Recent studies have showed that SASP may contribute to cell cycle arrest through autocrine/paracrine pathways.
In a previous research by means of LC-MS/MS analyses, we evaluated the SASP composition of bone marrow (BM) and adipose (A) MSCs following different genotoxic stress treatment.
This experiment aimed to determine whether SASP from H2O2 treated MSCs having silenced FLNB or CD13 were still able to induce senescence in healthy cells by paracrine mechanism.
Recent studies showed that senescent cells secrete a pool of molecules (SASP) such as inflammatory cytokines, chemokines, growth factors, and matrix metalloproteinases that can regulate and determine the senescence response.
Although many studies highlighted the importance of the SASP in regulating cellular response to senescence signaling, the identification of secreted factors is still a challenging issue, since the typology of secreted proteins strictly depends on genotoxic stress and cell type (2-4).
In the new work, the mechanism by which SASPs prevent this fatal reaction comes to light.
By studying SASPs, scientists may learn more about how the earliest cells survived the high ultraviolet levels present before the emergence of Earth's radiation-filtering stratospheric ozone layer, Mohr says.