PDGFB Forward PCR Primer (500bp position)
- Known as:
- PDGFB Forward PCR test kit Primer (500bp position)
- Catalog number:
- MP1163
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PDGFB Forward PCR Primer (500bp position)
Related genes to: PDGFB Forward PCR Primer (500bp position)
- Gene:
- PDGFB NIH gene
- Name:
- platelet derived growth factor subunit B
- Previous symbol:
- SIS
- Synonyms:
- SSV
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-01-14
Related products to: PDGFB Forward PCR Primer (500bp position)
Related articles to: PDGFB Forward PCR Primer (500bp position)
- : Recombinant human platelet-derived growth factor-BB (rhPDGF-BB) is intended to restore reparative signaling in diabetic wounds, yet its efficacy and the contribution of delivery systems remain uncertain. This systematic review evaluated its preclinical efficacy, mechanistic responses, safety, risk of bias, certainty, and attribution of effects. : Following PRISMA 2020 and an OSF-registered protocol, PubMed, Embase, Scopus, Web of Science, and ScienceDirect were searched from inception to 29 July 2026 for controlled in vivo diabetic wound studies. Compatible outcomes were pooled using random-effects models with restricted maximum-likelihood estimation and Hartung-Knapp adjustment. Non-poolable findings were synthesized using attribution-specific effect direction maps. Risk of bias and certainty were assessed with SYRCLE and preclinical GRADE, respectively. : Twenty-nine studies were included from 3844 records. For percentage wound closure at days 10-12, three studies comprising 113 animals yielded a favorable but imprecise pooled estimate (mean difference: 12.94 percentage points; 95% CI: -0.34 to 26.23; = 0.052; I = 54.6%). Two studies comprising 45 animals suggested a non-significant 4.28-day reduction in time to complete closure (95% CI: -27.98 to 19.42). In the exploratory effect direction synthesis, directly attributable macroscopic healing showed a favorable direction in 17 of 22 studies and was the only domain meeting the prespecified 70% concordance threshold; four of these studies had confirmed unit-of-analysis concerns, and other reparative domains were heterogeneous. Formulation-level comparisons met the same exploratory threshold across four reparative domains, but the isolated contribution of rhPDGF-BB could not be determined. Safety reporting was sparse. Certainty for the primary outcome was very low. : Directly attributable comparisons showed a predominantly favorable study-level pattern for macroscopic wound healing in the exploratory synthesis, but the pooled effects were imprecise and inconclusive. Formulation-level comparisons suggested broader reparative activity, although the independent contribution of rhPDGF-BB could not be isolated. Better controlled and clinically representative studies are required before confident translation. - Source: PubMed
Publication date: 2026/09/21
Muñoz-Carrillo José LuisGutiérrez-Coronado OscarLopez-Hernandez EdreiGutiérrez-Hernández RosalindaSabbagh-Permuth YaelZamora-Aguilar Ana KarolaRodríguez-Cortés NatalieChávez-Ruvalcaba FranciscaVillalobos-Gutiérrez Paola TrinidadChávez-Ruvalcaba María Isabel - contains β-carboline alkaloids with neuropharmacological and immunomodulatory properties, but their effects during prolonged exposure in established amyloid pathology remain poorly characterized. This study investigated whether chronic intermittent administration modifies behavioral performance, fibrillar amyloid pathology, and hippocampal microglial alterations in aged PDGFB-APPSwInd mice. : Male wild-type (WT) and PDGFB-APPSwInd transgenic (TG) mice aged 15-18 months received extract (1.5 mL/kg, oral gavage) or vehicle twice weekly for four weeks. Locomotor activity, anxiety-like behavior, and spatial recognition memory were assessed using the open-field, elevated-plus-maze, and object-location tests, respectively. Hippocampal fibrillar amyloid plaques were evaluated by Thioflavin-S staining, and microglial immunoreactivity and morphology were assessed using Iba1 immunofluorescence and morphometric analysis. : Chronic administration did not consistently modify locomotor activity, anxiety-like behavior, or spatial recognition memory. In TG mice, treatment increased the number of hippocampal Thioflavin-S-positive fibrillar amyloid plaques, without corresponding changes in total Thioflavin-S-positive area or median plaque size. Microglial alterations were predominantly genotype-associated, with TG mice exhibiting changes in Iba1-labeled cell quantification and morphology, particularly in the CA1 region. treatment did not significantly modify these genotype-associated morphological alterations. Chronic intermittent exposure was associated with a selective change in fibrillar amyloid plaque number without parallel changes in plaque area, plaque size, behavioral performance, or microglial morphology. These findings expand current evidence regarding the biological effects of repeated exposure in the context of established amyloid pathology. - Source: PubMed
Publication date: 2026/09/10
Bustelli Isabella BacciGraça Santhiago CalveloSantos Érica Victória DosLanaro RafaelLinardi AlessandraCaetano Ariadiny Lima - 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 - This study investigates the use of composite scaffolds composed of methacrylated hyaluronic acid (HAMA), methacrylated carboxymethyl chitosan (CMCSMA), and curcumin (Cur) in bone tissue regeneration. The repair of oral and maxillofacial bone defects poses a significant clinical challenge, and the development of innovative scaffold materials to facilitate bone regeneration is crucial. The objective of this study was to fabricate a composite scaffold that exhibits favorable biocompatibility and appropriate porosity (76%-87%), and to systematically assess its impact on the proliferation, migration, and osteogenic differentiation of osteoblasts (MC3T3 cells). The CMCSMA/HAMA/Cur composite scaffold was successfully synthesized through chemical processes and three-dimensional printing, followed by a thorough material characterization. In vitro cellular assays revealed that the CMCSMA/HAMA/Cur composite scaffold demonstrated excellent biocompatibility, with a hemolysis rate below 5%, and facilitated the sustained release of Cur, underscoring its potential for localized drug delivery. Furthermore, the scaffold notably enhanced cell proliferation and migration compared to the Control group and modulated the expression of key genes Vegfa, Tnc, Pdgfb in the PI3K-Akt signaling pathway, thereby suggesting its capacity to promote osteogenic differentiation. This study offers a novel approach and provides a theoretical framework for future advancements in bone tissue engineering and regenerative medicine, with the anticipation of further clinical evaluation and application. - Source: PubMed
Publication date: 2026/09/09
Guo YaxuanXue ZhijunLi HuiWang YingchengyaoHou YajingShen Jing - Brain tumors, particularly glioblastoma multiforme (GBM), remain among the most lethal forms of cancer due to their aggressive nature and the formidable challenge posed by the blood-brain barrier (BBB), which restricts the delivery of therapeutic agents. Conventional treatment modalities, including surgery, radiotherapy, and chemotherapy, often fail to achieve effective and targeted therapy without inducing systemic toxicity or damaging healthy brain tissue. In recent years, mesoporous silica nanoparticles (MSNs)have emerged as a versatile platform for targeted brain tumor therapy because of their high surface area, tunable pore structure, biocompatibility, and ease of surface functionalization. This review critically examines advanced surface functionalization strategies, including chemical functionalization (amine, thiol, carboxyl groups), ligand conjugation (antibodies, aptamers, peptides), and polymeric coatings (PEG, chitosan, PLGA) that enhance BBB penetration, facilitate tumor-specific targeting, and enable stimuli-responsive drug release (different types of exogenous and endogenous). We also explore the interactions of these modifications with key signaling pathways (e.g., Wnt/β-catenin, PDGF-B, TGF-β) that regulate BBB integrity and glioma progression. Special emphasis is placed on how surface-engineered MSNs can improve site-specific drug delivery, increase therapeutic accumulation in brain tumor tissue, and minimize off-target toxicity. Despite the considerable promise demonstrated by these techniques in preclinical glioma models, obstacles such as scalable synthesis, regulatory compliance, and long-term biosafety must be addressed to facilitate clinical translation. This review focuses specifically on brain tumor targeting via functionalized MSNs and provides mechanistic insights while highlighting emerging strategies to advance MSNs as next-generation therapeutics for brain tumor treatment. - Source: PubMed
Publication date: 2026/09/15
Sp RachanaPokale RahulDatta DeepanjanNaik Gaurisha Alias Resha RamnathJadhav Sandesh RamchandraKudarha RituMutalik SrinivasDhas Namdev