|MARKUS SCHOBER, Ph. D.|
Homeostasis, regeneration, and carcinogenesis in skin epithelium
Adult stem cells, which are capable to self-renewing and differentiating into various cell types, play an important role in maintaining all tissues and organs of our body. While generally tucked away in protected niches, quiescent adult stem cells become activated to balance normal wear and tear and maintain tissue homeostasis, as well as to regenerate damaged tissues and organs upon injury. Although adult stem cells are generally beneficial for human health, their inappropriate activation is also believed to contribute to diseases including cancer. Therefore, understanding the signaling mechanisms that govern tissue homeostasis and regeneration, and how their deregulation contributes to diseases including metastatic cancer is of general biomedical interest.
Mammalian skin is an excellent model system in which to investigate how cell signaling controls tissue homeostasis by balancing proliferation, differentiation, and apoptosis and how the deregulation of these processes contributes to carcinogenesis. The skin epithelium develops from a single cell layer, which is in direct contact with a basement membrane separating the epidermis from the dermis. As development proceeds, distinct cell types are specified within the single layered epithelium to a) differentiate into supra-basal cells driving epidermal stratification, and to b) develop into epidermal appendages such as hair follicles, sebaceous glands, and sweat glands, which grow downwards into the underlying dermis. Distinct populations of adult stem cells maintain homeostasis within the inter-follicular epidermis, the sebaceous gland, and the hair follicle and contribute to the regeneration of the skin epithelium and its appendages upon injury and imbalance in homeostasis. Although distinct cell populations with stem cell potential have been identified in the skin epithelium, the mechanisms which determine their stem cell potential remain largely unknown.
Our interest lies in understanding the molecular mechanisms by which growth promoting signals form receptor tyrosine kinases and integrin mediated cell matrix adhesions cooperate with growth restricting signals from the TGFβ pathway to control proliferation, survival, differentiation, and migration of stem- and progenitor cells in epidermal morphogenesis, homeostasis, regeneration, and carcinogenesis.
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