Project description:Olfactory ensheathing cells are one of the few central nervous system regenerative cells discovered so far. It is characterized by its lifelong nerve regeneration function, and it can also release a variety of neurotrophic factors and neural adhesion molecules. It is considered to be the glial cell with the strongest myelination ability. Olfactory ensheathing cells and Schwann cells have phenotypes in common, they can promote axon regeneration(R. Doucette, 1995). Olfactory ensheathing cells have the characteristics of Schwann cells and astrocytes, but the overall performance tends to be the former, which has two unique characteristics. First, it exists not only in the peripheral nerves (Schwann cells), but also in the central nervous system (astroglia); second, the olfactory mucosa has the ability to regenerate life-long, including human olfactory ensheathing cells(J. C. Bartolomei and C. A. Greer, 2000). Regeneration is a process in which olfactory ensheathing cells participate in efficient regulation, although the specific mechanism is not yet clear. Olfactory ensheathing cells are different from astrocytes and Schwann cells, but at the same time have the characteristics of these two cells(S. C. Barnett, 2004), like Schwann cells help axon growth, but more than Schwann cells It can make axons grow long distances, that is, it has stronger migration(A. Ramon-Cueto et al., 1998); there are also astrocytes that have a nutritional effect on the survival of neurons and the growth of axons, but olfactory ensheathing cells can also wrap neurons forms myelin sheath to support the growth of nerve processes(R. Devon and R. Doucette, 1992; J. Gu et al., 2019). There are two characteristics that make olfactory ensheathing cells the best choice for the treatment of neurological diseases(S. C. Chiu et al., 2009; J. Kim et al., 2018; M. Abdel-Rahman et al., 2018). Olfactory ensheathing cells are gradually used to treat spinal cord injuries and have shown amazing effects(J. C. Bartolomei and C. A. Greer, 2000; K. J. Liu et al., 2010; R. Yao et al., 2018). Olfactory ensheathing cells that have been used in research are usually derived from the olfactory bulb(E. H. Franssen et al., 2007), but it is easier to obtain olfactory ensheathing cells from the olfactory mucosa in clinical practice(M. Ryszard et al., 2006), so the difference between the olfactory ensheathing cells from the olfactory bulb and the olfactory mucosa There are more and more studies(B. M. U. et al., 2007), and previous studies have shown that they not only have many similar functions, but also have many differences(M. W. Richter et al., 2005; L. Wang et al., 2014; K. E. Smith et al., 2020). Because olfactory ensheathing cells derived from the olfactory bulb are not easy to obtain, olfactory ensheathing cells derived from the olfactory mucosa have become the focus of attention. Although we know that olfactory ensheathing cells from two sources have nerve repair functions, it is not clear why the two different sources of olfactory ensheathing cells have different therapeutic effects. Nicolas G. once studied that the genetic difference between the two cells and found that there are many genes related to wound repair and nerve regeneration(G. Nicolas et al., 2010). We have reason to guess that olfactory ensheathing cells from these two sources will also have a large difference in protein level. Our research group wants to use the current mature transcriptome and proteomic sequencing technologies to explore the difference between olfactory ensheathing cells from the olfactory bulb and olfactory mucosa, and explain why the two sources of olfactory ensheathing cells shows different therapeutic effects, hope to provide a new theoretical basis for future clinical treatment.
Project description:we mapped the locations of DNA segments occupied by GATA1 using chromatin immunoprecipitation (ChIP). We have produced genome-wide GATA1 ChIP datasets after restoration and activation in G1E-ER4 cells. we employed the sequence census methodology of ChIP-seq , using Illumina GA2 technology to produce 23 million reads (36 nucleotides long) uniquely mapped to the mouse genome (mm8 assembly) for the GATA1 ChIP DNA and 15 million mapped reads for the input DNA Examination of transcription factor GATA1 occupancy
Project description:This study involves characterization of four head and neck cancer cell lines -- NT8e, OT9, AW13516 and AW8507, established from Indian head and neck cancer patients, using SNP arrays, whole exome and whole transcriptome sequencing.
Project description:The dysregulation of exosomal microRNAs (miRNAs) play a crucial role in the development and progression of cancer. Differentially expressed miRNAs were identified in serum exosomes of GC patients and healthy individuals using next-generation sequencing and bioinformatics.
Project description:G1ME cells are GATA1-deficient murine bipotential megakaryocyte/erythrocyte progenitor cells derived from Gata1-negative murine ES cells. In order to assess the impact of GATA1 on gene regulation and cell differentiation, an expression construct was used to transiently produce high levels of GATA1. Cells transduced with this construct or a vector control were harvested at 18 and 42 hours, and gene expression was analyzed using Affymetrix MOE430 version 2 arrays. Both vector control and GATA1-expressing cells were isolated by FACS for GFP and 18 and 42 hours. Biologic triplicates were performed for each construct at each timepoint.
Project description:Contradictorily, both up- and downregulation of miR-25 can reverse heart failure. Importantly, these findings were based on the same animal model of pressure overloaded transverse aortic constriction (TAC) mice. How can we explain and, if possible, reconcile these two conflicting findings? Heart failure is a multi-step process that involves multiple organs, and we hypothesized that determining whether altering miR-25 alone could induce heart failure should provide a mechanistic basis for miR-25âs action in this process. Here, we show that overexpression of miR-25 in normal mice caused cardiomyocyte fibrosis and apoptosis but no obvious kidney impairment. By contrast, inhibition of miR-25 in normal mice led to hypertension, mild heart dilation, and severe kidney dysfunction. With the expectation that restoring miR-25 might ameliorate kidney injury, we demonstrated that increasing miR-25 reversed proteinuria and kidney fibrosis in diabetic nephropathy. MiR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. RNA sequencing of mouse kidneys with elevated and reduced miR-25 identified distinct alterations of a number of putative miR-25 target mRNAs, including those involved in the Ras signaling pathway, oxidant stress. In summary, differences in miR-25 expression during different stages of heart disease and its distinct roles in the heart and kidney, offer a new perspective for the role of miR-25 function in heart failure, which may begin to resolve this catch-22. Detect the mRNA alteration in wildtype and miR-25 agomir or antagomir treated mice
Project description:Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. Here, we found that Bach2 deficiency promotes the intestinal epithelial cell proliferation during homeostasis and facilitates the crypt regeneration after irradiation, resulting in a reduction of mortality. RNA-seq analysis of isolated crypts revealed that Bach2 deficiency altered expression of numerous genes including those regulating DSBs repair. Crypts were isolated from the small intestines of Bach2 KO and control mice (n=3, respectively) 10 days after tamoxifen administration. Total RNA was extracted for sequencing using RNA-Seq.
Project description:The experiment is for demonstrating the miRNA profiles in plasma exosomes derived from mild cognitive impairment and Alzheimer's disease patients and healthy donors.
Project description:The resulting heat map shows an increased expression of ECM and ECM regulatory genes, 'activated' fibroblast genes, and cell cycle genes in the THY1+HE- sorted cells and in Tie2 and Tbx18-derived cardiac fibroblasts from TAC relative to sham RNA-seq of Thy1+HE- cells isolated 7 days after injury in mice that underwent sham and transaortic constriction (TAC) operations.