mProX™ Human GPR83 Stable Cell Line

Zeng H, et al. "Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine ." Journal of neuroinflammation, 2023.
Spinal cord injury (SCI) is a detrimental disease of the central nervous system that results in loss of sensory and motor function below the level of injury. SCI-induced immunodeficiency syndrome (SCI-IDS) is a secondary immunosuppressive condition that increases vulnerability to infections and exacerbates neurological dysfunction. It is considered an independent risk factor for poor neurological prognosis, predominantly occurring after injury above the T5 levels. Despite studies suggesting the role of the sympathetic-adrenal medullary axis and the hypothalamus,Äípituitary,Äíadrenal (HPA) axis in SCI-IDS, the exact mechanism remains unclear. This study aimed to assess the concentrations of adrenocorticotropic hormone and cortisol, as well as changes in sympathetic activity in rats with high-level (T3) and low-level (T10) SCI. Through histology and multitissue transcriptomics, the researchers also explored the differential regulation of the gene network between the sympathetic-adrenal medullary axis and the HPA axis, revealing a disrupted neuroendocrine-immune network associated with SCI-IDS. Results showed marked atrophy of secondary immune organs in the high-level SCI group and elevated cortisol levels mediated by the adrenal glands. Downregulated differentially expressed genes (DEGs) in the high-level SCI group were significantly enriched in immunoregulation, while upregulated DEGs in the hypothalamus were enriched in inflammatory pathways and downregulated in pathways related to inhibitory Gi-mediated G protein-coupled receptors (Gi-GPCR) neurons and neuropeptide changes. Upregulated genes in the adrenal glands were enriched in cortisol secretion and circadian rhythm changes, while downregulated genes were significantly enriched in MHC-mediated immune responses. These findings suggest that SCI-induced neuroinflammation may contribute to immune suppression and disruption of nerve repair, ultimately leading to increased susceptibility to infection and poor neurological prognosis.
Pubmed: 37775760   DOI: 10.1186/s12974-023-02906-7

Li HZ, et al. "Nanomolar range of FAM237B can activate receptor GPR83.." Amino acids, 2023.
The recent study conducted by a group of researchers has confirmed that the mature neuropeptide FAM237A, also known as neurosecretory protein GL (NPGL), acts as a potent agonist for GPR83. This finding was in contrast to previous reports which showed that the paralog FAM237B was a weak agonist for GPR83. Through the use of an intein-fusion approach, the researchers were able to prepare mature human FAM237B and demonstrate its ability to significantly activate GPR83 at nanomolar concentrations (1,Äí10 nM) in a beta-arrestin recruitment assay. This suggests that FAM237B may be an additional endogenous agonist for GPR83, although further in vivo studies will be needed to confirm this.
Pubmed: 37689599   DOI: 10.1007/s00726-023-03328-8