Ask about this productRelated genes to: NT5E antibody
- Gene:
- NT5E NIH gene
- Name:
- 5'-nucleotidase ecto
- Previous symbol:
- NT5
- Synonyms:
- CD73, eN, eNT, CALJA
- Chromosome:
- 6q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-23
- Date modifiied:
- 2016-10-05
Related products to: NT5E antibody
Related articles to: NT5E antibody
- Extracellular purinergic signaling, mediated by nucleotides such as adenosine triphosphate (ATP) and adenosine, is a critical regulator of retinal homeostasis. Within the retina, this signaling pathway is indispensable for maintaining physiological functions. Dysregulation of extracellular purine balance is a key driver of retinal pathophysiology, contributing to inflammation, pathological angiogenesis, and neurodegeneration in diseases like diabetic retinopathy (DR), age-related macular degeneration (AMD), glaucoma, and retinopathy of prematurity (ROP). The hydrolysis of extracellular ATP to adenosine, primarily orchestrated by the sequential actions of NTPDase1/ENTPD1 (CD39) and ecto-5'-nucleotidase/NT5E (CD73), represents a fundamental mechanism for calibrating purinergic signals and shifting the microenvironment from pro-inflammatory to anti-inflammatory and protective. CD39 and CD73 are pivotal enzymes in regulating retinal purinergic equilibrium. Despite their well-characterized roles in tumor biology and cerebral pathophysiology, the expression, physiological functions, and pathological implications of CD39/CD73 in the retina remain understudied and lack systematic synthesis. This review synthesizes current understanding of the roles of CD39 and CD73 in retinal physiology and pathology, with a focus on their implications in DR, AMD, glaucoma, and ROP. Critically, this review provides the first systematic integration of their layer-specific spatial compartmentalization, context-dependent functional duality, and emerging metabolic roles in photoreceptor homeostasis. We also discuss emerging therapeutic strategies that target this pathway, addressing the growing need for translational research to preserve vision. - Source: PubMed
Publication date: 2026/09/08
Chen XinyiJi JingYao JiaxinChen PengfanZhang JialiLiu LongqianWen Xiangyi - Diabetic kidney disease (DKD) is commonly staged using albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR), yet complementary molecular markers are needed. We profiled urine and serum metabolites from 92 Korean participants (72 with type 2 diabetes and 20 healthy controls) using gas chromatography-tandem mass spectrometry (GC-MS/MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). An exploratory restricted Boltzmann machine framework compared five DKD staging criteria and prioritized candidate metabolites; robustness was assessed against LASSO, linear support vector machine (SVM), and random forest using nested cross-validation. ACR-based staging showed the highest metabolomic discrimination. Urinary adenosine and 5'-methylthioadenosine decreased, whereas serum N2,N2-dimethylguanosine and -aconitic acid increased across ACR stages. Integration with a public renal tubular microarray dataset suggested as a cross-study network hub. These cross-sectional findings define candidate metabolite signatures associated with DKD severity and require external longitudinal validation before clinical translation. - Source: PubMed
Publication date: 2026/09/12
Jung InhaPark SungjinJi MoongiPark So YoungLee Da YoungYu Ji HeeSeo Ji APaik Man-JeongPark Hyeong KyuKwon Soon HyoLee Dae HoKim Nan Hee - The underlying mechanisms of exosomes in chronic lung allograft dysfunction (CLAD) remain poorly understood. The primary challenge lies in the substantial functional heterogeneity of exosomes in CLAD. In this study, lung transplantation was initially performed, followed by the generation of a chronic rejection (CR) model in rats to simulate CLAD in humans. Exosomes from lung graft tissues were extracted, purified, and subjected to proximity barcoding assay-based single-vesicle membrane proteomic profiling. Additionally, bulk proteomic and metabolomic profiling of the graft tissues was conducted. Exosomes were categorized into 14 clusters. Compared with the syngeneic group, the CR group had significantly lower levels of clusters 7 (Nphs1), 13 (Aqp1), and 14 (Csf3r), and higher levels of clusters 2 (Lrp2 Mrc1) and 4 (Nt5e). The abundance of cluster 12 (Ilk) exosomes was strongly correlated with pleural thickness (r = -0.90, P < 0.001). Cluster 12 exosomes exhibited the greatest number of related differentially expressed proteins and metabolites. The proteins correlated with cluster 12 were enriched in the "complement and coagulation cascades", whereas the metabolites were enriched in the "glycerophospholipid metabolism". Further verification in patients with restrictive allograft syndrome revealed the same decrease in abundance of cluster 12 exosomes as that observed in the rat model. Finally, the core molecular network of cluster 12 that contributes to pleural thickening in CLAD was constructed. In this study, the heterogeneous composition of exosomes in lung grafts was mapped to expand the understanding of their effects and to drive their application in CLAD. - Source: PubMed
Publication date: 2026/09/17
Tian DongZheng XiangyunYu ZengweiWang DapengChen WeiyangLiu YalingLiu ZehuiXia BoyangJin XiaohanYan HaojiWu YeZhao YongshengZhang ChuanfenPu QiangChen JingyuSato MasaakiLiu Lunxu - Objective To investigate changes in the immune microenvironment of placental villous tissue in recurrent spontaneous abortion (RSA) based on transcriptomic analysis, and to preliminarily explore the potential relationship between the adenosine-NT5E/CD73 axis and macrophage state remodeling. Methods The placental villous tissue transcriptome dataset GSE237732, including RSA and normal pregnancy samples, was obtained from the gene expression omnibus (GEO) database. Candidate key genes were screened by differential expression analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) network analysis. Immune infiltration analysis was performed to assess the association between key genes and relative immune cell abundance, and gene set enrichment analysis (GSEA) was used to explore related signaling pathways. The placental microarray dataset GSE22490 was used for independent validation of NT5E expression and macrophage/inflammation-related signatures. The decidual CD45 immune cell single-cell dataset GSE164449 was also analyzed as an exploratory bypass dataset. Finally, a THP-1-derived macrophage model was used to evaluate the effects of CD73 inhibition and adenosine supplementation on inflammatory markers of M1 macrophages. Results Nine key genes were identified from GSE237732, including PDGFRB, DCN, COL6A1, COL5A2, PDGFRA, LTBP2, TIMP1, ENG, and NT5E. Immune infiltration analysis showed that all nine key genes were significantly correlated with M1 macrophages; ENG and NT5E were negatively correlated, whereas the other genes were positively correlated. GSEA indicated that NT5E was involved in multiple pathways related to immune dysregulation and inflammatory responses. In GSE22490, NT5E expression showed a decreasing trend in the recurrent miscarriage group, whereas CD86 and M1/inflammatory signatures showed increasing trends, although these changes were not statistically significant. The M2 macrophage signature was significantly increased, suggesting overall macrophage state remodeling rather than isolated M1 elevation. Exploratory single-cell analysis of GSE164449 showed increased macrophage-like cell proportions and increased M1- and M2-related scores in RPL-associated decidual CD45 immune cells. Quantitative real-time PCR and flow cytometry showed that APCP-mediated inhibition of NT5E/CD73 activity increased inflammatory factor expression and the CD86positive rate in M1 macrophages, whereas adenosine supplementation partially reversed these effects. Conclusion NT5E-encoded CD73 may participate in the regulation of macrophage inflammatory phenotypes through adenosine signaling and may be associated with immune microenvironment remodeling at the maternal-fetal interface in RSA. Together with independent dataset validation, public single-cell exploratory analysis, and cellular experiments, these findings suggest that the adenosine-NT5E/CD73 axis may be a candidate pathway related to immune imbalance in RSA. However, the current evidence cannot replace validation of NT5E/CD73 protein expression and spatial colocalization of CD68/CD86/CD206 in patient villous tissues. Further studies using larger clinical cohorts, tissue localization, and maternal-fetal interface-related experimental models are required. - Source: PubMed
Huang HeyingLiu Bing - Immune dysregulation characterized by persistent myeloid activation and associated impairment of regulatory T cell (Treg) function contributes to inflammatory signaling across peripheral and central compartments in neurodegenerative diseases. We evaluated whether combining a glucagon-like peptide-1 receptor agonist (GLP-1RA; semaglutide) with low-dose interleukin-2 (LD-IL2) could modulate myeloid-associated transcript expression and enhance Treg-associated regulatory transcripts in a subacute lipopolysaccharide (LPS)-induced model of systemic and CNS inflammation. Mice received LPS once daily for 5 days, while GLP-1RA, LD-IL2, or combination treatment was initiated 24 h after LPS onset and continued daily. Splenic immune populations were quantified, and transcript expressions were assessed in magnetically enriched CD11b myeloid cells and CD4CD25 Tregs, as well as in cortex and hippocampus. As monotherapies, GLP-1RA reduced myeloid expansion with modest modulation of pro-inflammatory and anti-inflammatory myeloid transcripts, whereas LD-IL2 selectively enhanced Treg numbers and increased transcripts associated with Treg stability and suppressive regulation, including (CD25), , , (HELIOS), (CD39), and (CD73). Combination treatment significantly reduced LPS-induced myeloid , , and expression and increased expression. Combination treatment further enhanced Treg-associated (CD25), , and expression relative to monotherapies. In cortical and hippocampal tissues, combination treatment produced more robust modulation of inflammatory transcripts compared with effects observed with monotherapies, including reductions in and and increases in and (CD206) expression. Together, these findings demonstrate coordinated and complementary changes in peripheral immune-cell populations and myeloid inflammatory and Treg-associated regulatory transcripts and warrant further evaluation of this combination in inflammation-driven neurodegenerative disease. - Source: PubMed
Publication date: 2026/09/02
Thome Aaron DWang JinghongFaridar AlirezaZhao WeihuaSaetzler ValerieBeers David RAppel Stanley H