Project description:A fuller study of UV-induced biological effects lies beyond the scope of this paper. I will focus on the genetic interaction of cells irradiated by UV. Accordingly, in respect to genomic, the regulation of the gene expressions in cells represents how they response to the stress and repair themselves. In the past, Northern Blot has been used to detect the expression level of a few genes in one experiment. Thus, this assay is always limited to a small scope of a huge unknown network of gene expression. However, to investigate gene expression networks made of thousands of genes, a powerful tool must be implemented. As anticipated, the interactions between regulated genes in UV irradiation time-course experiment can be analyzed by cDNA microarray analysis with experimental loop design. This study provides a platform to investigate the gene networks regulated by UV irradiation. Keywords: UV, cDNA microarray, mitochondria respiratory chain, ROS, carcinogenesis
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
Project description: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.
