PDGF-bb, human
- Known as:
- PDGF-bb, H. sapiens
- Catalog number:
- p716-10
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- 101bio
- Gene target:
- PDGF- human
Related genes to: PDGF-bb, human
- 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: PDGF-bb, human
Related articles to: PDGF-bb, human
- Fibroblast collagen deposition is regulated by macrophages and the circadian rhythm; understanding how these processes interact provides insights to collagenous tissue homeostasis. Here, we reveal that macrophage-fibroblast interaction enhances collagen deposition and requires a functional circadian rhythm. Macrophage polarization status determines how fibroblast responses were elicited, where naive and pro-inflammatory macrophages require direct cell-cell contact, and anti-inflammatory macrophages secrete soluble factors. One key secreted factor identified by mass spectrometry proteomics analysis is PDGFA. Crucially, macrophages lacking PDGFA, or treatment with PDGFRa inhibitor, showed diminished ability to modulate fibroblast circadian rhythms and collagen production. Impaired circadian rhythms in either cell type also led to a reduced collagen fibrillogenesis response. These results confirmed that the collagen deposition pathway is under circadian clock control in lung fibroblasts, and demonstrated that macrophages can re-synchronize fibroblast circadian rhythms to promote collagen deposition and extracellular remodeling, which are implicated in processes such as wound healing responses. - Source: PubMed
Publication date: 2026/09/21
Lowles KatherineZhang Xin-YangYao Xue-FengCutiongco Marie F AHughes Joshua JLi Shi-YangKnox JohnCoy MadeleineLin Wei-HsiangMacDonald Andrew SKadler Karl EMeng Qing-JunHussell TracyChang Joan - Oxidative stress is a well-recognized contributor to male reproductive dysfunction, yet discussion of this mechanism has focused almost exclusively on sperm damage. This focus overlooks the somatic and stromal networks that support testicular development, steroidogenesis, tissue architecture, and erectile function. Platelet-derived growth factor receptor alpha (PDGFRα) is expressed in heterogeneous interstitial and progenitor-enriched populations and has established roles in testicular development. This narrative review examines the evidence on PDGFRα in male reproductive tissues and considers the potential relevance of redox mechanisms identified predominantly in other organ systems. Genetic studies show that deficiency impairs the postnatal establishment of the adult Leydig-cell population, whereas deficiency disrupts fetal testis cord organization and Leydig-cell differentiation. Studies of the adult testis document receptor localization and, in cell-based models, downstream signaling capacity. Preclinical work has further identified PDGFRα-positive cavernosal fibroblasts associated with vascular remodeling in erectile dysfunction, although a receptor-specific function for these cells remains unproven. We propose that PDGFR-associated redox signaling may shape stromal responses to injury in the testis and penis; however, direct evidence for this mechanism in male reproductive tissue is currently lacking. Testing this hypothesis will require cell-resolved measurements of receptor phosphorylation and localized reactive oxygen species, together with lineage-restricted, receptor-specific perturbation. Establishing whether such a pathway exists could open a mechanistic link between oxidative stress and stromal, rather than purely germ-cell, contributions to male reproductive dysfunction-with implications for both testicular endocrine failure and vasculogenic erectile dysfunction. - Source: PubMed
Publication date: 2026/09/20
Ko Eun-AHwa Jeong SeokKang Dawon - Acute full‑thickness skin wounds represent a significant clinical challenge due to tissue loss, risk of bacterial contamination, and the need for rapid and effective regeneration. Injectable thermosensitive hydrogels incorporating antibacterial nanomaterials represent a promising strategy for advanced wound care. In this study, a multifunctional hydrogel composed of Graphene oxide (GO), branched polyethyleneimine (BPEI), and silver nanoparticles (AgNPs) dispersed in Pluronic F127 was developed and evaluated for wound healing applications. The GO-BPEI-AgNP nanocomposite was synthesized via amidation and microwave-assisted methods and characterized using DLS, UV-vis, FTIR, XRD, and SEM-EDX analyses. Biocompatibility was assessed in HaCaT keratinocytes using the Alamar Blue assay, while scratch assays and antibacterial activity against. In vivo wound healing efficacy and histopathological changes were evaluated in a rat full-thickness skin wound model, together with qRT-PCR analysis of wound-healing-related genes. The hydrogel exhibited favorable injectability, nanoscale morphology, and high biocompatibility (IC: 246.7 µg/mL). It significantly enhanced keratinocyte migration and demonstrated antibacterial activity. In vivo findings revealed accelerated wound closure, enhanced epidermal regeneration, and modulation of PDGFA, VEGFC, COL1A1, TIMP1, and MMP9 expression. Collectively, the GO‑BPEI‑AgNP hydrogel shows strong potential as an injectable antibacterial biomaterial for acute full‑thickness wound repair, with potential relevance to infection‑associated wound environments. - Source: PubMed
Bas KemalKarakurt Serdar - In the United States, sickle cell disease (SCD) is a rare inherited hemoglobinopathy affecting about 100,000 individuals, mostly with African ancestry. SCD causes damage to multiple organ systems and SCD nephropathy (SCDN) is a common complication associated with early mortality. We previously performed a genome-wide association study (GWAS) for SCDN and identified a modest number of genome-wide significant loci. Here, we leveraged the ancestral composition of participants from two well-characterized adult SCD cohorts to boost statistical power and perform a local ancestry-aware GWAS for estimated glomerular filtration rate (eGFR), resulting in the identification of novel genome-wide significant loci within the African (AFR) and European (EUR) ancestral components of participants. Meta-analysis identified 12 significant genomic regions in the AFR tract, including PPIL6, ARHGAP24, RAB11A, and STEAP3, and 38 regions in the EUR tract, including UBLCP1, ADAMTS6, JAZF1, MYO7B, MYO1C, PDGFA, GPC5, LRP1B, KANK1, and TRPV5. The identified regions encompass genes affecting inflammation, extracellular matrix (ECM) integrity, iron metabolism, magnesium ion homeostasis, B cell apoptosis, tumor necrosis factor (TNF) production, and estrogen signaling. Many of these genes and pathways are important not only for renal function, but also for SCD biology, providing additional support for the hypothesis that SCDN pathophysiology is unique from other forms of kidney disease. This study represents the largest local ancestry-aware analysis of SCDN to date, furthers our understanding of the genetic risk factors underlying SCDN, and proposes new targets that could be useful for the early identification and treatment of kidney dysfunction in SCD patients. - Source: PubMed
Publication date: 2026/08/19
Garrett Melanie ENouraie Seyed MehdiMachado Roberto FGordeuk Victor RGladwin Mark TTelen Marilyn JAshley-Koch Allison ETOPMed Nhlbi Trans-Omics For Precision Medicine - Fetal growth restriction (FGR) is a complex condition with highly heterogeneous clinical outcomes, making prenatal distinction between transient and persistent growth failure challenging. This study aims to identify amniotic fluid (AF) biomarkers capable of differentiating distinct FGR trajectories and characterizing persistent growth failure mechanisms. - Source: PubMed
Publication date: 2026/08/15
Cao YanHao WenjingWang YanChai ChongchongLi YouranLiu YingZhu HongyuanLu YifanWang DongZhai YanhongYan YoushengCao Zheng