Ask about this productRelated genes to: PDGFRB antibody
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PDGFRB antibody
Related articles to: PDGFRB antibody
- Storiform collagenoma is a rare benign dermal neoplasm recently shown to harbor concurrent PTEN and PDGFRB mutations. While most are sporadic, a subset occurs in the context of Cowden syndrome. We describe two storiform collagenomas with unusual morphology including infiltrative growth pattern and perivascular myoid differentiation. Confirmation of concurrent PTEN and PDGFRB mutations in both cases allowed for a more confident diagnosis of storiform collagenoma in these cases and their distinction from dermatofibrosarcoma protuberans. - Source: PubMed
Publication date: 2026/09/20
Scopelliti AmandaDorwal PranavCheah Alison - 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 - Metabolic dysfunction-associated steatohepatitis (MASH) progresses through macrophage activation and hepatic stellate cell (HSC)-driven fibrogenesis. As cell-level single-cell discoveries often suffer from pseudoreplication and fail to replicate across cohorts, in this study we critically re-evaluated human liver single-nucleus RNA-sequencing data using a rigorous per-donor statistical framework to dissociate invariant biological signals from technical artifacts. Macrophage and HSC compartments from dataset GSE202379 were profiled across clinical stages (healthy, metabolic dysfunction-associated steatotic liver disease, MASH). Cell-level statistics were aggregated into per-donor metrics, and continuous phenotypic shifts evaluated via the Jonckheere-Terpstra (JT) trend test. Key findings were tested for cross-cohort reproducibility in two independent cohorts (GSE136103 and GSE244832). A 249-gene scar-associated macrophage (SAMac) program showed reproducible, stage-dependent expansion in the discovery cohort (per-donor Jonckheere-Terpstra trend across the disease-only spectrum, MASLD to advanced MASH, z = 2.23, = 0.026 [primary]; z = 2.74, = 0.006 across all four stages including the healthy baseline) and directional replication in external data. Cell-cell communication analysis replicated the receptor-side topology of a conserved macrophage-to-HSC PDGF axis in both external cohorts and the ligand-driven PDGFC→PDGFRB edge in the external snRNA-seq cohort (GSE244832), with PDGFRB being a high-degree hub within the HSC fibrogenic interaction network. Importantly, a previously published global HSC activation module failed to validate (JT = 0.77); however, its core extracellular matrix and /2 sub-axis remained robust, whereas the widely claimed AP-1/ regulatory driver was not supported at the transcript level in the single-nucleus RNA-seq cohort data. These findings are consistent with an isolation-associated immediate-early gene response in enzymatically dissociated scRNA-seq data, given the flat-to-downward transcript-level trend in cryopreserved-tissue cohorts; transcript-level data cannot, however, exclude protein- or phosphorylation-level AP-1 activity. Targetable downstream components within the validated core architecture were annotated. By implementing per-donor verification, we successfully separated robust pathological features of MASH from platform-dependent artifacts. The validated SAMac program and the macrophage-HSC PDGF axis, together with an associated RUNX subprogram, represent high-confidence, reproducibility-filtered candidate therapeutic nodes that require functional validation. These findings establish a reproducibility-first standard for single-cell translational research, and the validated programs are consistent with emerging models of inter-organ inflammatory circuitry in MASH. - Source: PubMed
Publication date: 2026/09/05
Ling HaoQiu PeiyuHu Yanzhu - Progressive pulmonary fibrosis (PPF) comprises interstitial lung diseases characterized by progressive fibrosis and lung function decline. Nintedanib slows disease progression by inhibiting FGFR, VEGFR, and PDGFR signaling, but treatment response varies among patients. We investigated whether , , and gene variants are associated with nintedanib treatment outcomes, including changes in pulmonary function, diffusing capacity and adverse effects. This prospective study included 75 patients with PPF diagnosed according to ATS/ERS/JRS/ALAT criteria and treated with nintedanib at the Clinic of Pulmonology, University Clinical Center of Serbia. Spirometry and diffusing capacity were assessed at baseline and after 6 and 12 months. Genotyping of rs2071559 and rs1870377; rs2302273, rs2229562, and rs246395; and rs1800470 was performed using TaqMan assays. Carriers of the rs2302273 A allele more frequently experienced gastrointestinal adverse events (45.2% vs. 20.5%; = 0.022; OR 3.2, 95% CI 1.156-8.866) and diarrhea (38.7% vs. 15.9%; = 0.026; OR 3.3, 95% CI 1.129-9.869). Patients with the rs246395 TT genotype more frequently had a ≥15% decline in DLCO after one year (46% vs. 22%; = 0.038; OR 3.0, 95% CI 1.045-8.394). No significant associations were observed for the analyzed or variants. These findings suggest that variants may be associated with nintedanib treatment outcomes, although confirmation in larger cohorts is needed. - Source: PubMed
Publication date: 2026/08/23
Djurdjevic NatasaPjevic Marija DusanovićStjepanovic MihailoColic NikolaDimic-Janjic SanjaJankovic JelenaMaric NikolaZecevic AndrejTerzic MilicaGolubovic AleksaMilivojevic IvanOmcikus MajaIlic BranislavLukic KatarinaMijatovic SnjezanaGrk Milka - Gastric cancer (GC) remains a major cause of cancer-related mortality worldwide. Epigallocatechin gallate (EGCG), a natural polyphenol derived from green tea, exhibits anticancer properties; however, its molecular targets and regulatory mechanisms in GC are not fully elucidated. This study aimed to identify candidate EGCG-associated genes in GC and generate a hypothesis for future mechanistic investigation. - Source: PubMed
Publication date: 2026/07/21
Zhao YuboLi YuhangZheng Hongqun