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platelet derived growth factor

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The text is the summary of recent articles on platelet derived growth factor at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


(3)Department of Biomedical Sciences - Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA [1]. (4)Keizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil [2]. Here we show that impairment of platelet-derived growth factor-induced cell motility caused by extracellular α-Syn is mainly attributed to selective inhibition of sphingosine 1-phosphate (S1P) signalling [3]. The grafted veins were obtained 1, 2 and 4 weeks after operation, HE staining and Masson staining were preformed for histological changes of grafted vein wall, proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor (PDGF) immunohistochemistry staining were conducted for proliferation and expression and Distribution of PDGF of the grafted vein [4]. Additionally, Surgical Excision resulted in re-emergence of a mesenchymal cell population marked by expression of platelet-derived growth factor receptor-α (PDGFRα) and present in the initial developing HO Lesion but absent in mature HO [5].

(2)Departments of Physiology and Biophysics, Stony Brook University, Stony Brook, NY, 11794-5281, USA [6]. Fibroblasts were stimulated with transforming growth factor β1 (TGF-β1), and then treated either with a specific Fibrosis pathway inhibitor targeting TGF-β receptor type 1 (TβRI), platelet-derived growth factor receptor (PDGFR), Epidermal growth factor receptor (EGFR) or Vascular endothelial growth factor receptor (VEGFR) [7]. Nintedanib is a tyrosine kinase inhibitor targeting three angiogenesis-related transmembrane receptors (vascular endothelial growth factor, fibroblast growth factor, and platelet-derived growth factor) [8]. The most important study was the phase III LUME-Lung 1 trial, which investigated the combination of nintedanib with docetaxel for second-line treatment in advanced NSCLC patients [9]. Higher levels of Epidermal growth factor (EGF), transforming growth factor (TGF)‑β and platelet-derived growth factor (PDGF), and lower levels of basic fibroblast growth factor (bFGF) were observed in the wound tissue treated with NP compared to the wound tissue exposed to PP [10].

NP induced a statistically significant increase in the expression of fibronectin (FN) on days 3 and 10 compared to PP [11]. In addition, proliferation was blocked by palmitate and stearate (two SCD substrates) but not by palmitoleate and oleate (two SCD products) [12]. Conversely, knockdown of PDGF-B expression in cancer Cells undergoing EMT, or treatment with a PDGF-receptor inhibitor, decreased the invasion ability of both CAFs and cancer Cells [13]. By analyzing the gene expression profiles of 442 patients with lung adenocarcinomas, we established that high expression of PDGF-B and presentation of mesenchymal-like tumors were significantly associated with a high rate of disease Recurrence and poor patient prognosis [14]. This study was designed to evaluate the contents of major growth factors in CGF and compare them with those found in PRP (platelet-rich plasma) and PRF (platelet-rich fibrin) [15].

Concentrations of five representative growth factors in platelets were measured with enzyme-linked immunosorbent assay (ELISA): platelet-derived growth factor-BB (PDGF-BB), transforming growth factor β-1 (TGF-β1), insulin-like growth factor-1 (IGF-1), Vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) [16]. For other growth factors, such as PDGF-BB, TGF-β1, IGF-1, and VEGF, the levels did not differ significantly among activated PRP, PRF, and CGF [17]. Our findings extended the currently available data on the release and measurement of growth factors in CGF and other platelet gels [18]. Pericytes and Vascular smooth Muscle Cells, are known to play fundamental roles during these processes, their characteristics during Vascular development remain incompletely understood [19]. Furthermore, the combination of Pdgfrb and NG2 gene (Cspg4) driven reporter expression increased the specificity of brain Vascular mural cell labeling at later stages [20].

The expression of other known pericyte markers revealed time-, region- and marker-specific patterns, suggesting heterogeneity in mural cell maturation [21]. Group A consisted of 10 patients whose pathological TNM stage was IIIC (T3-4N2M0), while another 10 patients with synchronous liver Metastasis (TNM stage IV) were recruited for group B [22]. The current study was designated to investigate the effects of a phenanthrene derivative, 5,7-dimethoxy-1,4-phenanthrenequinone (DMPQ), on cell adhesion molecule (CAM) expression in Vascular ECs and migration in VSMCs [23]. These suggest that DMPQ affects CAM expression by affecting NF-κB signaling [24]. Meanwhile, DMPQ could also inhibit platelet-derived growth factor (PDGF)-induced VSMC migration toward collagen by affecting cellular PDGF signaling, including PDGFRβ, PLCγ, ERK1/2, and Akt phosphorylation [25].

In this regard, growth factors clearly play important roles in regulating cellular fate [26]. However, uncontrolled release of growth factors has been demonstrated to produce severe side effects on the surrounding tissues [27]. In this study, poly(lactic-co-glycolic acid) (PLGA) microspheres (MS) incorporated three-dimensional (3D) CORAGRAF scaffolds were engineered to achieve controlled release of platelet-derived growth factor-BB (PDGF-BB) for the differentiation of stem Cells within the 3D polymer network [28]. The platelet-derived growth factor (PDGF)/AKT signaling pathway plays complex roles in Tumor suppression [29]. MTT assay and flow cytometry showed that PD inhibited cell proliferation and induced apoptosis in Hep-2 and AMC-HN-8 Cells [30].

We also found that MERTK (a proto-oncogene which is overexpressed in several malignancies) and PDGFRB (a member of the platelet-derived growth factor family whose expression is high in breast-cancer Cells that have become resistant to endocrine therapy) were among the genes with a higher differential regulation by simvastatin [31]. Release of growth factors from the loaded bone substitutes was measured based on the platelet-derived growth factor isoform (PDGF-BB) and thrombin immunoassays [32]. This pro-mitogenic capacity of the supernatants decreased over the observation period [33]. Attractive targets are established by receptor tyrosine kinases, such as platelet-derived growth factor receptors (PDGFRs) and c-Kit as mostly Irregular signaling, which is due to either over expression or Mutation that is associated with tumorigenesis and cell proliferation [34]. In this research, we studied how imatinib mesylate would exert effect on MCF7 and T-47D breast cancer and MCF 10A epithelial cell lines, the gene and protein expression of PDGFR-β, c-Kit and their relevant ligands platelet-derived growth factor (PDGF)-BB and stem cell factor (SCF) [35].

The MTS assay was conducted in therapeutic relevant concentration of 2-10 µM for 96, 120 and 144 h treatment [36]. In the present study, we examined simultaneously the transcript levels of Vascular endothelial growth factor (VEGF), transforming growth factor β1 (TGF‑β1), basic fibroblast growth factor 2 (bFGF2), platelet derived growth factor (PDGF) isoforms and receptors, epidermal growth factor (EGF) and insulin growth factor‑1 (IGF‑1) in herniated and control ID specimens and investigated their correlation with the clinicopathological profiles of patients suffering from symptomatic lumbar ID herniation [37]. VEGF mRNA expression was significantly increased in the protruding compared with the extruded discs [38]. Increased VEGF expression possibly induces the neovascularization process in the earliest stages of ID herniation [39]. But ambiguities in existed studies on the clinical efficacy of rhGFs do not permit either the identification of the specific growth factors effective for therapeutic interventions or the optimal concentration of them [40].

Neither is it known whether the same rhGF can stimulate regeneration of both soft tissue and bone, or whether different patient populations call for differential use of the growth factors [41]. Particular attention was given to the therapeutic impact of fibroblast growth factor 2(FGF-2) and platelet derived growth factor BB (PDGF-BB) [42]. We previously found that hypoxia modulates the phenotype of primary corpus cavernosum smooth Muscle Cells (CCSMCs) in rats, but the underlying molecular mechanism is still unknown [43]. We also discuss the role of the S1P₁-Platelet derived growth factor receptor β functional complex (which deploys G-protein/β-arrestin and receptor tyrosine kinase signaling) in regulating cell migration [44]. CD117, CD34 desmin, vimentin, S-100 and smooth Muscle actin were immunohistochemically tested to achieve a diagnosis of GIST [45].

To date, it remains unknown as to whether AdipoRon regulates vascular smooth Muscle cell (VSMC) proliferation, which plays a major role in neointima formation [46]. Under in vitro conditions, AdipoRon treatment led to significant inhibition of platelet-derived growth factor (PDGF)-induced VSMC proliferation, DNA synthesis, and cyclin D1 expression [47]. Both are soluble and stable at physiologic conditions, which is a key factor for retaining viable Cells and active growth factor [48]. However, a long time (3-4 weeks) required to prepare a cultured epidermis sheet is a disadvantage [49]. Since there is no evidence of the role of anti-PDGF receptor autoantibodies in the pathogenesis of SSc Vascular lesions, we investigated the biologic effect of agonistic anti-PDGF receptor autoantibodies from SSc patients on human Pulmonary artery smooth muscle cells and the signaling pathways involved [50].

The synthetic (proliferation, migration, and type I collagen gene α1 chain expression) and contractile (smooth muscle-myosin heavy chain and smooth muscle-calponin expression) profiles of human Pulmonary artery smooth Muscle Cells were assessed in vitro after incubation with SSc anti-PDGF receptors stimulatory autoantibodies [51]. This phenotypic profile is mediated by increased generation of reactive oxygen species and expression of NOX4 and mTORC1 [52]. Cell proliferation was induced by the culture solution with basic fibroblast growth factor and platelet-derived growth factor, and the proliferation of OPCs was determined by MTT assay [53]. The present study has examined the likely regulatory effects of sulforaphane (SFN, an antioxidant) on Nrf2 activation and platelet-derived growth factor (PDGF)-induced mTOR signaling in VSMCs [54].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 ,

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