Project description:We have identified Epigallocatechin Gallate (EGCG) as a potent modulator of microglia function. Our aim was to determine whether EGCG affects the transcriptome of microglia and identify genes and gene sets that may underly the effects of EGCG on microglia function.
Project description:To elucidate the mechanism by which epigallocatechin gallate (EGCG) promotes the differentiation of epidermal stem cells (EpSCs), we performed RNA sequencing (RNA-seq) on EpSCs treated with or without 2 μM EGCG for 3 days. This analysis revealed the transcriptome profile regulated by EGCG.
Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection. A total of 7 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 1uM EGCG for 24h (n=3) in addition to the vehicle control (n=4).
Project description:Obesity has progressively become a global concern. It contributes to adipose tissue dysfunction, leading to metabolic disorders, and chronic systemic inflammation. Our previous study showed that the conjugation between chitooligosaccharides (COS) and epigallocatechin-3-gallate (EGCG) diminished lipid accumulation and promoted browning of white adipose tissue (WAT) in high fat diet (HFD)-induced obese rats.
Project description:The epigenetic regulation of transcription factor genes is critical for T cell lineage specification. A specific methylation pattern within a conserved region of the lineage specifying transcription factor gene FOXP3, the Treg-specific demethylated region (TSDR), is restricted to regulatory T (Treg) cells and required for stable expression of FOXP3 and suppressive function. We analyzed the impact of hypomethylating agents 5-Aza-2`-deoxycytidine and Epigallocatechin-3-gallate (EGCG) on human CD4+CD25- T for generating Treg cell specific DNA methylation pattern within FOXP3-TSDR and inducing functional Treg cells. Gene expression, including lineage specifying transcription factors of the major T cell lineages and their leading cytokines, functional properties and global transcriptome changes were analyzed. 5-Aza-2`-deoxycytidine induced FOXP3-TSDR methylation and expression of Treg cell specific genes FOXP3 and LRRC32. Proliferation of 5-Aza-2´deoxycytidine treated cells was reduced, but they did not show suppressive function. Hypomethylation was not restricted to FOXP3-TSDR and expression of master transcription factors and leading cytokines of Th1 and Th17 cells were induced. EGCG induced global DNA hypomethylation to a lower degree than 5-Aza-2´deoxycitidine, but no relevant hypomethylation within FOXP3-TSDR or expression of Treg cell specific genes. Both DNMT inhibitors did not induce full functional human Treg cells. Although 5-Aza-2`-deoxycytidine treated cells phenotypically appeared to be Treg cells, they did not suppress proliferation of responder cells, which is an essential capability to be used in Treg cell transfer therapy. In this study we analyze the potency of the two hypomethylating agents 5-Aza-2`-deoxycytidine (5-Aza-dC) and Epigallocatechin-3-gallate (EGCG) for in vitro induction of functional Treg cell cells through generation of a specific methylation pattern within FOXP3-TSDR. We analyzed the expression of Treg cell specific genes and for their functional properties from CD4+CD25- T cells. 5-Aza-dC is a derivative of 5-Azacytidine. Both substances are inhibitors of DNA methyltransferases (DNMTs) and used for therapy of patients with myelodysplastic syndrome and acute myeloid leukaemia. In these patients, 5-Azacytidine has been reported to augment regulatory T cell expansion in blood. EGCG is the most abundant catechin of green tea and has been reported to have cardio protective, anti-cancer, anti-infective properties and protective effects on autoimmune diseases. EGCG has also been described as a potent inhibitor of DNMTs and to induce Foxp3 in Jurkat T cell line.
Project description:Epigallocatechin-3-gallate (EGCG) is the most plentiful polyphenol in green tea and has antiviral, antioxidant, anti-aging, anti-inflammatory, and neuroprotective effects . Studies have shown that EGCG can inhibit a diversity of biological processes of tumor progression, including cell proliferation, invasion, metastasis, and angiogenesis, and can also induce apoptosis and cell cycle arrest. In order to investigate the role of EGCG in multiple myeloma (MM), we carried out this study. We found that EGCG could inhibit myeloma cell activity and promote myeloma cell apoptosis. To further explore the mechanism of EGCG promoting apoptosis in myeloma cells, cells were treated with EGCG and subjected to RNA sequencing.
Project description:We reported the molecular mechanisms of low combination doses of epigallocatechin-3-gallate and hydroxychavicol (EGCG+HC) in glioma cell lines 1321N1 and LN18. Using high throughput RNA sequencing, combined EGCG+HC exerted its anticancer effect by downregulating the axon guidance process and metabolic pathways, while simultaneously interfering with endoplasmic reticulum unfolded protein response pathway. Furthermore, EGCG+HC exerted its apoptotic effect through the alteration of mitochondrial genes such as MT-CO3 and MT-RNR2 in 1321N1 and LN18 cells respectively. EGCG+HC dynamically altered DYNLL1 alternative splicing expression in 1321N1 and DLD splicing expression in LN18 cell lines.