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
- In Alzheimer's disease (AD), neurovascular unit and blood-brain barrier (BBB) abnormalities are assessed using biologically distinct readouts, often across separate cohorts, complicating interpretation across clinical stages and biomarker domains. - Source: PubMed
Publication date: 2026/07/30
Wang WenchuanXu HanyingWu TongZhang YibinTao MengqiZhao XuanhengLu JingTang XiaoleiZhang ShuoZhang YingNan Hongmei - Decorin, a proteoglycan shown to inhibit transforming growth factor β1 (TGF-β1) signaling, has been increasingly considered as a potential anti-fibrotic agent to aid in therapies addressing corneal scarring and blindness. Decorin is also known to interact with a wide range of other growth factors, such as platelet-derived growth factor (PDGF), which has been shown to stimulate corneal cell migration to repopulate the decellularized region of the wounded cornea. In other tissues, decorin has been shown to inhibit PDGF-mediated migration and prolong wound healing. However, our understanding of the effect of decorin on PDGF signaling in the corneal stroma environment is limited. Specifically, thus far, there have been no studies investigating the interaction between decorin and PDGF in the context of the uniquely organized fibrillar collagen extracellular matrix (ECM), which provides topographic cues that guide cell migration during wound healing. The purpose of this study is to use an in vitro model of decorin-coated aligned collagen fibrils analogous to the corneal stroma ECM to investigate this interaction. With this in vitro model, we demonstrate that decorin inhibits the response of PDGF-BB-stimulated keratocytes to a 2-dimensional (2D) aligned collagen fibril ECM, reducing cell alignment, motility, PDGF receptor β (PDGFRβ) phosphorylation, and wound closure. We observed that when presented with a decellularized wound region, cells on the decorin-coated substrates migrated more randomly and were less aligned with the underlying aligned collagen fibrils than cells on uncoated fibrils, resulting in slower wound closure. Furthermore, PDGF-BB-stimulated cells on the decorin coating had increased branching and reduced solidity, representing a shift from the elongated, bipolar morphology typically resulting from PDGF-BB treatment towards the stellate, branched keratocyte phenotype. While decorin seems to be an effective agent against TGF-β1-mediated fibrosis, its interaction with PDGF-BB appears to present other challenges to wound healing that should be considered in the development of therapies for healthy corneal wound healing. - Source: PubMed
Publication date: 2026/07/30
Tjahjono Nathaniel SSubramanian DivyaShihabeddin Tarik ZTyagi NishthaZlotnikova MaryaMiron-Mendoza MiguelVarner Victor DPetroll W MatthewSchmidtke David W - Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointima formation, is a main cause of in-stent restenosis after coronary stent implantation, resulting in poor patient prognosis. Inhibition of VSMC proliferation, migration, and synthetic phenotype transition holds promise for preventing and treating neointimal hyperplasia and restenosis. GW0742, a peroxisome proliferator-activated receptor (PPAR)-β/δ agonist, has been reported to suppress atherosclerosis and myocardial ischemia-reperfusion injury. However, its role in neointima formation has not been previously studied. In this study, we found that GW0742 significantly inhibited carotid artery injury-induced neointimal hyperplasia in mice. In vitro experiments including cell counting, EdU staining, and proliferation marker detection revealed that GW0742 markedly suppressed Platelet-derived growth factor-BB (PDGF-BB)-induced proliferation of human aortic smooth muscle cells (HASMCs). Flow cytometry analysis showed that GW0742 treatment arrested cells in the G2/M phase. Transwell assays demonstrated that GW0742 inhibited HASMCs migration. Moreover, GW0742 reduced the expression of migration-associated proteins matrix metalloproteinases 2 (MMP2) and matrix metalloproteinases 9 (MMP9), while increasing contractile markers alpha-smooth muscle actin (α-SMA) and calponin 1 (CNN1), suggesting that GW0742 suppresses HASMC proliferation, migration, and phenotypic switching, thereby preserving the contractile phenotype. RNA sequencing revealed that GW0742 regulates fatty acid metabolism by upregulating fatty acid binding protein 3 (FABP3) expression to counteract PDGF-BB-induced VSMC phenotypic switching. Knockdown of FABP3 significantly abrogated the inhibitory effects of GW0742 on VSMC proliferation, migration, and synthetic phenotype transition. Taken together, our findings demonstrate that GW0742 upregulates FABP3 expression, leading to the inhibition of VSMC proliferation, migration, and phenotypic switching, and ultimately suppressing neointima formation. These results underscore the therapeutic potential of GW0742 for the prevention and treatment of vascular restenosis. - Source: PubMed
Publication date: 2026/08/12
Wang XueshengChen JingjieHuo BoWu XingliangLin WenxinJiang Ding-ShengZhang Yu-SongFeng XinGong Fu-Han - [This corrects the article DOI: 10.1016/j.heliyon.2025.e43767.]. - Source: PubMed
Publication date: 2025/12/05
Yi HaoLiu Hao-HanDing Jia-TongZhou Hao-NanHuang Hao-YuLiu JiangHuang Ying-FengZhou Tai-ChengZong Zhen - Platelet-derived growth factors (PDGFs) and their cognate receptors (PDGFRα/β) play critical roles in breast cancer progression and metastasis. This review summarizes current evidence of PDGF ligand and receptor expression patterns, oncogenic functions, prognostic significance and therapeutic targetability, with a specific focus on small molecule inhibition. PDGF-PDGFR signaling is known to contribute to epithelial to mesenchymal transition, cancer stem cell maintenance, desmoplasia, angiogenesis, and immune modulation. Additionally, the four PDGF ligands have distinct oncogenic functions. PDGFA and PDGFB have been implicated in breast cancer associated brain metastasis, while PDGFC has been shown to play a crucial role in fibroblast activation. PDGFD, while less studied, may activate epithelial to mesenchymal transition in breast cancer. High expression of PDGFA, PDGFB, PDGFC, and stromal PDGFRβ correlate with poor patient survival, highlighting their potential as candidate biomarkers. We specifically focus on evaluating current therapeutic strategies which target the PDGF-PDGFR axis, including neutralizing antibodies, aptamers, and small molecule inhibitors, which show preclinical promise but limited clinical success in breast cancer to date. We discuss future research directions with emphasis on identifying selective inhibitors, utilizing PDGF-PDGFR signaling components for patient stratification, and combination with immunotherapies. - Source: PubMed
Publication date: 2026/08/07
Reardon Jesse JMossing Alexis APackard Rebecca LShah SajitaSizemore Gina M