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
- Idiopathic pulmonary fibrosis is a chronic, progressive fibrosing interstitial lung disease with a poor prognosis, carrying a median survival of two to three years without antifibrotic therapy. Nintedanib, an oral intracellular tyrosine kinase inhibitor (TKI) targeting vascular endothelial growth factor receptors (VEGFRs 1-3), platelet-derived growth factor receptor (PDGFR)-α/β, and fibroblast growth factor receptors (FGFRs) 1-3, has emerged as a cornerstone of therapy, reducing the rate of forced vital capacity (FVC) decline by approximately 50% in the INPULSIS trials. While diarrhea is the most common adverse event, generalized body swelling has not been previously described with nintedanib, although it is a well-recognized class effect of several oncologic TKIs, including imatinib and mesenchymal-epithelial transition factor (MET) inhibitors. We report a 66-year-old male ex-smoker with a 45-pack-year smoking history and comorbidities including ischemic heart disease, bronchial asthma, and gastroesophageal reflux disease who presented with five months of progressive dyspnea, classified as modified Medical Research Council grade III. High-resolution computed tomography revealed bilateral peripheral reticulation with mild honeycombing, traction bronchiectasis, and basal predominance without ground-glass opacities, fulfilling the criteria for a definite usual interstitial pneumonia pattern. Spirometry demonstrated a moderate restrictive pattern (FVC, 65%), and autoimmune screening was comprehensively negative. Following multidisciplinary review, nintedanib was initiated at 100 mg twice daily and subsequently escalated to the standard 150 mg twice-daily dose. The patient developed mild generalized body swelling at initiation, which worsened markedly after dose escalation. Extensive cardiology, nephrology, endocrine, hepatic, and metabolic evaluations identified no alternative cause. Discontinuation of nintedanib resulted in near-complete resolution of swelling within two months. Rechallenge at a tertiary interstitial lung disease center precipitated recurrence of identical generalized swelling within one month, necessitating a second discontinuation. The temporal relationship, dose dependence, and reproducible recurrence on rechallenge strongly suggest a causal association between nintedanib and generalized body swelling in this patient. This previously unreported adverse event warrants clinician vigilance and formal pharmacovigilance reporting. - Source: PubMed
Publication date: 2026/08/31
Alghulayqah Abdulaziz I - Stem cells reside within specialized microenvironments, termed niches, composed of vascular networks, stromal cells, extracellular matrix (ECM), immune components, and neural elements, which collectively regulate quiescence, self-renewal, and lineage commitment of stem cells. Platelet-derived growth factor receptor-β (PDGFRβ), a class III receptor tyrosine kinase (RTK) predominantly expressed in perivascular and mesenchymal stromal cells, has been associated with vascular-stromal organization across multiple stem cell systems. Rather than acting mainly as a direct determinant of stemness-associated transcriptional programs, PDGFRβ may influence stem cell behavior indirectly by modulating vascular stability, matrix remodeling, metabolic gradients, and biomechanical signaling. Evidence from hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs), neural stem cells (NSCs), tumor stem cells (TSCs), renal glomerular cells, and limbal stem cells (LSCs) indicates that PDGFRβ stromal or perivascular cells contribute to niche architecture and function in a context-dependent manner. Through interactions with platelet-derived growth factor-B (PDGF-B), vascular endothelial growth factor (VEGF), hypoxia-related signaling, inflammatory mediators, and integrin-dependent mechanotransduction, PDGFRβ is linked to angiogenesis, stromal cell activation, ECM remodeling, and niche biomechanics. Under physiological conditions, such regulation may support tissue maintenance, repair, and regeneration, whereas persistent or dysregulated activation may contribute to fibrosis, vascular dysfunction, tumor progression, and disruption of stem cell equilibrium. This review summarizes the current understanding of PDGFRβ as a vascular-stromal component associated with stem cell niche regulation, with emphasis on cross-tissue mechanisms and context-dependent differences. Particular attention is given to the LSC niche, where PDGFRβ limbal niche cells (LNCs) are discussed in relation to the Palisades of Vogt, limbal vessels, basement membrane/ECM organization, and epithelial progenitor maintenance. We distinguish established evidence for PDGFRβ expression and LNC-associated stromal identity from proposed mechanisms involving vascular-stromal support, ECM remodeling, biomechanical regulation, and LSC repair. Because receptor-specific functional evidence for PDGFRβ in limbal microenvironmental cells remains limited, the limbal component of this review is presented as a hypothesis-generating framework rather than as established evidence that PDGFRβ functionally regulates the limbal niche. Collectively, available evidence supports PDGFRβ as a candidate link between vascular-stromal organization and stem cell functional states, while underscoring the need for direct PDGFRβ perturbation studies in LNCs to define its functional relevance in limbal niche stability and corneal epithelial regeneration. This framework may guide future studies of PDGFRβ-associated stromal regulation in corneal epithelial regeneration and LSC niche dysfunction. - Source: PubMed
Publication date: 2026/09/22
Liao ShuyingLi Guigang - Atypical teratoid/rhabdoid tumor (ATRT) is the most common brain tumor in children less than one-year-old. Previous studies have identified three epigenetic subgroups of ATRT: ATRT-SHH, ATRT-TYR, and ATRT-MYC. Interestingly, it was found that ATRT-TYR/MYC (mesenchymal) subgroups are sensitive to receptor-tyrosine kinase inhibitors (RTKIs), particularly those that inhibit the platelet-derived growth factor receptor B (PDGFRB), highlighting the importance of PDGF signaling in ATRTs. In addition, the ATRT-TYR/MYC subgroups show upregulation of the macrophage migration inhibitory factor (MIF), with dysregulation of the MIF signaling pathway, which was found to have immunosuppressive effects in other cancers. While PDGF and MIF pathways have been found to promote tumorigenesis of other cancers including glioma, their roles in ATRTs remain unknown. We hypothesized that PDGF and MIF signaling pathways contribute to maintaining malignant phenotypes in ATRT-TYR/MYC subgroups. - Source: PubMed
Publication date: 2026/09/09
Choutri Yacine AXu LimingYao FupanHuang Annie - Butyrylcholinesterase (BuChE) is a metabolic enzyme implicated in Alzheimer's disease, detoxification and depression. Although reduced BuChE expression is recognised in cirrhosis, its functional role in fibrogenesis remains undefined. - Source: PubMed
Publication date: 2026/09/23
Tao LeLiu NuoyaZhang WeiYang ZongguoXing WenyaWu LiuHou LinqiWei PingtingXie YuanyuanHan WeiLiu YunqiJin YesenXiang LianlianLiu XulingMa WentingHu PingpingLi WeiZhou WenjunWang SaiChen HongzhuanLiu PingYin DongminLi YingDooley StevenZhang LiXu JianrongJi GuangLiu Cheng - 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