GPR32 Membrane Protein Introduction

Introduction of GPR32

GPR32, also known as probable G-protein coupled receptor 32 or resolvin D1 receptor, is a protein which is encoded by the human GPR32 gene and belongs to the rhodopsin-like subfamily of G-protein coupled receptors. It was initially identified and defined as coding for an Orphan receptor, namely a protein with an amino acid sequence similar to known receptors but having no known ligand(s) to which it responds and no known function. During the past years, the role of GPR32 has been widely studied.

Function of GPR32 Membrane Protein

As a member of the rhodopsin-like subfamily of G-protein coupled receptors, GPR32 is produced physiologically from the sequential oxygenation of docosahexaenoic acid (DHA) by 15- and 5-lipoxygenase and function to dampen excessive neutrophil trafficking to the site of inflammation. Studies have suggested that GPR32 can be expressed in various human cells, which including but not limited to neutrophils, lymphocytes, macrophages, and small airway epithelial cells. It has also been reported that GPR32 has the ability to inhibit the Cyclic adenosine monophosphate signaling pathway under both baseline and forskolin-stimulated conditions. Recently, a report described that RvD1 has the ability to suppress the EMT of A549 cells via ALX/FPR2 and GPR32 receptors, all of which lead to suppression of ZEB1 expression. Furthermore, research has found that triggering GPR32 could induce a pro-resolution macrophage phenotype with reduced secretion of proinflammatory cytokines, low chemotaxis, and increased phagocytosis of microbial particles.

Fig.1 Schematic view of the overall structure of a G protein-coupled receptor (GPCR). (Fossépré, 2014)

Application of GPR32 Membrane Protein in Literature

1. Taylan A., et.al. S1000A12, chitotriosidase, and resolvin D1 as potential biomarkers of familial Mediterranean fever. Journal of Korean medical science. 2015, 30(9):1241-5. PubMed ID: 26339162
   
   

   This article finds that serum level of resolvin D1 is elevated in both the attack and silent periods of familial Mediterranean fever (FMF) patients compared to controls. It indicates that resolvin D1 may be helpful to restrict inflammation.

2. Hsiao H.M., et.al. Resolvin D1 Attenuates Polyinosinic-Polycytidylic Acid-Induced Inflammatory Signaling in Human Airway Epithelial Cells via TAK1. The Journal of Immunology. 2014, 193(10):4980-7. PubMed ID: 25320283
   
   

   This article suggests that RvD1 could inhibit the phosphorylation of TAK1 (TGF-β-activated kinase 1) by inhibiting the formation of a poly (I:C)-induced signaling complex composed of TAK1, TAB1 (TAK1 binding protein), and TRAF6 (TNF receptor-associated factor 6). It indicates that RvD1 has the potential to be used as an anti-inflammatory and pro-resolving agent, possibly in the context of exuberant host responses to damaging respirable agents such as viruses.

3. Zhao X.W., et.al. Effect of diclofenac on the levels of lipoxin A4 and Resolvin D1 and E1 in post-ERCP pancreatitis. Digestive diseases and sciences. 2014, 59(12):2992-6. PubMed ID: 25030943
   
   

   This article reveals that intramuscular diclofenac after endoscopic retrograde cholangiopancreatography can reduce the incidence of preventing pancreatitis, which may be related to the fact that diclofenac can increase the levels of LxA4, RvD1, and RvE1.

4. Lee H.J., et.al. Resolvin D1 inhibits TGF-β1-induced epithelial mesenchymal transition of A549 lung cancer cells via lipoxin A4 receptor/formyl peptide receptor 2 and GPR32. The international journal of biochemistry & cell biology. 2013, 45(12):2801-7. PubMed ID: 24120851
   
   

   This article suggests that resolvin D1 has the ability to inhibit TGF-β1-induced EMT via ALX/FPR2 and GPR32 by reducing the expression of ZEB1.

5. Krishnamoorthy S., et.al. Resolvin D1 binds human phagocytes with evidence for proresolving receptors. Proceedings of the National Academy of Sciences. 2010,107(4):1660-5. PubMed ID: 20080636
   
   

   This article indicates that RvD1 could specifically interact with both ALX and GPR32 on phagocytes and suggest that each plays a role in resolving acute inflammation.

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Reference

1. Fossépré, et.al. (2014). On the modularity of the intrinsic flexibility of the µ opioid receptor: a computational study. PloS one, 9(12), e115856.

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