Ask about this productRelated genes to: EMR1 antibody
- Gene:
- ADGRE1 NIH gene
- Name:
- adhesion G protein-coupled receptor E1
- Previous symbol:
- TM7LN3, EMR1
- Synonyms:
- -
- Chromosome:
- 19p13.3-p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-31
- Date modifiied:
- 2018-02-13
Related products to: EMR1 antibody
Related articles to: EMR1 antibody
- Macrophages play a key role in kidney inflammation and fibrosis. The oxysterol receptor G protein-coupled receptor 183 (GPR183) is an important immunomodulatory receptor, but its role in kidney disease is undefined. In this study, we investigated the contribution of GPR183 to renal injury using adenine diet-induced chronic kidney disease and folic acid-induced nephropathy models. Both models exhibited marked upregulation of the cholesterol hydroxylases CH25H and CYP7B1, along with increased GPR183 expression in the kidney. Immunofluorescence analysis demonstrated that GPR183 colocalized with M1 macrophage markers within injured kidneys. Genetic deletion of GPR183 selectively reduced renal M1 macrophage accumulation and proinflammatory cytokine expression without affecting M2 macrophage infiltration, leading to improved renal function. GPR183 deficiency also significantly attenuated renal fibrosis, as evidenced by decreased collagen deposition and reduced expression of fibronectin and α-smooth muscle actin. In primary bone marrow-derived macrophages, GPR183 deletion suppressed lipopolysaccharide (LPS) and interferon γ (IFN-γ)-induced M1 polarization through inhibition of NF-κB signaling. Finally, analysis of publicly available human single-cell RNA sequencing data demonstrated substantial GPR183 expression in immune cells, including macrophages, in patients with chronic kidney disease. These findings identify GPR183 as a key regulator of macrophage phenotype in kidney injury and demonstrate that activation of the oxysterol-GPR183 axis promotes inflammatory and fibrotic renal remodeling. Targeting GPR183 may therefore represent a novel therapeutic strategy for the treatment of progressive kidney disease. This study identifies GPR183 as a previously unrecognized regulator of macrophage polarization and renal fibrogenesis. We demonstrate that kidney injury activates an oxysterol-GPR183 signaling axis that promotes NF-κB-dependent M1 macrophage polarization. Genetic deletion of GPR183 selectively limits inflammatory macrophage accumulation, attenuates fibrosis, and preserves renal function, establishing GPR183 as a novel therapeutic target in progressive kidney disease. - Source: PubMed
Publication date: 2026/04/09
Zhang QianWang YanFan YuHan Seung SeokXie HanRhee Eugene PWen Donghai - Chronic kidney disease is closely associated with kidney inflammation and fibrosis. Macrophage plays a critical role in the pathogenesis of kidney inflammation and fibrosis. However, the molecular mechanisms underlying macrophage activation remain poorly elucidated. In this work, we examined the role of macrophage RNA polymerase II subunit 5 -mediating protein (RMP) in kidney inflammation and fibrosis. - Source: PubMed
Publication date: 2026/03/17
Nie JiayiLiu BenquanXiong HengGao YingLi ShuiyingChen ShuangquanYu WenqiangLiang Hua - The adhesion G-protein coupled receptors (aGPCRs) are a family of 33 G-protein receptors consisting of ADGRA1-3, ADGRB1-3, ADGRC1-3, ADGRD1-2, ADGRE1-5, ADGRF1-5, ADGRG1-7, ADGRL1-4, and ADGRV1. Recent studies have unveiled the role of aGPCRs in numerous brain functions, including in neurodevelopment, synapse formation and maintenance, establishment of the blood-brain barrier, and myelination. Further, dysfunction of aGPCRs have been associated with disorders such as gliomas, depression, and epilepsy, among many others. Herein, we review generalized properties of aGPCRs, their brain-specific expression, associations with neurological and psychiatric diseases, and potential as future pharmacological targets. - Source: PubMed
Publication date: 2025/11/24
Lee Brandon HMeyer Christina MSpeca David JDíaz Elva - Muscle hematomas can exacerbate inflammation, delay healing, and reduce function after muscle injury. This study examined whether early hematoma removal promoted recovery in a rat model of tibialis anterior muscle laceration. Hematomas were surgically removed 6 h after injury and compared with untreated animals. Histological analysis revealed that the hematoma removal group had a significantly reduced hematoma size 24 h after injury and a significantly reduced abnormal tissue area on days 3 and 14. Furthermore, the hematoma removal group demonstrated better muscle strength recovery at 3, 14, and 28 days post-injury. Gene expression analysis of the injured muscle tissue revealed that the expression levels of several genes related to inflammation and inflammatory pain (IL-6, IL-10, IL-1β, TNF-α, IL-1Ra, COX-1, COX-2, NGF) and macrophage marker molecules (CD68, ADGRE1, CD206, Arg1) during the acute phase were significantly lower in the hematoma removal group compared to the control group. No significant differences were observed in the transcription levels of the genes related to myogenic differentiation. In summary, early surgical hematoma removal in a rat laceration model reduced inflammation and abnormal tissue volume and promoted muscle strength recovery. This study provides new evidence suggesting that early hematoma removal after skeletal muscle injury is beneficial. - Source: PubMed
Publication date: 2026/01/25
Ren YujieKanamoto TakashiMiyazaki RyoZhang ZiyangHuang RenyanEbina KosukeTanaka HiroyukiNakata Ken - Atherosclerosis is a chronic inflammatory disease driven by dysregulated lipid metabolism and macrophage dysfunction. However, the role of and activin membrane-binding inhibitor (), a pseudoreceptor that antagonizes superfamily signaling, in modulating these processes remains incompletely characterized. - Source: PubMed
Publication date: 2025/12/24
Chen XiaochangTan SiyuLi SitingSu PeihongGuan HuaXiang AoqiZhang LushaWang HaopingYu Qi