Speaker
Description
The term "cellular senescence" refers to an irreversible cell cycle arrest that can be caused by a variety of stressors and is accompanied by an accumulation of damage, changes in cell shape and secretory profile, and epigenetic abnormalities in primary cells. There is an accumulation of senescent cells in development, aging and tissue regeneration; all of which are conditions with increased damage and pro-growth stimuli. Importantly, while the reason for this accumulation is unclear, the senescent cells which persist in the tissue directly contribute to the pathology of age-related diseases, chronic wounds and tumor growth. This presentation is aimed at sharing unpublished results on the kinetics of senescent cell
accumulation at the sites of wounds in mice and pigs, particularly in acute mechanical wounds. BALB/c mice were wounded on the mid-back with 1 cm diameter full-thickness wounds, while minipigs were injured using a standard 6 mm biopsy punch. Wound samples were taken at various
time points to characterize the kinetics of healing and senescence induction. In addition to elaborating on the temporal relationship between senescence and wound healing, we will also reveal our novel results on the spatial relationship between the site of wounding and senescence induction. Moreover, we demonstrate a clear correlation between senescence markers and features of healing such as reepithelialization and trans-differentiation of fibroblasts. Finally, we will describe the candidate proteins and pathways involved in the induction of cellular senescence at wounds.
20941819044
