Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control- with 4-OHT-treated. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of 4-OHT-induced degeneration of photoreceptor cells in the 3D-retinas. 4-OHT-induced gene expression in the 3D-retinas was measured at DD 26 when the photoreceptor cells were degenerated. Two-condition experiment, vehicle control- vs. 5 µM 4-OHT-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1 replicate.
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control with 4-OHT-treated w/o supplements. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of protective effects of representative ophthalmic supplements for treating the photoreceptor degeneration. 4-OHT w/o supplements-induced gene expression in the 3D-retinas was measured at DD 25 when the photoreceptor cells started to be degenerated. Four-condition experiment, vehicle control- vs. 5 µM 4-OHT- vs. 5 µM 4-OHT with 400 µM vitamin E- vs. 5 µM 4-OHT with 200 nM lutein-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1replicate.
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control- with 4-OHT-treated. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of 4-OHT-induced degeneration of photoreceptor cells in the 3D-retinas.
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control with 4-OHT-treated w/o supplements. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of protective effects of representative ophthalmic supplements for treating the photoreceptor degeneration.
Project description:3D LCMS using C18 functionality in all three dimensions (HFBA-pH10-Formic Acid).
1D LC-MS, 90 minutes; 2D LC-MS, 21 fractions x 90 minutes; 3D LC-MS, 126
fractions x 90 minutes. Jurkat cell digest.
Project description:Previously, we have shown that broad spectrum antibiotic treatment reduces reactive astrocyte phenotypes in the APPPS1-21 model of AD-related amyloidosis. We have also found that antibiotics selectively increases propionate levels and exogenous propionate treatment recapitulates phenotypes observed in antibiotic treated mice. In the current study, we wanted to assess astrocyte transcriptional state using bulk RNA sequencing. To accomplish this we used translating ribosome affinity purification (TRAP) sequencing, a ribosomal protein L10a is fused to eGFP under the control of a cell type specific promoter in a transgenic mouse model. We crossed APPPS1-21 mice to the Aldh1l1-eGFP/Rpl10a bacTRAP mouse model and progeny were treated with antibiotics, propionate, or VHL and performed bulk TRAPseq.