Project description:We utilized whole genome sequencing of mRNA (RNA-seq) to understand the extent to which the senescence-associated secretory phenotype is regulated by p38MAPK Examination of replicates of young, senescent or p38MAPK-inhibited senescent BJ human foreskin fibroblasts.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:Background: Mutations of mitochondrial (mt)DNA cause a variety of human diseases and are also implicated in ageing processes. Results: Primary fibroblasts of the conplastic mouse strain C57BL/6J-mtALR/LTJ with a mutation at position nt4738 resulting in a single nucleotide exchange (leucine to methionine) in the mitochondrial NADH dehydrogenase subunit 2 (Nd2) gene of the respiratory chain show higher enzyme activity and ATP production and lower ROS production than control fibroblasts. Furthermore, Nd2-mutant fibroblasts show a higher proliferation rate and a reduction of senescence markers. Transcriptome analysis reveals members of the p38MAPK pathway as being significantly downregulated in Nd2-mutant mice as compared with controls. In line with this, inhibition of p38MAPK with SB203580 enhanced the proliferation and reduced cytokine secretion in senescent Nd2-mutant fibroblasts. Conclusion: Taken together, we report Nd2 as a new mitochondrial gene with age-protective function in mice, and possibly in humans, which interferes with age-related signaling pathways. MouseRef-8 v2.0 Expression BeadChips of 8 samples of skin fibroblasts; 4 samples of fibroblasts from 4 mice of C57BL/6J-mtALR/LtJ (Nd2-mutant) and 4 samples of fibroblasts from 4 mice of C57BL/6J-mtAKR/J (control)
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.
