mProX™ Human GPR3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 GPR3 of exogenous origin exerts a moderating effect on the proliferation of cerebellar granule neurons in rodents induced by Shh, demonstrating a partial inhibitory influence on this cellular process.
Rat cerebellum-derived GCPs at postnatal day 7 underwent electroporation with either a GPR3/EGFP vector or a control vector via the AMAXA nucleofector system. Subsequently, Shh (1 µg/ml) was introduced six hours later. Thirty hours into the experiment, BrdU (10 µM final concentration) was administered 12 hours before fixation. Evaluation of cell proliferation was conducted by assessing BrdU incorporation using immunohistochemistry with a specific BrdU monoclonal antibody (displayed in panels a and b). As a positive control, dbcAMP (100 µM) was employed as a chemical cAMP activator. Panel a illustrates representative fields from the Shh and control vector group (top row), Shh and GPR3/EGFP-electroporated group (middle row), and the Shh, control vector group, and dbcAMP (bottom row), visualized through BrdU immunohistochemistry (in red), EGFP fluorescence (in green), and the merged image. Each dish (n = 3) selected five random fields, with at least one hundred GFP-positive neurons counted in each field. Additionally, doubly labeled cells (appearing in yellow) were enumerated per dish. The results were expressed as the percentage of doubly-labeled cells among the total GFP-positive cells in the Shh+GPR3 group or Shh+GPR3+dbcAMP groups, in comparison to the Shh group (as shown in panel b). Simultaneously, cell proliferation was assessed using an ELISA assay based on BrdU incorporation during DNA synthesis (Panel C). Variations between the percentages of cells in panel b and c are likely attributed to differences in the assays employed, involving visual counting versus colorimetry-based counting.
Ref: Tanaka, Shigeru, et al. "The Gs-linked receptor GPR3 inhibits the proliferation of cerebellar granule cells during postnatal development." PloS one 4.6 (2009): e5922.
Pubmed: 19526062
DOI: 10.1371/journal.pone.0005922
Research Highlights
Jiang Y, et al. "Chronic stress induces meiotic arrest failure and ovarian reserve decline via the ." Frontiers in endocrinology, 2023.
The causal role of chronic stress in female subfertility is of interest, though the mechanisms driving this phenomenon remain unclear. In a recent study, researchers examined the impact of chronic stress on the cyclic adenosine 3',5'-monophosphate (cAMP) signaling pathway in mice, resulting in an observed decline in ovarian reserve. Utilizing a restraint stress model over the course of 8 weeks, the stress-exposed group displayed an elongated estrous cycle and a significant increase in the number of atretic follicles. Furthermore, stress-exposed oocytes showed signs of meiotic arrest failure (MAF) with condensed metaphase chromosomes, assembled spindles or polar bodies. Analysis using the CUBIC method confirmed a significant decrease in both quiescent and growing oocytes in the stress group. Subsequent examination of meiotic arrest maintenance pathways via real-time quantitative polymerase chain reaction (RT-qPCR) revealed downregulation of Gpr3, Nppc, and Npr2 in the stress group. Overall, these results suggest that inhibited cAMP production contributes to MAF and a decline in ovarian reserve. This study provides a better understanding of the mechanisms underlying chronic stress-induced oocyte loss and possible targets for preserving ovarian reserve.
Pubmed:
37720535
DOI:
10.3389/fendo.2023.1177061
Lu Y, et al. "Molecular insights into orphan G protein-coupled receptors relevant to ." British journal of pharmacology, 2023.
This article focuses on the relationship between GPR3, GPR6, GPR12, GPR52, GPR85, GPR88, and GPR139 and schizophrenia. The authors review the expression, signalling mechanisms, and cellular function of these receptors, along with the development of small molecule therapeutics and structural insights. Through this review, they aim to present the current evidence and potential for new classes of therapeutics for schizophrenia.
Pubmed:
37605621
DOI:
10.1111/bph.16221
