mProX™ Human GPBAR1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Silencing of TGR5 abolishes the inhibitory effects of INT-777 on IL-1β- induced chondrocytes senescence signaling.
The suppressive impact of INT-777 on SA-β-Gal activity was nullified upon TGR5 silence. Following a 24-hour transfection with siTGR5, cells were exposed to IL-1β (10 ng/ml) with or without INT-777 (10 μM) for another 24 hours (*, #, $, p < 0.01 vs. prior group, n = 4-6).
Ref: Huang, He, et al. "Activation of the bile acid receptor GPBAR1 (TGR5) ameliorates interleukin-1β (IL-1β)-induced chondrocytes senescence." Biomedicine & Pharmacotherapy 106 (2018): 1713-1719.
Pubmed: 30119246
DOI: 10.1016/j.biopha.2018.06.154
Research Highlights
Leonhardt J, et al. "Immunosuppressive effects of circulating bile acids in human endotoxemia and ." Critical care (London, England), 2023.
In critically ill patients, sepsis-induced immunosuppression can lead to opportunistic infections and death. To develop effective treatments, there is a need for a deeper understanding of the underlying mechanisms. Recently, it was discovered that certain bile acids, known for their immunosuppressive effects, are present in the bloodstream of critically ill patients. The aim of this study was to investigate whether these immunosuppressive bile acids are present in patients with endotoxemia and septic shock, and if they pose a higher risk to certain individuals. Results showed that patients with severe liver failure had significantly higher levels of circulating bile acids capable of inducing immunosuppression compared to healthy controls. It is suggested that future research should explore the potential benefits of regulating bile acid metabolism in septic shock patients with severe liver failure for better clinical outcomes.
Pubmed:
37759239
DOI:
10.1186/s13054-023-04620-5
Xiong H, et al. "Exosomal EIF5A derived from Lewis lung carcinoma induced adipocyte wasting in ." Cellular signalling, 2023.
In this study, the role of tumor-derived extracellular vesicles (EVs) in cancer cachexia was investigated. The researchers extracted and characterized EVs from Lewis lung carcinoma (LLC) cells. They then used these EVs to stimulate 3T3-L1 and HIB1B adipocytes and establish a cancer cachexia mouse model. Results showed that the EVs were taken up by the adipocytes and contained high levels of hypusinated eukaryotic initiation factor 5A (EIF5A). This protein was found to induce lipolysis in adipocytes by directly binding to the mRNA of G protein-coupled bile acid receptor 1 (GPBAR1) and activating the cAMP response element binding protein (CREB) signaling pathway. The researchers demonstrated that the reduction of lipolysis in adipocytes could be achieved through silencing EIF5A or treating with a pharmacological inhibitor. In addition, suppressing the expression of EIF5A in LLC cells by infected with shRNA or pharmacologic inhibitor treatment partly alleviated lipolysis in white and brown adipose tissue in vivo. These findings suggest that exosomal EIF5A is a potential target for treating cancer cachexia.
Pubmed:
37743008
DOI:
10.1016/j.cellsig.2023.110901
