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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.


In skin, CPs intake significantly down-regulated placenta growth factor (PIGF-2), insulin-like growth factor (IGF)-binding protein (IGFBP) -2 and IGFBP-3, and up-regulated platelet factor 4 (PF4), serpin E1 and transforming growth factor (TGF)-β1 [1]. Vascular endothelial growth factor (VEGF) function was to form new blood vessels produced by various Cells one of them was macrophages [2]. In this study, we performed drug repositioning using human platelet-derived growth factor receptor α (PDGFRα)-positive mesenchymal progenitors that have been proved to be an origin of ectopic adipocytes in skeletal Muscle [3]. Recently, inhibition of platelet-derived growth factor receptor (PDGFR)-α by the monoclonal Antibody olaratumab showed promising clinical activity [4]. Fibrocytes are bone marrow-derived progenitor Cells that produce growth factors and contribute to fibrogenesis in the Lungs [5].

The expression of growth factors and their receptors in fibrocytes was analyzed using ELISA and Western blotting [6]. Matriptase also cleaves the ECD of the Vascular endothelial growth factor receptor 2 (VEGFR2) and the angiopoietin receptor Tie2 [7]. We co-expressed the proteases in an epithelial cell line with Her2, Her3, Her4, insulin receptor (INSR), insulin-like growth factor I receptor (IGF-1R), the platelet-derived growth factor receptors (PDGFRs) α and β, or nerve growth factor receptor A (TrkA) [8]. Matriptase cleaves phosphorylated Her2 at Arg558 and Arg599 and the Arg599 cleavage produces a CTF not recognized by the monoclonal antibody trastuzumab/Herceptin [9]. Her2 cleavages by matriptase can be inhibited by the hepatocyte growth factor activator inhibitor 1 (HAI-1) in the MDA-MB-231 human breast cancer Cells [10].

Aberrant platelet-derived growth factor (PDGF) activity can lead to hyperproliferation of PASMC, however, little is known about the role of long noncoding RNA (lncRNA) in this process [11]. Depletion of 4 lncRNAs affected proliferation of RPASMC, as measured by EdU incorporation assay [12]. In the in vitro study Vascular smooth Muscle Cells (VSMC) were cultured, proliferation stimulated with platelet-derived growth factor-BB (PDGF-BB) (20 ng/ml) and TCS at 1, 2, or 4 μM added [13]. Herein we showed that loss of TSC1 or TSC2 downregulation of platelet-derived growth factor receptor α (PDGFRα) expression was mediated by mTORC1 [14]. Moreover, mTORC1 inhibited PDGFRα expression via suppression of forkhead box O3a (FOXO3a)-mediated PDGFRα gene transcription [15].

In addition, ectopic expression of PDGFRα promoted AKT activation and enhanced proliferation and tumorigenic capacity of Tsc1- or Tsc2-null mouse embryonic fibroblasts (MEFs), and vice versa [16]. Western blot and real-time PCR (RT-PCR) were used to study PDGFRα protein and gene expression levels [17]. Topical NTX accelerated DNA synthesis, as measured by BrdU incorporation, increased mast Cells, and enhanced expression of platelet-derived growth factor (PDGF) and Vascular endothelial growth factor (VEGF), a marker for angiogenesis [18]. Regranex had little effect on DNA synthesis, mast Cells, and VEGF expression relative to vehicle-treated wounds, and it only temporarily increased PDGF expression [19]. In the present study, we investigated the effects of prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and high fact diet after weaning on body growth and expression of platelet-derived growth factor receptor β in the brain in rat pups [20].

Recent investigations have explored to improve the healing process by growth factor delivery from the sutures [21]. However, it is difficult to conjugate growth factors to nylon or other synthetic sutures [22]. This study explores the performance of a novel electrochemically aligned collagen suture in a flexor tendon repair model with and without platelet derived growth factor following complete tendon laceration in vivo [23]. Heparin was covalently bound to electrochemically aligned collagen sutures (ELAS) to facilitate affinity bound delivery of platelet-derived growth factor-BB (PDGF-BB) [24]. The cell-surface glycome of activated HSCs facilitated Gal-1 binding, which upon recognition of the N-glycans on neuropilin (NRP)-1, activated platelet-derived growth factor (PDGF)- and transforming growth factor (TGF)-β-like signals to promote HSC migration and activation [25].

In addition, blocking endogenous Gal-1 expression suppressed PDGF- and TGF-β1-induced signaling, migration, and gene expression in HSCs [26]. Stem Cells require contact with extracellular matrices as well as signals from growth factors to proliferate and to retain their stemness [27]. The StemTrix scaffold is comprised of chitosan with immobilized heparin which in turn tethers heparin-binding growth factors [28]. When FGF-2 and heparin-binding EGF are tethered to the StemTrix cultureware neural stem cells grow ∼3 times faster and remain in a more primitive state as determined by both Western Blot and gene expression analyses [29]. In the in vitro study, DPN attenuated the transformation of quiescent HSCs to activated phenotype, suppressed Collagen I and α-SMA expression [30].

The Vascular endothelial growth factor (VEGF) family and other angiogenic factors, including fibroblast growth factor and platelet-derived growth factor, promote the growth of newly formed vessels from preexisting vessels and change the Tumor microenvironment [31]. Further, when the two cysteines were individually mutated in gO GT1c no impairment in cell-free infectivity was observed [32]. This, however, was in sharp contrast to gO GT4, in which both of the corresponding cysteine Mutations led to a substantial reduction in cell-free infectivity which was even more pronounced upon Mutation of GT4-C336 than of GT4-C216 [33]. SHP2 oxidation requires NADPH oxidases (NOXs), and oxidized SHP2 co-localizes with platelet-derived growth factor receptor and NOX1/4 [34]. Our results showed that PDGF dose- and time-dependently induced PASMC proliferation, and this was accompanied by an increase of HDAC1 and cyclin-dependent kinase 4 (CDK4) protein expression as well as a reduction of microRNA-124 (miR-124) [35].

In addition, over-expression of miR-124 reversed CDK4 protein elevation and PASMC proliferation caused by PDGF [36]. We further found that pre-incubation of PASMCs with pioglitazone, an agonist of PPARγ receptors, significantly increased PPARγ expression and activity, and blocked PDGF-stimulated cell proliferation by regulating HDAC1-mediated miR-124 and CDK4 expression [37]. Stenosis due to intimal Hyperplasia development often occurs after placement of arteriovenous synthetic grafts used for hemodialysis [38]. The effect of conditioned media from the culture of fat with ROS or PGZ on i) platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation of human venous smooth Muscle Cells (SMC) was measured by a DNA-binding assay, and ii) lipopolysaccharide (LPS)-induced human monocyte release of Tumor necrosis factor-alpha (TNFα) was assessed by ELISA [39]. The proliferation of SMC was inhibited in the presence of media conditioned by fat/ROS cultures [40].

External jugular vein exposed to fat incorporated with PGZ had increased adiponectin expression compared to vein exposed to fat alone [41]. The study we proposed exhibited high sensitivity toward platelet-derived growth factor BB (PDGF-BB) with the detection limit of 52 fM [42]. Pain and functional improvements were assessed using the visual analog scale (VAS), Modified Mayo Clinic Performance Index for the elbow, and magnetic resonance imaging (MRI) [43]. White blood cell count, platelet count, and levels of platelet-derived growth factor-AB (PDGF-AB), PDGF-BB, transforming growth factor-β (TGF-β), Vascular endothelial growth factor, epithelial growth factor, and interleukin-1 β in PRP were measured and investigated for statistical correlation with the clinical score [44]. TGF-β level significantly correlated with Mayo Clinic performance score and MRI grade improvement [45].

Platelet-derived growth factor (PDGF)-A in Tumor CM was shown to induce ALDH expression in HMVEC [46]. Afterwards, platelet derived growth factor (PDGF)-induced primary rat airway smooth Muscle cell (ASMC) model and ovalbumin (OVA)-induced rat asthma model were used to continue our following research [47]. The down-regulation of transforming growth factor β1 (TGF-β1) and interleukin-1β (IL-1β) upon ISOF treatment might be responsible for its anti-remodeling and anti-inflammation roles [48]. In conclusion, ISOF can reduce cough and sputum, as well as inhibit airway remodeling and Inflammation by regulating the expression of TGF-β1 and IL-1β [49]. This leads to a hypoxic Tumor microenvironment further reinforcing the activation of PSCs by stimulating their secretion of growth factors and chemokines [50].

This defect could not be overcome by the stimulation with platelet-derived growth factor [51]. Furthermore, miR-22-3p expression was negatively correlated with HMGB1 expression in ASO tissue specimens [52]. PDGFRα mRNA and protein expression levels were both significantly increased in colonic smooth muscle tissue, but PDGFRβ expression was unchanged [53]. Meanwhile, the expression of PDGF ligands, including both PDGFα and PDGFβ, was significantly increased in diabetic colonic smooth Muscle tissue [54]. However, the expression of P-FOXO3 protein was significantly decreased [55].

FOXO3 could bind to a site on the PDGFRα promoter, and the basal expression of PDGFRα was significantly reduced when endogenous FOXO3 expression was knocked down with FOXO3 short hairpin RNA (shRNA) in NIH Cells [56]. The expression of ECM component genes in keratocytes was upregulated by MSC-CM [57]. However, sorafenib did not affect MC proliferation and apoptosis, suggesting that it stimulated MC maturation from resident precursors [58]. In recent years, the over-expression of platelet-derived growth factor (PDGF) has been shown to produce Tumors in experimental rodent models that closely resemble this human disease, specifically the proneural subtype of glioblastoma [59]. All growth factors were stable for at least nine months post-storage at -70˚C [60].

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 , 55 , 56 , 57 , 58 , 59 , 60 ,

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