Project description:Gene Expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice Affymetrix GeneChip® Mouse Genome 430 array was used to study the gene expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice Gene Expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice
Project description:Gene Expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice Affymetrix GeneChip® Mouse Genome 430 array was used to study the gene expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice
Project description:To examine whether MFG-E8 deficiency affects gene expression in spleen. Total RNA samples were extracted whole spleen of 4 month old B6 and MFG-E8 deficient mice
Project description:The mammary gland is a unique apocrine gland made up of a branching network of ducts that end in alveoli. It is an ideal system to study the molecular mechanisms associated with cell proliferation, differentiation, and oncogenesis. MFG-E8, also known as Lactadherin, is a vital glycoprotein related to the milk fat globule membrane and initially identified to get secreted in bovine milk. Our previous report suggests that a high level of MFG-E8 is indicative of high milk yield in dairy animals. Here, we showed that MFGE-E8 controls the cell growth and morphology of epithelial cells through a network of regulatory transcription factors. To understand the comprehensive action, we downregulated its expression in MECs by MFG-E8 specific shRNA. We generated a knockdown proteome profile of differentially expressed proteins through a quantitative iTRAQ experiment on a high-resolution mass spectrometer (Q-TOF). The downregulation of MFG-E8 resulted in reduced phagocytosis and cell migration ability, whereas it also leads to more lifespan to knockdown vis-a-vis healthy cells, which is confirmed through BrdU, MTT, Neutral red, and Caspase 3/7. The bioinformatics analysis revealed that MFG-E8 knockdown perturbs a large number of intracellular signaling, eventually leading to cessation in cell growth. Based on the Weighted Gene Coexpression Network Analysis and directed network, we found that MFG-E8 is activated by CX3CL1, TP63, and CSF2 and leads to the activation of SOCS3 and CCL2 for the regulation of cell proliferation. We further proved that the depletion of MFG-E8 resulted in activated cytoskeletal remodeling by MFG-E8 knockdown, which results in the activation of three independent pathways ZP4/JAK-STAT5, DOCK1/STAT3, and PIP3/AKT/mTOR. Overall, this study suggests that MFG-E8 expression in mammary epithelial cells is an indication of intracellular deterioration in cell health. To date, to the best of our knowledge, this is the first study that explores the downstream targets of MFG-E8 involved in the regulation of mammary epithelial cell health.
Project description:The wounds were made on the back skin of Snhg26 knockout (KO) and wild type (WT) mice. The wound edge and skin tissue were collected and the epidermis were separated by incubate the tissue with dispaseII. Total RNA was extracted from the epidermis. The global transcriptome analysis of the epidermis were performed by using Affymetrix arrays.
Project description:Wound healing is orchestrated by a spatial and temporal network of intercellular communication between epithelial cells, the stromal compartment, and the immune system. We found that Hgfac KO mice showed delayed wound healing in an endoscopic wound model. To dissect the celluar and molecular mechanisms of tissue healing, we collected tissues from day2 wounds or intact tissues from Hgfac WT and KO mice using a skin biopsy punch and dissociated cells for scRNA-seq analysis.
Project description:To investigate the roll of ARID1A in the regulation of effector CD8+ T cell responses, we crossed GzmB-Cre P14 Thy1.1 mice with Arid1a-fl/fl mice to generate Arid1a Het and KO mice. We then performed gene expression profiling analysis of WT, Het, and KO cells in vivo at d3, d5, and d8 post-LCMV Armstrong infection.
Project description:To investigate the role of ARID1A in the regulation of transcription factor binding and histone modifications in effector CD8+ T cell responses, we crossed GzmB-Cre P14 Thy1.1 mice with Arid1a-fl/fl mice to generate Arid1a KO mice. We then performed CUT&RUN against ARID1A, BATF, ETS, Tbet, H3K27ac, H3K27me3 in WT, Arid1a KO, or Tbx21 (Tbet) KO cells in vivo at d0, 48h in vitro activated, d5, and d8 post-LCMV Armstrong infection.
