Project description:SDF-1 has been reported to trigger ADAMTS4,5 overexpression through activating CXCR4 signaling in chondrocytes. Here we described the transcriptional changes of SDF-1-treatment as well as natural products CXCR4 antagonists treatment.
Project description:To examine the effects of DPP4 overexpression and its modulation by 4,5-Dicaffeoylquinic acid on chondrocytes, we established C28/I2 cell lines with DPP4 overexpression (DPP4OE), control empty vector (OENC), and DPP4OE treated with 4,5-Dicaffeoylquinic acid. Gene expression profiling analysis was performed using RNA sequencing (RNA-seq) with biological replicates to investigate the global transcriptomic changes associated with these conditions.
Project description:In order to study the role of piR_019914 in C28/I2 cells, we established piR_019914_mimics to overexpress piR_019914 in C28/I2 cells We then performed gene expression profiling analysis using data obtained from RNA-seq of piR_019914 overexpression C28/I2 cells and mimics_NC C28/I2 cells.
Project description:Fatty acid-binding protein 4 (FABP4) plays an essential role in metabolism and inflammatory. However, the role of FABP4 in alcoholic steatohepatitis (ASH) remains unclear. This study aimed to investigate the function of FABP4 and the underlying mechanisms in the progression of ASH.
Project description:Analysis of gene expression profiling in FABP4 modulation UM-UC14 and Um-UC9 cells. The overall objective was to identify genes regulated by PPARγ signaling pathway in particular FABP4 Total RNA was obtained from FABP4 modulated (either by FABP4 knockdown or rosiglitazone treatment) UM-UC14 or UM-UC9 cells compared to untreated control
Project description:We report here the overexpression of DPP4 in C28/I2 chondrocyte cells to investigate the changes induced by elevated levels of this gene. DPP4 is known as a marker of cellular senescence, yet its regulatory mechanisms remain unclear. In this study, we utilized the C28/I2 cell line to overexpress DPP4 and analyzed the resultant effects on gene expression and cellular behavior. Our findings reveal that DPP4 overexpression influences several pathways associated with chondrocyte function and senescence. Specifically, we observed alterations in pathways related to extracellular matrix organization, inflammatory response, and cellular aging. These results suggest that DPP4 plays a significant role in the modulation of chondrocyte senescence and may provide new insights into the mechanisms of cellular aging. Taken together, our data provide a molecular framework for understanding how DPP4 overexpression impacts chondrocyte physiology and offers potential targets for therapeutic intervention in age-related cartilage diseases.
Project description:Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4. RAW264.7 macrophages were treated with and without 200 nM recombinant FABP4 in the absence and presence of 0.2 mM palmitic acid.
Project description:Fatty acid-binding protein 4 (FABP4), a key lipid protein in metabolism and inflammation, has been suggested to be linked to osteoporosis (OP), though direct evidence is scarce. Here, we present the first clear evidence of FABP4's significant role in OP, supported by clinical data and comprehensive in vivo and in vitro experiments. Elevated serum FABP4 in OP patients inversely correlates with bone mineral density (BMD), with similar trends observed in OVX mice. While FABP4 does not influence osteoblast differentiation, it promotes osteoclast formation and bone resorption. The FABP4 inhibitor BMS309403, with an IC50 of 0.89 μM, inhibits osteoclast differentiation by modulating calcium ions and suppressing the Ca2+-Calcineurin-NFATc pathway. Oral BMS309403 increased BMD in OVX mice, albeit less effectively than alendronate, whereas bone-targeted PLGA nanoparticles showed comparable efficacy to alendronate. This research identifies FABP4 as a promising therapeutic target for OP, with significant clinical implications.
