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Pig platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Pig, Sample Type serum, plasma

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[#CSB-EL017709PI] Pig platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Pig, Sample Type serum, plasma

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CSB-EL017709PI | Pig platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Pig, Sample Type serum, plasma, 96T
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(1) Comparative immunohistochemical characterization of interstitial cells in the urinary bladder of human, guinea pig and pig.[TOP]

Pubmed ID :29464320
Publication Date : //
Interstitial cells (ICs) are thought to play a functional role in urinary bladder. Animal models are commonly used to elucidate bladder physiology and pathophysiology. However, inter-species comparative studies on ICs are rare. We therefore analyzed ICs and their distribution in the upper lamina propria (ULP), the deeper lamina propria (DLP) and the detrusor muscular layer (DET) of human, guinea pig (GP) and pig. Paraffin slices were examined by immunohistochemistry and 3D confocal immunofluorescence of the mesenchymal intermediate filament vimentin (VIM), alpha-smooth muscle actin (αSMA), platelet-derived growth factor receptor alpha (PDGFRα) and transient receptor potential cation channel A1 (TRPA1). Image stacks were processed for analysis using Huygens software; quantitative analysis was performed with Fiji macros. ICs were identified by immunoreactivity for VIM (excluding blood vessels). In all species ≥ 75% of ULP ICs were VIM/PDGFRα and ≥ 90% were VIM/TRPA1. In human and pig ≥ 74% of ULP ICs were VIM/αSMA, while in GP the percentage differed significantly with only 37% VIM/αSMA ICs. Additionally, over 90% of αSMA ICs were also TRPA1 and PDGFRα in human, GP and pig. In all three species, TRPA1 and PDGFRα ICs point to an active role for these cells in bladder physiology, regarding afferent signaling processes and signal modification. We hypothesize that decline in αSMA-positivity in GP reflects adaptation of bladder histology to smaller bladder size. In our experiments, pig bladder proved to be highly comparable to human urinary bladder and seems to provide safer interpretation of experimental findings than GP.

Authors : Steiner Clara, Gevaert Thomas, Ganzer Roman, De Ridder Dirk, Neuhaus Jochen,



(2) PDGFRα Regulated by miR-34a and FoxO1 Promotes Adipogenesis in Porcine Intramuscular Preadipocytes through Erk Signaling Pathway.[TOP]

Pubmed ID :29140299
Publication Date : //
Suitable intramuscular fat (IMF) content improves porcine meat quality. The vital genes regulating IMF deposition are necessary for the selection and breeding of an IMF trait. However, the effect and mechanism of on IMF deposition are still unclear. Here, is moderately expressed in porcine longissimus dorsi muscle (LD), whereas it highly expressed in white adipose tissue (WAT). Moreover, -positive cells were located in the gaps of LD fibers which there were IMF adipocytes. Compared with 180-day-old and lean-type pigs, the levels of were much higher in one-day-old and fat-type pigs. Meanwhile the levels of gradually decreased during IMF preadipocyte differentiation. Furthermore, promoted adipogenic differentiation through activating Erk signaling pathway. Based on upstream regulation analysis, we found that the knockdown of repressed lipogenesis by downregulating , and miR-34a inhibited adipogenesis through targeting . Collectively, is a positive regulator of IMF deposition. Therefore, we suggest that is a possible target to improve meat quality.

Authors : Sun Yun-Mei, Qin Jin, Liu Shu-Ge, Cai Rui, Chen Xiao-Chang, Wang Xiang-Ming, Pang Wei-Jun,



(3) Autologous fat transplants to deliver glitazone and adiponectin for vasculoprotection.[TOP]

Pubmed ID :28867378
Publication Date : //
The insulin sensitizing glitazone drugs, rosiglitazone (ROS) and pioglitazone (PGZ) both have anti-proliferative and anti-inflammatory effects and induce adipose tissue (fat) to produce the vaso-protective protein adiponectin. Stenosis due to intimal hyperplasia development often occurs after placement of arteriovenous synthetic grafts used for hemodialysis. This work was performed to characterize the in vitro and in vivo effects of ROS or PGZ incorporation in fat and to determine if fat/PGZ depots could decrease vascular hyperplasia development in a porcine model of hemodialysis arteriovenous graft stenosis. Powdered ROS or PGZ (6-6000μM) was mixed with fat explants and cultured. Drug release from fat was quantified by HPLC/MS/MS, and adiponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture media were measured by ELISA. 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. In a porcine model, pharmacokinetics of PGZ from fat depots transplanted perivascular to jugular vein were assessed by HPLC/MS/MS, and retention of the fat depot was monitored by MRI. A porcine model of synthetic graft placed between carotid artery and ipsilateral jugular vein was used to assess effects of PGZ/fat depots on vascular hyperplasia development. Both ROS and PGZ significantly induced the release of adiponectin and inhibited release of MCP-1 from the fat. TNF production from monocytes stimulated with LPS was inhibited 50-70% in the presence of media conditioned by fat alone or fat and either drug. The proliferation of SMC was inhibited in the presence of media conditioned by fat/ROS cultures. Fat explants placed perivascular to the external jugular vein were retained, as confirmed by MRI at one week after placement. PGZ was detected in the fat depot, in the external jugular vein wall and in adjacent tissue at clinically relevant levels, whereas levels in plasma were below detection. External jugular vein exposed to fat incorporated with PGZ had increased adiponectin expression compared to vein exposed to fat alone. However, the development of hyperplasia within the arteriovenous synthetic grafts was unchanged by treatment with fat/PGZ depots compared to no treatment.

Authors : Sanders William G, Li Huan, Zhuplatov Ilya, He Yuxia, Kim Seong-Eun, Cheung Alfred K, Agarwal Jayant, Terry Christi M,



(4) Reprogramming Bone Marrow Stem Cells to Functional Endothelial Cells in a Mini Pig Animal Model.[TOP]

Pubmed ID :28814711
Publication Date : //
BACKGROUND The aims of this study were to compare the morphological, biochemical, and functional properties of reprogrammed bone marrow stem cell (BMSC)-derived arterial endothelial cells (AECs) and venous endothelial cells (VECs), following adenosine triphosphate (ATP)-stimulation in a mini pig animal model. MATERIAL AND METHODS Bone marrow aspiration was performed in six adult mini pigs. Harvested mononuclear cells were isolated, cultured, and treated with vascular endothelial growth factor (VEGF) (16 µg/ml). Transformed cells were characterized using immunofluorescence staining for CD31 and von Willebrandt factor (vWF) and expression of endothelial nitric oxide synthase (eNOS). Cell release of nitric oxide (cNO) was measured using spectrophotometry. Matrigel assays were used to investigate angiogenesis in transformed BMSCs. RESULTS Reprogrammed BMSCs in culture showed a typical cobblestone-like pattern of growth. Immunofluorescence staining was positive for CD31 and vWF expression. Expression of eNOS, using immunofluorescence staining and Western blot, showed no difference between the reprogrammed BMSCs and VECs. Spectrophotometric examination following stimulation with 10mmol/l ATP, showed comparable cNO release for reprogrammed BMSCs (10.87±1.76 pmol/106 cells/min) and VECs (13.23±2.16 pmol/10^6 cells/min), but reduced cNO release for AECS (3.44±0.75 pmol/10^6 cells/min). Matrigel assay for angiogenesis showed vascular tube formation of differentiated BMSC endothelial cells (grade 3.25). BMSCs cultured without VEGF did not demonstrate vascular tube formation. CONCLUSIONS The findings of this study showed that eNOS expression and release of NO could be used to show that BMSCs can be reprogrammed to functional VECs and AECs.

Authors : Schlegel Franziska, Appler Marco, Halling Michelle, Smit Francis Edwin, Mohr Friedrich-Wilhelm, Dhein Stefan, Dohmen Pascal Maria,



(5) Efficacy of platelets in bone healing: A systematic review on animal studies.[TOP]

Pubmed ID :28643535
Publication Date : //
In presence of large bone defects, delayed bone union, non-union, fractures, and implant surgery, bone reconstruction may be necessary. Different strategies have been employed to enhance bone healing among which the use of autologous platelet concentrates. Due to the high content of platelets and platelet-derived bioactive molecules (e.g., growth factors, antimicrobial peptides), they are promising candidates to increase bone healing. However, a high heterogeneity of both preclinical and clinical studies resulted in contrasting results. Aim of the present systematic review was to evaluate the efficacy of platelet concentrates in animal models of bone regeneration, considering the possible factors which might affect the outcome. An electronic search was performed on MEDLINE and SCOPUS databases. Animal studies with a minimum follow up of 2 weeks and a sample size of five subjects per group, using platelet concentrates for bone regeneration, were included. Articles underwent risk of bias assessment and further quality evaluation was done. Sixty studies performed on six animal species (rat, rabbit, dog, sheep, goat, and mini-pig) were included. The present part of the review considers only studies performed on rats and rabbits (35 articles). The majority of the studies were considered at medium risk of bias. Animal species, healthy models, platelet, growth factors and leukocytes concentration, and type of bone defect seemed to influence the efficacy of platelet concentrates in bone healing. However, final conclusions were not be drawn, since only few included studies evaluated leukocyte, growth factor content, or presence of other bioactive molecules in platelet concentrates. Further studies with a standardized protocol including characterization of the final products will provide useful information for clinical application of platelet concentrates in bone surgery.

Authors : Marcazzan Sabrina, Weinstein Roberto Lodovico, Del Fabbro Massimo,



(6) Characterization of bladder acellular matrix hydrogel with inherent bioactive factors.[TOP]

Pubmed ID :28532019
Publication Date : //
Bladder acellular matrix (BAM) hydrogel may have great potential in tissue engineering due to outstanding biocompatibility and the presence of inherent bioactive factors in BAM. In this study, we prepared the BAM hydrogel by the method of enzymatic solubilization with pepsin and characterize the microrheological properties of the BAM precursor solution. The structures of the BAM hydrogel were characterized by scanning electron microscope (SEM), Fourier-transform infrared spectroscopy (FTIR) and differential scanning calorimetry (DSC). Furthermore, the growth factors including vascular endothelial growth factor (VEGF), platelet-derived growth factor B (PDGF-BB), keratinocyte growth factor (KGF) were quantified by ELISA. The biological performances of the hydrogels were evaluated by cultivating porcine iliac endothelial cells (PIECs) in vitro. Lyophilized BAM showed porous structure with pore diameter ranging from 50 to 100μm. BAM 4-G hydrogel (4mg/mL) with a short gelation time of 3.95±0.07min presents better thermal stability than BAM 6-G hydrogel (6mg/mL). Growth factors in the BAM hydrogel maintain valuable biological activity even after digestion process. The BAM hydrogel supported the adhesion and growth of PIECs well and has great potential for further tissue engineering.

Authors : Jiang Dan, Huang Jianwen, Shao Huili, Hu Xuechao, Song Lujie, Zhang Yaopeng,



(7) Neuropilin 1 binds PDGF-D and is a co-receptor in PDGF-D-PDGFRβ signaling.[TOP]

Pubmed ID :28254885
Publication Date : //
Platelet-derived growth factor (PDGF)-D is a PDGF receptor β (PDGFRβ)-specific ligand implicated in a number of pathological conditions, such as cardiovascular disease and cancer, but its biological function remains incompletely understood. In this study, we demonstrate that PDGF-D binds directly to neuropilin 1 (NRP1), in a manner that requires the PDGF-D C-terminal Arg residue. Stimulation with PDGF-D, but not PDGF-B, induced PDGFRβ-NRP1 complex formation in fibroblasts. Additionally, PDGF-D induced translocation of NRP1 to cell-cell junctions in endothelial cells, independently of PDGFRβ, altering the availability of NRP1 for VEGF-A-VEGFR2 signaling. PDGF-D showed differential effects on pericyte behavior in sprouting assays compared to PDGF-B. Furthermore, PDGF-D-induced PDGFRβ-NRP1 interaction can occur in between molecules located in different cells (endothelial cells and pericytes). In summary, we show that NRP1 can act as a co-receptor for PDGF-D-PDGFRβ signaling and is possibly implicated in intercellular communication in the vascular wall.

Authors : Muhl Lars, Folestad Erika Bergsten, Gladh Hanna, Wang Yixin, Moessinger Christine, Jakobsson Lars, Eriksson Ulf,



(8) The MEK1 inhibitors UO126 and PD98059 block PDGF-AB induced phosphorylation of threonine 292 in porcine smooth muscle cells.[TOP]

Pubmed ID :28235676
Publication Date : //
PDGF-AB and FGF-2 (GFs) induce smooth muscle cell (SMC) proliferation which is indispensible for arteriogenesis. While there is common agreement that GFs stimulate SMC proliferation through phosphorylation (P-) of MEK1/2 at Ser218/222, we previously demonstrated that the MEK inhibitors PD98059 and UO126 did not inhibit P-Ser218/222 as originally proposed but caused strong hyperphosphorylation. Here, we demonstrate that GFs increased phosphorylation of MEK1 at Thr292 while UO126 and PD98059 blocked this phosphorylation. This was again surprising since phosphorylation of Thr292 is regarded as a negative feedback loop. Our findings suggest that inhibition of Thr292 phosphorylation in combination with hyperphosphorylation of Ser218/222 serves as an "off" switch of SMC proliferation and potentially of arteriogenesis.

Authors : Kubin Thomas, Cetinkaya Ayse, Schönburg Markus, Beiras-Fernandez Andres, Walther Thomas, Richter Manfred,



(9) Validation of Cross-Species Reactivity of the VEGF-A/PDGFRβ Bifunctional Antibody PF-06653157.[TOP]

Pubmed ID :27736501
Publication Date : //
PF-06653157 is a bifunctional antagonist monoclonal antibody (mAb) that targets human VEGF-A ligand and PDGF-Rβ. With the advent of PF-06653157 as an angiogenesis inhibitor and potential treatment for angiogenesis deregulation diseases, a relevant toxicology species is needed for toxicity and efficacy studies. Investigative studies were conducted to validate the mAb dual antagonist properties in a human system and determine its cross-reactive pharmacology in nonhuman cells.

Authors : Ashoor Roshan, Lee Dong, Cheng Alvan, Jessen Bart, Huang Wenhu,



(10) Arsenite suppresses angiogenesis of vascular endothelial cells mediated by Platelet Derived Growth Factor Receptor-beta.[TOP]

Pubmed ID :27475902
Publication Date : //
The present study aimed to investigate the effects of sodium arsenite (NaAsO2) on the angiogenesis of human umbilical vein endothelial cells (HUVECs) and the mechanism involved. Firstly, a Matrigel-based in vitro angiogenesis assay demonstrated that arsenite suppressed the angiogenesis of HUVECs in a dose-dependent manner. Then by using a global inhibitor for multiple growth factor receptors (E7080) and a specific inhibitor of PDGFR-beta (CP-673451), we found that E7080 completely prevented and CP-673451 significantly decreased the angiogenesis of HUVECs. This suggested that angiogenesis of HUVECs depends on the signal pathway mediated by tyrosine kinase receptors and that among them, PDGFR-beta has an important regulatory function. Finally by using porcine aortic endothelial cells which stably express human PDGFR-beta, we found that arsenite suppressed the angiogenesis mediated by PDGFR-beta. Based on these results, we conclude that arsenite suppressed the angiogenesis of the vascular endothelial cells, that this effect is mediated by PDGFR-beta, and postulate that it might contribute to the injuries of blood vessel in arsenism.

Authors : Wang Xiaotong, Mou Yan, Yue Zhen, Zhang Haiying, Su Xuejin, Wang Yang, Li Ronggui, Sun Xin,