Expression profile of UVB-induced premature senescent fibroblasts
Skin aging is a multifaceted process influenced by various factors including intrinsic factors, such as genetics and natural aging processes and extrinsic factors, such as exposure to UV radiation. UV radiation, especially, leads to the formation of reactive oxygen species (ROS), DNA damage, and the activation of inflammatory pathways, ultimately causing the accumulation of senescent cells. UV radiation can indeed induce cellular senescence in various skin cell types, including dermal fibroblasts. Fibroblasts are crucial cells in the dermis responsible for producing extracellular matrix components like collagen. Understanding the mechanisms by which UV radiation induces cellular senescence in skin cells is crucial for developing strategies to prevent and counteract the aging effects of sun exposure. Studying the gene expression profile of UVB-induced senescent fibroblasts provides insights into the molecular mechanisms underlying the skin's response to UV radiation and helps identify potential targets for interventions aimed at preventing or mitigating the effects of UV-induced skin aging. In the current study, we induced premature senescence in normal human dermal fibroblasts (NHDFs) from foreskins of young donors by exposure to narrowband (NB)-UVB irradiation. We also confirmed that our repeated UVB exposure protocol led to stress-induced premature senescence (UVB-SIPS).  Gene expression profile of UVB-induced premature senescent NHDFs were investigated using RNA-seq data analysis. By comparing the transcriptomes of UVB-exposed fibroblasts to those of unexposed fibroblasts, we identified 430 upregulated genes and 216 downregulated genes in response to UVB radiation.
Skin aging is a multifaceted process influenced by various factors including intrinsic factors, such as genetics and natural aging processes and extrinsic factors, such as exposure to UV radiation. UV radiation, especially, leads to the formation of reactive oxygen species (ROS), DNA damage, and the activation of inflammatory pathways, ultimately causing the accumulation of senescent cells. UV radiation can indeed induce cellular senescence in various skin cell types, including dermal fibroblasts. Fibroblasts are crucial cells in the dermis responsible for producing extracellular matrix components like collagen. Understanding the mechanisms by which UV radiation induces cellular senescence in skin cells is crucial for developing strategies to prevent and counteract the aging effects of sun exposure. Studying the gene expression profile of UVB-induced senescent fibroblasts provides insights into the molecular mechanisms underlying the skin's response to UV radiation and helps identify potential targets for interventions aimed at preventing or mitigating the effects of UV-induced skin aging. In the current study, we induced premature senescence in normal human dermal fibroblasts (NHDFs) from foreskins of young donors by exposure to narrowband (NB)-UVB irradiation. We also confirmed that our repeated UVB exposure protocol led to stress-induced premature senescence (UVB-SIPS).  Gene expression profile of UVB-induced premature senescent NHDFs were investigated using RNA-seq data analysis. By comparing the transcriptomes of UVB-exposed fibroblasts to those of unexposed fibroblasts, we identified 430 upregulated genes and 216 downregulated genes in response to UVB radiation.
Research Unit on Cellular Biology