Project description:The affection of Sirt1 on astrocyte is not well understanded. Here we studied the change of RNA expression profile after Sirt1 knockout in primary astrocyte after stimulating with A1 astrocyte inducing cocktails. To analyze the change of RNA expression profile after Sirt1 knockout in astrocytes, we built Sirt1 knockout and control astrocytes using crispr technique, and analyzed RNA expression profiles of Sirt1 KO and control astrocytes after treating with cocktail (C1q, IL-1α, TNF-α) by using microarray.
Project description:Direct current electric field mimicking a physiological electrical field from transepithelial potential difference can direct cell migration (electrotaxis)and cellular signaling. While the transcriptome in dcEF has been reported and more studied, the miRNA expression of cells under dcEF stimulation is less understood. We use a reversibly sealed dcEF stimulation bioreactor to apply uniform dcEF to glioblastoma cell lines and primary astrocytes and investigate if dcEF can induce differential expression of cellular miRNA and exosomal miRNA expression that can regulate the gene expression
Project description:In order to understand the mechanism associated with SIRT1-mediated development of prostate cancer progression, we conducted RNA-sequencing analysis in SIRT1 suppressed hormone sensitive prostate cancer cells (LNCaP) under conditions of androgen sufficiency, deprivation, androgen stimulation or AR suppression.
Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-DE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.
Project description:Sirtuin 1 (SIRT1) is involved in both aging and circadian-clock regulation, yet the link between the two processes in relation to SIRT1 function is not clear. Using Sirt1-deficient mice, we found that Sirt1 and Period 2 (Per2) constitute a reciprocal negative regulation loop that plays important roles in modulating hepatic circadian rhythmicity and aging. Sirt1-deficient mice exhibited profound premature aging and enhanced acetylation of histone H4 on lysine16 (H4K16) in the promoter of Per2, the latter of which leads to its overexpression; in turn, Per2 suppresses Sirt1 transcription through binding to the Sirt1 promoter at the Clock/Bmal1 site. This negative reciprocal relationship between SIRT1 and PER2 was also observed in human hepatocytes. We further demonstrated that the absence of Sirt1 or the ectopic overexpression of Per2 in the liver resulted in a dysregulated pace of the circadian rhythm. The similar circadian rhythm was also observed in aged wild type mice. The interplay between Sirt1 and Per2 modulates aging gene expression and circadian-clock maintenance.
Project description:Sirtuin 1 (SIRT1) is involved in both aging and circadian-clock regulation, yet the link between the two processes in relation to SIRT1 function is not clear. Using Sirt1-deficient mice, we found that Sirt1 and Period 2 (Per2) constitute a reciprocal negative regulation loop that plays important roles in modulating hepatic circadian rhythmicity and aging. Sirt1-deficient mice exhibited profound premature aging and enhanced acetylation of histone H4 on lysine16 (H4K16) in the promoter of Per2, the latter of which leads to its overexpression; in turn, Per2 suppresses Sirt1 transcription through binding to the Sirt1 promoter at the Clock/Bmal1 site. This negative reciprocal relationship between SIRT1 and PER2 was also observed in human hepatocytes. We further demonstrated that the absence of Sirt1 or the ectopic overexpression of Per2 in the liver resulted in a dysregulated pace of the circadian rhythm. The similar circadian rhythm was also observed in aged wild type mice. The interplay between Sirt1 and Per2 modulates aging gene expression and circadian-clock maintenance. To investigate hepatic SIRT1-dependent aging related genes, livers from wild type mice at 3 months (young), 12 months (middle age), and 19 months (old) of age, as well as Sirt1-deficient mice at 3 months of age were snap frozen and subject to RNA isolation and microarray analysis.