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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.

The lowest immunoexpression of CD34, podoplanin, PDGFA, EGFR has been noticed in the Rapamycin-treated group without important differences correlated to dosage and time [1]. In the present study, the role of leukocytes contained in PRP was assessed to verify their in vitro effect on fibroblasts and endothelial Cells, which have a leading role in the biological processes associated with wound healing (including angiogenesis and matrix remodeling) [2]. The two aliquots were used in in vitro tests in order to verify the effects of leukocytes on proliferation, wound healing and tube formation, and in molecular analyses of growth factor and enzyme content [3]. Here, we investigated the CAF phenotype in cutaneous malignant Tumors based on their histology and immunohistochemical expression of CAF-related markers, including adipocyte enhancer-binding protein 1 (AEBP1), podoplanin, platelet derived growth factor receptor α (PDGFRα), PDGFRβ, fibroblast activating protein (FAP), CD10, S100A4, α-smooth Muscle actin (α-SMA), and EMT-related markers (Zeb1, Slug and Twist) [4]. Immunohistochemical evaluation finds that most rectal GIST Tumors are CD117 (KIT) positive, and are sometimes CD34, platelet-derived growth factor receptor alpha (PDGFRA), smooth muscle actin, S-100, or vimentin positive [5].

The airway remodeling induced by abnormal airway smooth Muscle (ASM) cell proliferation is an important cause of asthma [6]. MicroRNAs (miRNAs) are important regulators of ASM cell proliferation [7]. Numerous studies have reported that miR-20b-5p is a critical regulator for cell proliferation [8]. However, whether miR-20b-5p is involved in regulating ASM cell proliferation remains unknown [9]. Overall, our results show that miR-20b-5p impedes PDGF-induced proliferation of Fetal ASM Cells through targeting STAT3 [10].

DDR1 Deficiency led to reduced expression of the genes encoding vascular endothelial growth factor (VEGF)-A, VEGF-C, and platelet-derived growth factor-B [11]. After redissolution, lyophilized powder HPLs were compared with liquid HPLs, as well as human peripheral serum (HPS) and Fetal bovine serum (FBS) in liquid or redissolved lyophilized powder forms [12]. Concentrations of epidermal growth factor (EGF), transforming growth factor-β1 (TGF-β1), platelet-derived growth factor-AB (PDGF-AB) and platelet-derived growth factor-BB (PDGF-BB) were evaluated by enzyme-linked immunosorbent assay (ELISA) [13]. Cell differentiation was examined by transepithelial electrical resistance (TEER) [14]. In vitro experiments on cell migration, proliferation and differentiation and rat models on wound healing demonstrated no significant difference between the liquid and redissolved lyophilized powder forms for HPLs, HPS and FBS [15].

However, the epiblast and primitive endoderm can not be identified in late blastocysts, and those TE or ICM lineage-specific genes were low expressed in blastomeres from the morula [16]. Chondrosarcomas harbor molecular abnormalities, such as overexpression of platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, which are required for cancer development, progression, and Metastasis [17]. Pazopanib is a potent and selective multitargeted tyrosine kinase inhibitor, which co-inhibits stem cell growth factor receptor (c-KIT), fibroblast growth factor receptor (FGFR), PDGFR, and vascular endothelial growth factor receptor (VEGFR) and has demonstrated clinical activity in patients with advanced previously treated soft tissue Sarcoma [18]. Previous reports have demonstrated that human fibroblast growth factor (hFGF)-21 is a multifunctional protein that exhibits potential therapeutic value for metabolic diseases [19]. Results also demonstrated that hFGF-21 treatment downregulated Inflammatory cytokines [20].

PDGF-BB stimulation decreased TMF-1 binding to the transcriptional regulator Brahma-related gene 1 (Brg-1) and released Brg-1 from the SWI-SNF chromatin remodeling complex [21]. CM/FGF-18 significantly promoted cell proliferation, alkaline phosphatase activity, and mineralization compared to CM alone [22]. Alveolar mesenchymal Cells deposit elastic fibers which limit cellular strain, but while the elastic fiber network is incomplete, this function is also served by the intracellular cytoskeleton [23]. Test groups had PDGF-BB, TGF-β1, IGF-1, or a combination of all three added to the culture medium, whereas the control group received no growth factor [24]. Cardiac involvement in hypereosinophilia, especially Loeffler Endocarditis, carries a poor prognosis and significant mortality [25].

In addition, higher expressions of pre-oligodendrocyte markers were detected in the Cells transduced with miR-219 lentivirus in comparison with the Cells treated with triiodothyronine (T3) [26]. We identified paracrine crosstalk between cancer cells expressing platelet-derived growth factor (PDGF)-CC and CAFs expressing the cognate receptors in human basal-like mammary carcinomas [27]. VHL loss increases the expression of hypoxia-inducible factors (HIFs) and their targets, including Epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) [28]. HIFs are upstream of the crosstalk between the growth factors, and these factors may regulate the expression of VEGR, EGF, PDGF and other growth factors [29]. The frequent VHL loss in ccRCC increases HIF expression, and HIFs may be an ideal candidate to overcome the TKI resistance [30].

As a step toward engineering these transitional zones, we initially analyzed how different (topographical or biological) cues affect tenogenic differentiation of adipose-derived stem Cells (ADSCs) [31]. We immobilized platelet-derived growth factor - BB (PDGF-BB) using polydopamine (PD) chemistry on random and aligned nanofibers and investigated ADSC proliferation and tenogenic differentiation [32]. Interestingly, the PDGF immobilized aligned nanofiber group showed a synergistic effect with maximum expression of tenogenic markers for 14 days [33]. A gradient of immobilized PDGF was able to control the phenotypic differentiation of ADSCs into tenocytes in a spatially controlled manner, as confirmed by analysis of the expression of tenogenic markers and immunofluorescence staining [34]. In contractile experiments, the colonic smooth muscles were more sensitive to the SK3 agonist and antagonist (CyPPA and apamin) and the P2Y1 agonist and antagonist (MRS2365 and MRS2500) in STZ-treated mice [35].

Intracellular recordings showed the responses of membrane potentials in colonic smooth Muscle Cells to CyPPA, apamin, MRS2365, and MRS2500 were more sensitive in STZ-treated mice [36]. Overexpression and inhibition of miR-1281 in PASMCs promoted and suppressed, respectively, the cell proliferation and migration [37]. LX-2 Cells induced by platelet-derived growth factor-BB (PDGF-BB) were used to evaluate the anti-fibrogenic effect of propranolol in vitro [38]. Platelet-rich plasma (PRP), one of the most studied sources of growth factors, has demonstrated to promote wound healing in vitro and in vivo [39]. The authors set out to compare the effects of these two growth factor sources in cell proliferation and migration (scratch) assays of keratinocyte, fibroblast, endothelial and adipose derived stem Cells [40].

Growth factors involved in wound healing were measured: keratinocyte growth factor, Epidermal growth factor, insulin-like growth factor, interleukin 6, platelet-derived growth factor beta, Tumor Necrosis factor alfa, transforming growth factor beta and Vascular endothelial growth factor [41]. PRP showed higher growth factor concentrations, except for keratinocyte growth factor, that was present in adipose tissue in greater quantities [42]. Although, activation of lipolysis by exercise induces adipocyte hypotrophy and reduction of fat Mass, it is poorly understood whether exercise regulates angiogenesis by altering angiogenic gene expression in WAT [43]. Therefore, the purpose of this study was to evaluate the effect of 6 weeks voluntary wheel running exercise on angiogenic gene expression in adipose tissues [44]. At 24 hr after the last exercise training, tibialis anterior (TA), soleus (Sol), epididymal WAT (eWAT), inguinal WAT (iWAT), and Brown adipose tissue (BAT) were isolated and then the expressions of vascular endothelial growth factor A (VEGFA), angiopoietin1 (Ang1), Ang2, platelet-derived growth factor B (PDGF-B) and their corresponding receptors were analyzed by reverse transcription-polymerase chain reaction [45].

In skeletal muscles, VEGFA expression was upregulated in TA and Sol and PDDGF-B expression was increased in Sol after exercise training [46]. In eWAT, the expressions of VEGFA and Flk-1 were dramatically downregulated, whereas Ang2 and PDGFRβ was upregulated after exercise training [47]. In iWAT, VEGF expression was increased with the downregulation of Ang1 [48]. To study retinal proteome changes in BRVO following an intervention with a dexamethasone (DEX) implant this study combined an experimental model of BRVO with proteomic techniques [49]. Dexamethasone intervention reduced the retinal levels of platelet-derived growth factor receptor-α (PDGFR-α), and Vascular endothelial growth factor receptor 2 (VEGFR-2) [50].

We investigated whether minoxidil stimulates ASCs and if increased growth factor secretion by ASCs facilitates minoxidil-induced Hair growth [51]. Treatment with CXCL1, PD-ECGF, or PDGF-C also increased the proliferation index in DP Cells [52]. Minoxidil stimulates ASC motility and increases paracrine growth factor signaling [53]. Minoxidil-stimulated secretion of growth factors by ASCs may enhance hair growth by promoting DP proliferation [54]. The patient experienced a local Recurrence and distant metastasis after Surgical intervention [55].

The Surgical specimen analyzed in this study resisted the molecular target reagent cetuximab, which is an Epidermal growth factor receptor inhibitor [56]. Our cell death assay revealed that SpCC cell death was induced by the anticancer drug imatinib, which is known to inhibit protein tyrosine kinase activity of ABL, platelet-derived growth factor receptor α (PDGFRα), and KIT [57]. Mast Cells contribute to the aggressiveness of the pancreatic ductal Carcinoma enhancing the expression of several pro-angiogenic factors such as Vascular endothelial growth factor, fibroblast growth factor-2, platelet-derived growth factor and angiopoietin-1 as well as stimulating the pancreatic cancer Cells proliferation by IL-13 and tryptase [58]. Cell with distinctive prolongations called telopodes) has recently been identified in the stroma of various organs in humans [59]. Moreover, synovial telocytes coexpressed CD34 and platelet-derived growth factor receptor α [60].

The JMJD3 expression and proliferation markers in RA-FLS were higher than those in healthy-FLS and were upregulated in platelet-derived growth factor (PDGF)-induced FLS [61]. PDGFR-β small interfering RNA (siRNA) and IRF9 siRNA were injected intracerebroventricularly 48 h before SAH [62]. CatK gene deletion increased osteoblast differentiation via enhanced OCP and OC secretion of platelet-derived growth factor (PDGF)-BB and sphingosine 1 phosphate [63]. However, the effects of TRIM37 on airway smooth Muscle Cells (ASMCs) proliferation and migration are still unknown [64]. The Wnt/β-catenin pathway activator LiCl significantly reversed the inhibitory effects of TRIM37 on cell proliferation and migration in PDGF-BB-stimulated ASMCs [65].

Remodeling of the bronchial airways in COPD includes changes in both the bronchial epithelium and the subepithelial extracellular matrix (ECM) [66]. Sema3B and Sema3F expression was significantly lower in Arthritis patients fulfilling classification criteria for RA compared with those who did not [67]. FLS expression of Sema3A was induced after stimulation with TNF, IL-1β or lipopolysaccharides (LPS), while Sema3B and Sema3F expression was downregulated [68].

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 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 ,

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I have varied research interests ranging from eHealth, Health Information Exchange, Clinical Trials and Research, Contact Dermatitis, Bioinformatics, and Cosmetic Dermatology. I have work experience in Canada as an eHealth analyst, and in Dubai and India as a Specialist Dermatologist.


Bell Raj Eapen
Hamilton, ON