Dataset Information

CUT&RUN seq of HSF4 and COIL after UV stimulation of NIH-3T3 cells

ABSTRACT: Intense ultraviolet (UV) exposure can cause phototoxic reactions, such as skin inflammation, resulting in injury. UV is believed to be the direct cause of DNA damage, but the mechanisms of transcriptional regulation within cells after DNA damage are unclear. The bioinformatic analysis of transcriptome sequencing data from UV-irradiated and non-UV-irradiated skin showed that transcription-related proteins, such as HSF4 and COIL, mediate the cellular response to UV irradiation. HSF4 and COIL could form a complex under UV irradiation, and the preference for binding target genes changed. This is due to the presence of a large number of R-loops in the cells under UV irradiation and the ability of COIL to recognize the R-loops. The regulation of target genes was altered by the HSF4-COIL complex, and the expression of inflammation and aging-related genes, such as ATG7, TFPI, and LIMS1, were enhanced. A drug screen was performed for the recognition sites of COIL and R-loop. N6-(2-hydroxyethyl)-adenosine (HEA) could competitively bind COIL and inhibit the binding of COIL to R-loop. Thus, the activation of downstream inflammation-related genes and inflammatory skin injury were inhibited.

ORGANISM(S): Mus musculus

PROVIDER: GSE233680 | GEO | 2023/08/08

REPOSITORIES: GEO

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Project description:Dr. Liu's research group is interested in studying the expression and functions of galectin-3, -7 and -12, in particular the roles of these proteins in inflammation and neoplasm. Members of the galectin family are known to participate in cellular homeostasis by modulating cell growth, controlling cell cycle progression, and inducing or inhibiting apoptosis. It is known that some galectins have similar functions. However, it is not fully understood whether they work cooperatively or not. As the outermost barrier of the body, skin is directly and frequently exposed to a prooxidative environment, including solar ultraviolet A (UVA), ultraviolet B (UVB) radiation, and air pollution. Several reports have shown that exposure of cells to UV increase or decrease the levels of galectins. For example, the amounts of galectin-7 mRNA and protein are increased rapidly after UVB irradiation of keratinocytes (Proc. Natl. Acad. Sci. USA 1999; 96:11329-34). Heat shock and subculturing decrease, while alkylating agents and UV-light increase galectin-3 (Cell Physiol Biochem 2000; 10:149-58). To analyze the change of all galectin gene expression profiles after UVB irradiation and to determine the presence or absence of coordinate regulation, we analyzed the gene expression profiles of keratinocytes exposed to UVB. Normal human epidermal keratinocytes (NHEK) were irradiated with 200 J/m2 of UVB. Total RNA will be extracted at 0, 6, 12 and 24 h after irradiation (duplicate) for analysis on the Glyco gene chip. Several reports have shown that exposure to UV light can regulate levels of galectin in skin. This study seeks to analyze the changes in all galectin gene expression profiles post-UVB irradiation to determine the presence or absence of coordinate regulation. In this study, normal human keratinocytes were irradiated with 200J/m2 of UVB. Total RNA was extracted at 0, 6, 12, and 24-hour post irradiation time points, in duplicate. Samples were hybridized and analyzed using the GLYCOv2 array.

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CUT&RUN seq of HSF4 and COIL after UV stimulation of NIH-3T3 cells

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