Skin ageing is an inevitable consequence of life and accelerated by exposure to ultraviolet (UV) rays. Senescence is an irreversible growth arrest and senescent cells accumulate in ageing tissues, including human skin, at sites of age-related pathologies and in pre-neoplastic lesions. Traditionally, senescent cells have been detected by “senescence associated-β-galactosidase (SA-β-gal) activity”, a procedure that is technically challenging and requires enzymatic activity, which is lost in cryopreserved tissue samples. Moreover, SA-β-gal activity and other senescence markers lack specificity and are difficult to quantify. Therefore, we need better markers to detect and quantify senescent cells in vivo.
We previously demonstrated that loss of lamin B1 is a novel marker to identify senescent cells in vitro as well as in aged human skin in vivo1,2. In addition, we demonstrated that loss of lamin B1 can be used to detect and quantify senescent cells upon UV-exposure in vitro. To test the physiological relevance of these findings in vivo, we used a mouse model to quantify the accumulation and clearance of senescent cells upon chronic UV-exposure and skin regeneration, respectively3. Our goal is to use these and other biomarkers to study the impact of senescence on different skin cell types and skin compartments during ageing, 2) distinguish senescent from proliferating cells in pre-neoplastic lesions, and 3) investigate how senescence changes the function of different skin cell types.
1Dreesen O et al., (2013). Consequences of Lamin B1 fluctuations on cellular proliferation and senescence. Journal of Cell Biology
2Dreesen O, Ong PF, Chojnowski A, Colman A (2013). The contrasting roles of lamin B1 in cellular aging and human disease. Nucleus
3Wang AS, Ong PF, Chojnowski A, Clavel C, Dreesen O (2017) Loss of lamin B1 is a biomarker to quantify cellular senescence in photoaged skin. Scientific Reports