skin barrier function and are reflected in many skin disorders, such as psoriasis, eczema, etc.. In addition, improper removal of damaged cells by the keratinocyte terminal differentiation program can result in cancerous lesions.

Our research group tries to understand the role of molecules involved in homeostasis, cell death and inflammation in the skin. Therefore we developed substantial expertise in the field of molecular signal transduction in cell death and inflammation using in vitro and in vivo model systems (about 100 publications in the field of expertise). Currently, we focus on studying the involvement of caspases, RIP kinases and regulators thereof in skin homeostasis and pathology.

Schematic representation of the differentiating keratinocyte layers in the epidermis. Eckhart, Lippens, Tschachler and Declercq, BBA, 2013. Click to enlarge.
Schematic representation of the differentiating keratinocyte layers in the epidermis. Eckhart, Lippens, Tschachler and Declercq, BBA, 2013. Click to enlarge.

Areas of expertise

  • Cell death and NF-κB signaling
  • In vivo mouse gene targeting and development of skin inflammation mouse models
  • Study of the molecular pathways involving caspases and RIP kinases

Technology transfer potential

  • Development of mouse models for inflammatory skin diseases
  • Identification of therapeutic targets in cell death and inflammation

Selected publications

  1. Hoste E et al. Caspase-14-deficient mice are more prone to the development of parakeratosis.
    Journal of Investigative Dermatology, 133, 742-50. 2013
  2. Duprez L et al. RIP kinase-dependent necrosis drives lethal systemic inflammatory response syndrome.
    Immunity, 35, 908-18, 2011.
  3. Lippens S et al. Keratinocyte-specific ablation of the NF-κB regulatory protein A20 (TNFAIP3) reveals a role in the control of epidermal homeostasis.
    Cell Death and Differentiation, 18, 1845-53, 2011.
  4. Declercq W et al. RIP kinases at the crossroads of cell death and survival.
    Cell, 138, 229-232, 2009.
  5. Denecker G et al. Caspase-14 protects against epidermal UVB photo-damage and water loss.
    Nature Cell Biology, 9, 666-674, 2007.

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