Project description:To determine what signalling pathways are affected by LILRB1 in MM cells, ARP-1 MM cell lines were transfected with lentivirus to knockdown LILRB1, injected to nsg mice, sorted from the bone marrow of NSG mice and sent for RNA-seq. Total RNAs of 2 x 10^6 CTR-KD ARP-1 cells or LILRB1-KD ARP-1 cells were extracted by RNeasy Mini Kit (Qiagen). 5-10 µg RNA samples were sent to Cancer Genomics Center at The University of Texas (Houston, TX) for RNA-seq followed by data analysis. We use the RNA-seq data to determine differential expression of genes in CTR-KD ARP-1 cells and LILRB1-KD ARP-1 cells.
Project description:Nonalcoholic steatohepatitis (NASH) is an aggressive liver disease threatening public health, however its natural history is poorly understood. Unlike ob/ob mice, Lep∆I14/∆I14 rats develop unique NASH phenotype with an inflection point of inflammation at postnatal week 16. Using Lep∆I14/∆I14 rats, we studied the natural history of NASH progression by performing an integrated analysis of hepatic transcriptome from postnatal week 4 to 48. Leptin deficiency leads to the precipitously increasing expression of genes encoding rate-limiting enzymes in lipid metabolism. However, hepatic inflammation related genes, pathways and immune-cell infiltration are restricted after week 16, implying an essential role of LEPTIN in regulating hepatic inflammation. Lep∆I14/∆I14 rats share more genes with NASH patients than known mouse models, therefore will provide a better genetic platform for studying NASH than mice.