It is my great pleasure to invite you to the second seminar of the “Ster lectures” series, which will take place next Thursday, April 20th at 3pm in the CN hall.
By invitation of Grégory Petrazzo, a PhD student from the Laboratory of the Molecular Bases of Aging led by prof. Ewa Sikora, we will host prof. Maria Cavinato head of the Laboratory of Cellular Senescence and Skin Biology at the Institute for Biomedical Aging Research of the University of Innsbruck.
Prof Cavinato will give a lecture entitled: Mechanisms of mitochondria quality control in skin aging and disease.
Accumulation of dysfunctional mitochondria due to impaired mitophagy is a major characteristic of senescent cells as well as of several human age-related conditions and cancer. Mitophagy receptor NIX has been shown to drive epidermal differentiation through control of mitochondrial fragmentation. Furthermore, NIX epidermal expression is decreased during aging and leads to the accumulation of dysfunctional mitochondria in this tissue, suggesting that NIX-dependent mitophagy is an important mechanism for the maintenance of skin homeostasis. Recently, the release of extracellular vesicles (EVs) containing damaged mitochondria has been proposed to act as an alternative mechanism of mitochondria quality control to outsource mitophagy. However, it is unknown if such mechanisms are involved in the process of senescence of human dermal fibroblasts (HDF) as well as if they participate in aging and disease of human skin. We have thus investigated the role of NIX-dependent mitophagy in cellular senescence, skin aging and skin tumorigenesis, the release of EVs containing mitochondria as a compensatory mechanism to outsource mitophagy and to explored the implication of these mechanisms in skin homeostasis and disease. Based on our preliminary data we have observed that NIX-dependent mitophagy plays a crucial role in HDF homeostasis. Impairment of this mechanism induces senescence of HDF, even in the absence of UVB, characterized by secretion of different SASP factors, including EVs containing mitochondria. Work with 3D skin equivalents demonstrated that absence of NIX in dermal fibroblasts induce hyperproliferation and impaired differentiation of epidermal keratinocytes suggesting that factors secreted by NIX-depleted fibroblasts can modulate skin homeostasis and induce skin carcinogenesis.
The seminar will be followed by a get together.
With best regards,