Project description:HUC model includes three cell lines: HUC-BC, HUC-PC, and MCT11. They were all originally derived from human uroepithelium. However, three cell lines have different malignant potential. We here performed micro array to examine the differences in gene expression among three cell lines.
Project description:HUC model includes three cell lines: HUC-BC, HUC-PC, and MCT11. They were all originally derived from human uroepithelium. However, three cell lines have different malignant potential. We here performed micro array to examine the differences in gene expression among three cell lines.
Project description:Peripheral infusion of human umbilical cord mesenchymal stem cells (hUC-MSCs) can profoundly suppress the activation of c-Mos and remarkably improve hepatic histology, suppress the systemic inflammatory reaction, and promote animal survival in a large non-human primate model of acute liver failure (ALF). The mechanism through which hUC-MSCs inhibits c-Mos activation in vivo remains unclear. We hypothesized that hUC-MSCs can adaptively produce certain inhibitory cytokines in response to the pro-inflammatory microenvironment. To confirm this, we stimulated cultured hUC-MSCs with inflammatory monkey serum (serum isolated at day 1 following toxin challenge). After a 30-min stimulation, the cells were collected for microarray gene expression analysis. A whole human genome oligo microarray analysis was performed to reveal the altered gene expression profiles of the hUC-MSCs
Project description:Neuromyelitis optica (NMO) is a severe autoimmune inflammatory disease of the central nervous system that affects motor function and causes relapsing disability. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) have been used extensively in the treatment of various inflammatory diseases, due to their potent regulatory roles that can mitigate inflammation and repair damaged tissues. However, their use in NMO is currently limited, and the mechanism underlying the beneficial effects of hUC-MSCs on motor function in NMO remains unclear. In this study, we investigate the effects of hUC-MSCs on the recovery of motor function in an NMO systemic model. Our findings demonstrate that milk fat globule epidermal growth 8 (MFGE8), a key functional factor secreted by hUC-MSCs, plays a critical role in ameliorating motor impairments. We also elucidate that the MFGE8/Integrin αvβ3/NF-κB signaling pathway is partially responsible for structural and functional recovery, in addition to motor functional enhancements induced by hUC-MSC exposure. Taken together, these findings strongly support the involvement of MFGE8 in mediating hUC-MSCs-induced improvements in motor functional recovery in an NMO mouse model. In addition, this provides new insight on the therapeutic potential of hUC-MSCs and the mechanisms underlying their beneficial effects in NMO.
Project description:To uncover the dysregulated genes in BCa, we performed the RNA-seq to detect the gene expression levels in four BCa cells (5637, UMUC3, T24, and J82) and human immortalized urothelial cell SV-HUC-1. To search for the differentially expressed genes of for cell lines (5637, J82, UMUC3, and T24) compared to the normal cell line SV-HUC-1.
Project description:hUC-MSCs exhibit the biological characteristics and potential for neural differentiation.The different gene involved in the neural differentiation were not clear. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during the process of neural differentiation.
Project description:Mesenchymal stem cells (MSCs) exist in almost all tissues and participate in tissue regeneration and homeostasis. MSCs based therapy is applied to some refractory immune diseases to control inflammation, such as lupus nephritis, Crohn’s disease and rheumatoid arthritis. However, accumulating studies showed that the immunomodulatory capacity of naïve MSCs is mild and limited. To enhance MSCs immunomodulatory function, researchers innovated a new method to reprogram MSCs via pre-treatment with inflammatory cytokines. In this work, we firstly used a cocktail of three cytokines, IL-1β, TNF-a and IFN-γ, to treat hUC-MSCs (human MSCs from umbilical cord). We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 untreated hUC-MSCs (ctrl) and 3 cytokines-treated hUC-MSCs (primed).
Project description:To study the genes and pathway involved in cigarette smoke induced lung inflammation, and treatment with hUC-MSC-EV and hUC-MSC we have employed microarray expression profiling to identify the differentially expressed genes
Project description:Human umbilical cord mesenchymal stem cells (hUC-MSCs) are broadly applied in clinical treatment due to easy availability, low immunogenicity, and no ethical issues involved. However, the microenvironment of inflammatory tissues may cause oxidative stress and induce senescence in transplanted hUC-MSCs, which will further reduce the proliferation, migration ability, and the final therapeutic effects of hUC-MSCs. Beta-nicotinamide mononucleotide (NMN), and coenzyme Q10 (CoQ10) are famous antioxidants and longevity medicines that could reduce intracellular reactive oxygen species levels by different mechanisms.Transcriptomic analysis revealed that NMN and CoQ10 both increased DNA repair ability and cyclin expression, and downregulated TNF and IL-17 inflammatory signaling pathways, thereby contributed to the proliferation of advanced stem cells and aging due to oxidative stress. These findings suggest that antioxidants can improve the survival and efficacy of hUC-MSCs in stem cell therapy for inflammation-related diseases.
