Project description:Here we found Rosa roxburghii fruit extracts effectively increase TERT expression and telomerase activity in cultured human mesenchymal stem cells. Both Rosa roxburghii fruit extracts by freeze drying and spray drying methods increase the activity of telomerase. Rosa roxburghii fruit freeze drying extracts is able to reduce reactive oxygen species levels, enhance SOD activity and resistance to oxidative stress, and reduce DNA damage caused by oxidative stress or radiation. Rosa roxburghii fruit extracts promoted cell proliferation, improved senescent cell morphology, delayed replicative cellular senescence, attenuated cell cycle supressors and alleviated the senescence-associated secretory phenotype. Transcriptome and metabolic profilings found that Rosa roxburghii fruit extract promote cell proliferation and DNA repair pathways, decreased triglycerides as well. Overall, we provided a theoretical basis for the application of Rosa roxburghii fruit as an anti-aging natural product.
Project description:To examine the role of Evi1 in HSC specification, we generated Tie2-Cre::ROSA-Evi1 mice, which can induce Evi1 in endothelial cells. We observed five-fold increase of HSCs In Tie2-Cre::ROSA-Evi1 embryo. To characterize the induced HSCs in Tie2-Cre::ROSA-Evi1 embryos, we analyzed the gene expression profile of HSCs.
Project description:Only a few small regulatory RNAs (sRNAs) have been characterized in B. subtilis, the paradigm of Gram-positive bacteria, and one of the major challenges is target identification. Here we use global in vivo RNA psoralen cross-linking to identify RNA-RNA partners in Bacillus subtilis. Two sRNAs, RoxS and FsrA, play key roles in balancing the metabolic state of the cell in response to carbon sources and iron limitation, respectively. In this study, we identify new mRNA targets for both RoxS and FsrA, and a small RNA (S345/RosA) that is able to interact with both sRNAs. We report that RosA controls the maturation and degradation of RoxS and acts as a sponge to limit the efficacy of RoxS on its targets. Expression of RosA is catabolically repressed by the transcription factor CcpA. We provide evidence that the RosA/RoxS interaction plays a key role in regulating metabolism in response to a switches in carbon source.
