Recombinant Mouse PDGF-AA Protein
- Known as:
- Recombinant Mouse PDGF-AA Protein
- Catalog number:
- pdgfa-019
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Mouse PDGF- Protein
Related genes to: Recombinant Mouse PDGF-AA Protein
- Gene:
- PDGFA NIH gene
- Name:
- platelet derived growth factor subunit A
- Previous symbol:
- -
- Synonyms:
- PDGF1, PDGF-A
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- PDGFRA NIH gene
- Name:
- platelet derived growth factor receptor alpha
- Previous symbol:
- -
- Synonyms:
- CD140a, PDGFR2, GAS9
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2019-04-23
- 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: Recombinant Mouse PDGF-AA Protein
Related articles to: Recombinant Mouse PDGF-AA Protein
- Angiogenesis is a pivotal process for tumor progression and metastasis in non-small cell lung cancer (NSCLC). However, the molecular mechanisms by which WNT1-inducible signaling pathway protein 3 (WISP-3) contributes to NSCLC angiogenesis remain poorly defined. This study investigated the role of WISP-3 in regulating pro-angiogenic signaling in lung adenocarcinoma (LUAD) cells. Conditioned medium from H1299 and A549 cells treated with recombinant WISP-3 (0-100 ng/mL) significantly and dose-dependently enhanced the tube formation of human umbilical vein endothelial cells (HUVECs). WISP-3 selectively upregulated platelet-derived growth factor A (PDGF-A) expression at both mRNA and protein levels in NSCLC cell lines, while other angiogenic factors remained unaffected. Notably, knockdown of PDGF-A using siRNA markedly abolished WISP-3-induced HUVEC tube formation, confirming PDGF-A as a critical mediator in this process. Mechanistically, WISP-3 rapidly triggered the phosphorylation of p38 and JNK signaling pathways. These activations led to the phosphorylation of the transcription factor c-Jun, which in turn promoted PDGF-A gene expression. Pharmacological inhibition of p38 (Adezmapimod), JNK (SP600125), or c-Jun (T-5224) effectively suppressed WISP-3-induced c-Jun activation, PDGF-A expression, and subsequent angiogenesis. Collectively, our findings identify a novel WISP-3/p38-JNK/c-Jun/PDGF-A signaling axis that drives vascular remodeling in NSCLC. Targeting WISP-3 or its downstream effectors may represent a promising therapeutic strategy for anti-angiogenic treatment in lung cancer. - Source: PubMed
Publication date: 2026/03/25
Chang En-MingLin Syuan-LingCheng Ching-YuanTang Chih-HsinChen Yu-ChenLee Chiang-WenLin Chih-Yang - Differentiating between malignant and benign biliary strictures remains a clinical challenge because current diagnostic tools have limited sensitivity. The detection of tumour-related biomarkers directly in bile, which is in close contact with the lesion, may enhance diagnostic accuracy. This study aimed at evaluating the diagnostic and prognostic values of biliary concentrations of VEGF, PDGF-AA, IGF and MMPs in patients with extrahepatic cholangiocarcinoma (CCA), pancreatic ductal adenocarcinoma (PDAC), or benign obstruction. - Source: PubMed
Gigante EUntereiner VCaruso SRhaiem RGrados LBoulagnon-Rombi CAdam SSockalingum G DGarnotel RThiefin G - The clinical treatment of castration-resistant prostate cancer (CRPC) is currently a major challenge. This study explored a new combination strategy for CRPC that targeted androgen receptor (AR)-dependent and AR-independent mechanisms. First, the degradation efficiency of AR by ARV-110 was verified. CCK-8 and CellTiter-Glo assays were used to evaluate the viability of CRPC cells after treatment. The combination index of platelet-derived growth factor receptor (PDGFR) inhibitors combined with ARV-110 was calculated using CompuSyn software. Transcriptome sequencing was used to explore the in-depth mechanisms of the combination strategy. Chromatin immunoprecipitation and dual-luciferase reporter assays were used to clarify the transcriptional regulatory relationships. Coimmunoprecipitation was used to evaluate protein interactions. The results showed that ARV-110 significantly promoted AR degradation. The combination of ARV-110 and ponatinib exerted a significant inhibitory and synergistic effect on CRPC cells. The effective targets were AR and PDGFR. The combination of ARV-110 and the PDGFR-selective inhibitor JNJ10198409 effectively induced the apoptosis of CRPC cells. ARV-110 alone promoted the transcription of PDGFA. And the combination strategy further induced JNK signaling pathway activation and promoted cell apoptosis by inhibiting PDGFR activity. Additionally, the substantial accumulation of reactive oxygen species induced by the combination strategy was related to the joint downregulation of catalase by the two drugs through different mechanisms. In conclusion, this study described a new strategy for the treatment of CRPC and clarified the molecular mechanisms of the combination strategy, providing a new theoretical basis for the precision treatment of CRPC. - Source: PubMed
Publication date: 2026/04/10
Fu YangSun ShanshanLiu GuangxuDong QingzhuoWang YutaoZheng HaoyuanPiao ChiyuanBi Jianbin - Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects. - Source: PubMed
Yasavoli-Sharahi HamedShahbazi RoghayehAlsadi NawalSahebi Nasim BondarCuenin CyrilleCahais VincentChung Felicia Fei-LeiHerceg ZdenkoMatar Chantal - Colorectal cancer (CRC) remains one of the most important causes of cancer-related mortality worldwide, underscoring the need to better understand systemic inflammatory pathways across the colorectal neoplasia spectrum. In this exploratory case-control study, we characterized plasma levels of key inflammatory mediators in healthy individuals and patients with colorectal polyps or CRC. Healthy controls ( = 10), patients with colorectal polyps (CP, n = 16), early-onset CRC (EO-CRC, n = 11), and late-onset CRC (LO-CRC, n = 51) were prospectively enrolled. Plasma levels of sTNF-R, total TNF-α, PDGF-AA, IL-17A, and IL-1β were measured by ELISA. Group comparisons used Kruskal-Wallis tests with epsilon-squared effect sizes. PDGF-AA showed the strongest differences between controls and all neoplastic groups (ε ≥ 0.15), and these comparisons remained significant after Benjamini-Hochberg false discovery rate correction. IL-17A levels were slightly higher in EO-CRC than in LO-CRC; however, this difference did not remain significant after adjustment for multiple testing. TNF-α and IL-1β showed no significant differences across groups. Overall, this study primarily provides descriptive and hypothesis-generating evidence of differential inflammatory patterns across colorectal neoplasia, with PDGF-AA emerging as the most robust signal in this exploratory dataset. These findings do not support immediate diagnostic application and require validation in larger, prospectively recruited cohorts. - Source: PubMed
Publication date: 2026/03/13
Ionescu Vlad-AlexandruGheorghe GinaTurculet Claudiu StefanGeorgescu Teodor FlorinBratu Razvan MateiMambet CristinaEnache ValentinGheorghiu MihaelaPasarica DanielaDiaconu Camelia CristinaDiaconu Carmen CristinaBleotu Coralia