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

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[#CSB-EL017709CA] Cat platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Cat, Sample Type serum, plasma


CSB-EL017709CA | Cat platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Cat, Sample Type serum, plasma, 96T
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(1) Platelet-Derived Growth Factor BB Influences Muscle Regeneration in Duchenne Muscle Dystrophy.[TOP]

Pubmed ID :28618254
Publication Date : //
Duchenne muscular dystrophy (DMD) is characterized by a progressive loss of muscle fibers, and their substitution by fibrotic and adipose tissue. Many factors contribute to this process, but the molecular pathways related to regeneration and degeneration of muscle are not completely known. Platelet-derived growth factor (PDGF)-BB belongs to a family of growth factors that regulate proliferation, migration, and differentiation of mesenchymal cells. The role of PDGF-BB in muscle regeneration in humans has not been studied. We analyzed the expression of PDGF-BB in muscle biopsy samples from controls and patients with DMD. We performed in vitro experiments to understand the effects of PDGF-BB on myoblasts involved in the pathophysiology of muscular dystrophies and confirmed our results in vivo by treating the mdx murine model of DMD with repeated i.m. injections of PDGF-BB. We observed that regenerating and necrotic muscle fibers in muscle biopsy samples from DMD patients expressed PDGF-BB. In vitro, PDGF-BB attracted myoblasts and activated their proliferation. Analysis of muscles from the animals treated with PDGF-BB showed an increased population of satellite cells and an increase in the number of regenerative fibers, with a reduction in inflammatory infiltrates, compared with those in vehicle-treated mice. Based on our results, PDGF-BB may play a protective role in muscular dystrophies by enhancing muscle regeneration through activation of satellite cell proliferation and migration.

Authors : Piñol-Jurado Patricia, Gallardo Eduard, de Luna Noemi, Suárez-Calvet Xavier, Sánchez-Riera Carles, Fernández-Simón Esther, Gomis Clara, Illa Isabel, Díaz-Manera Jordi,

(2) Everolimus (RAD001) inhibits the proliferation of rat vascular smooth muscle cells by up-regulating the activity of the p27/kip1 gene promoter.[TOP]

Pubmed ID :27163533
Publication Date : //
We investigated whether the inhibitory effect of the immunosuppressant everolimus (RAD001) on vascular smooth muscle cell (VSMC) proliferation is mediated by p27/kip1 gene promoter activity.

Authors : Ran Boli, Li Minfeng, Li Yeqing, Lin Yang, Liu Weimin, Luo Qiulin, Fu Yongxin, Tang Qianmei, Yang Ya, Pu Yunfei,

(3) Chlorogenic acid protects against liver fibrosis in vivo and in vitro through inhibition of oxidative stress.[TOP]

Pubmed ID :27017478
Publication Date : //
Liver fibrosis is a scaring process related to chronic liver injury of all causes and as yet no truly effective treatment is available. Chlorogenic acid (CGA) is a phenolic compound and exerts anti-inflammatory and anti-oxidant activities. Our former studies suggested that CGA could prevent CCl-induced liver fibrosis through inhibition of inflammatory signaling pathway in rats. However, whether the anti-oxidant activity is involved in the anti-fibrotic effect of CGA on liver fibrosis is not yet fully understood. This study examined whether CGA may prevent CCl-induced liver fibrosis by improving anti-oxidant capacity via activation of Nrf2 pathway and suppressing the PDGF-induced profibrotic action via inhibition of NOX/ROS/MAPK pathway. The studies in vivo showed that the liver fibrosis degree, hydroxyproline content and expression of α-SMA, Collagen Ⅰ, Collagen Ⅲ and TIMP-1 were increased in CCl-injected rats and which were alleviated markedly by CGA. Furthermore, CGA significantly decreased CYP2E1 expression and increased the expression of nuclear Nrf2 and Nrf2-regulated anti-oxidant genes (HO-1, GCLC and NQO1). CGA decreased MDA level and increased GSH, SOD and CAT levels in liver tissues. In vitro studies PDGF could induce NOX subunits (p47phox and gp91phox) expression, ROS production, p38 and ERK1/2 phosphorylation, HSCs proliferation and profibrotic genes expression in HSCs, all of which were reduced by CGA treatment. In conclusion, the results suggest that CGA protects against CCl-induced liver fibrosis, at least in part, through the suppression of oxidative stress in liver and hepatic stellate cells.

Authors : Shi Haitao, Shi Ameng, Dong Lei, Lu Xiaolan, Wang Yan, Zhao Juhui, Dai Fei, Guo Xiaoyan,

(4) Cancer Stem-like Cells Act via Distinct Signaling Pathways in Promoting Late Stages of Malignant Progression.[TOP]

Pubmed ID :26719534
Publication Date : //
Cancer stem-like cells (CSC) play key roles in long-term tumor propagation and metastasis, but their dynamics during disease progression are not understood. Tumor relapse in patients with initially excised skin squamous cell carcinomas (SCC) is characterized by increased metastatic potential, and SCC progression is associated with an expansion of CSC. Here, we used genetically and chemically-induced mouse models of skin SCC to investigate the signaling pathways contributing to CSC function during disease progression. We found that CSC regulatory mechanisms change in advanced SCC, correlating with aggressive tumor growth and enhanced metastasis. β-Catenin and EGFR signaling, induced in early SCC CSC, were downregulated in advanced SCC. Instead, autocrine FGFR1 and PDGFRα signaling, which have not been previously associated with skin SCC CSC, were upregulated in late CSC and promoted tumor growth and metastasis, respectively. Finally, high-grade and recurrent human skin SCC recapitulated the signaling changes observed in advanced mouse SCC. Collectively, our findings suggest a stage-specific switch in CSC regulation during disease progression that could be therapeutically exploited by targeting the PDGFR and FGFR1 pathways to block relapse and metastasis of advanced human skin SCC.

Authors : da Silva-Diz Victoria, Simón-Extremera Pilar, Bernat-Peguera Adrià, de Sostoa Jana, Urpí Maria, Penín Rosa M, Sidelnikova Diana Pérez, Bermejo Oriol, Viñals Joan Maria, Rodolosse Annie, González-Suárez Eva, Moruno Antonio Gómez, Pujana Miguel Ángel, Esteller Manel, Villanueva Alberto, Viñals Francesc, Muñoz Purificación,

(5) Cancer metastases: challenges and opportunities.[TOP]

Pubmed ID :26579471
Publication Date : //
Cancer metastasis is the major cause of cancer morbidity and mortality, and accounts for about 90% of cancer deaths. Although cancer survival rate has been significantly improved over the years, the improvement is primarily due to early diagnosis and cancer growth inhibition. Limited progress has been made in the treatment of cancer metastasis due to various factors. Current treatments for cancer metastasis are mainly chemotherapy and radiotherapy, though the new generation anti-cancer drugs (predominantly neutralizing antibodies for growth factors and small molecule kinase inhibitors) do have the effects on cancer metastasis in addition to their effects on cancer growth. Cancer metastasis begins with detachment of metastatic cells from the primary tumor, travel of the cells to different sites through blood/lymphatic vessels, settlement and growth of the cells at a distal site. During the process, metastatic cells go through detachment, migration, invasion and adhesion. These four essential, metastatic steps are inter-related and affected by multi-biochemical events and parameters. Additionally, it is known that tumor microenvironment (such as extracellular matrix structure, growth factors, chemokines, matrix metalloproteinases) plays a significant role in cancer metastasis. The biochemical events and parameters involved in the metastatic process and tumor microenvironment have been targeted or can be potential targets for metastasis prevention and inhibition. This review provides an overview of these metastasis essential steps, related biochemical factors, and targets for intervention.

Authors : Guan Xiangming,

(6) Expression of platelet-derived growth factor BB, erythropoietin and erythropoietin receptor in canine and feline osteosarcoma.[TOP]

Pubmed ID :26189892
Publication Date : //
The discovery of expression of the erythropoietin receptor (EPO-R) on neoplastic cells has led to concerns about the safety of treating anaemic cancer patients with EPO. In addition to its endocrine function, the receptor may play a role in tumour progression through an autocrine mechanism. In this study, the expression of EPO, EPO-R and platelet-derived growth factor BB (PDGF-BB) was analysed in five feline and 13 canine osteosarcomas using immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR). EPO expression was positive in all tumours by IHC, but EPO mRNA was only detected in 38% of the canine and 40% of the feline samples. EPO-R was expressed in all samples by quantitative RT-PCR (RT-qPCR) and IHC. EPO-R mRNA was expressed at higher levels in all feline tumours, tumour cell lines, and kidney when compared to canine tissues. PDGF-BB expression was variable by IHC, but mRNA was detected in all samples. To assess the functionality of the EPO-R on tumour cells, the proliferation of canine and feline osteosarcoma cell lines was evaluated after EPO administration using an alamarBlue assay and Ki67 immunostaining. All primary cell lines responded to EPO treatment in at least one of the performed assays, but the effect on proliferation was very low indicating only a weak responsiveness of EPO-R. In conclusion, since EPO and its receptor are expressed by canine and feline osteosarcomas, an autocrine or paracrine tumour progression mechanism cannot be excluded, although in vitro data suggest a minimal role of EPO-R in osteosarcoma cell proliferation.

Authors : Meyer F R L, Steinborn R, Grausgruber H, Wolfesberger B, Walter I,

(7) Metformin reduces hepatic resistance and portal pressure in cirrhotic rats.[TOP]

Pubmed ID :26138461
Publication Date : //
Increased hepatic vascular resistance is the primary factor in the development of portal hypertension. Metformin ameliorates vascular cells function in several vascular beds. Our study was aimed at evaluating the effects, and the underlying mechanisms, of metformin on hepatic and systemic hemodynamics in cirrhotic rats and its possible interaction with the effects of propranolol (Prop), the current standard treatment for portal hypertension. CCl4-cirrhotic rats received by gavage metformin 300 mg/kg or its vehicle once a day for 1 wk, before mean arterial pressure (MAP), portal pressure (PP), portal blood flow (PBF), hepatic vascular resistance, and putative molecular/cellular mechanisms were measured. In a subgroup of cirrhotic rats, the hemodynamic response to acute Prop (5 mg/kg iv) was assessed. Effects of metformin ± Prop on PP and MAP were validated in common bile duct ligated-cirrhotic rats. Metformin-treated CCl4-cirrhotic rats had lower PP and hepatic vascular resistance than vehicle-treated rats, without significant changes in MAP or PBF. Metformin caused a significant reduction in liver fibrosis (Sirius red), hepatic stellate cell activation (α-smooth muscle actin, platelet-derived growth factor receptor β polypeptide, transforming growth factor-βR1, and Rho kinase), hepatic inflammation (CD68 and CD163), superoxide (dihydroethidium staining), and nitric oxide scavenging (protein nitrotyrosination). Prop, by decreasing PBF, further reduced PP. Similar findings were observed in common bile duct ligated-cirrhotic rats. Metformin administration reduces PP by decreasing the structural and functional components of the elevated hepatic resistance of cirrhosis. This effect is additive to that of Prop. The potential impact of this pharmacological combination, otherwise commonly used in patients with cirrhosis and diabetes, needs clinical evaluation.

Authors : Tripathi Dinesh M, Erice Eva, Lafoz Erica, García-Calderó Héctor, Sarin Shiv K, Bosch Jaime, Gracia-Sancho Jordi, García-Pagán Juan Carlos,

(8) Correlation between mutational status and survival and second cancer risk assessment in patients with gastrointestinal stromal tumors: a population-based study.[TOP]

Pubmed ID :25885906
Publication Date : //
Gastrointestinal stromal tumors are sarcomas of the digestive tract characterized by mutations mainly located in the c-KIT or in the platelet-derived growth factor receptor (PDGFR)-alpha genes. Mutations in the BRAF gene have also been described. Our purpose is to define the distribution of c-KIT, PDGFR and BRAF mutations in a population-based cohort of gastrointestinal stromal tumors (GIST) patients and correlate them with anatomical site, risk classification and survival. In addition, as most of the GIST patients have a long survival, second cancers are frequently diagnosed in them. We performed a second primary cancer risk assessment.

Authors : Rubió-Casadevall Jordi, Borràs Joan Lluis, Carmona-García Maria Carme, Ameijide Alberto, Gonzalez-Vidal Allan, Ortiz Maria Rosa, Bosch Ramon, Riu Francesc, Parada David, Martí Esther, Miró Josefina, Sirvent Juan Jose, Galceran Jaume, Marcos-Gragera Rafael,

(9) Genomic characterisation of the feline sarcoid-associated papillomavirus and proposed classification as Bos taurus papillomavirus type 14.[TOP]

Pubmed ID :25840470
Publication Date : //
Feline sarcoids are rare mesenchymal neoplasms of domestic and exotic cats. Previous studies have consistently detected short DNA sequences from a papillomavirus (PV), designated feline sarcoid-associated papillomavirus (FeSarPV), in these neoplasms. The FeSarPV sequence has never been detected in any non-sarcoid sample from cats but has been amplified from the skin of cattle suggesting that feline sarcoids are caused by cross-species infection by a bovine papillomavirus (BPV). The aim of the present study was to determine the genome of the PV that contains the FeSarPV sequence. Using the circular nature of PV DNA, four specifically designed 'outward facing' primers were used to amplify two approximately 4,000 bp DNA segments from a feline sarcoid. The two PCR products were sequenced using next generation sequencing and the full genome of the PV, consisting 7,966 bp, was assembled and analysed. Phylogenetic analysis revealed the PV was closely related to the species 4 delta BPVs-1, -2, and -13, but distantly related to any carnivoran PV genus. These results are consistent with feline sarcoids being caused by a BPV type and we propose a classification of BPV-14 for this novel PV. Initial analysis suggests that, like other delta BPVs, the BPV-14 E5 protein could cause mesenchymal proliferation by binding to the platelet derived growth factor beta receptor. Interestingly BPV-14 has not been detected in any equine sarcoid suggesting that BPV-14 has a host range that is limited to bovids and felids.

Authors : Munday John S, Thomson Neroli, Dunowska Magda, Knight Cameron G, Laurie Rebecca E, Hills Simon,

(10) Clinical outcome, PDGFRβ and KIT expression in feline histiocytic disorders: a multicentre study.[TOP]

Pubmed ID :25665137
Publication Date : //
Information about histiocytic disease in cats is limited. The aim of this study was to document clinical findings and outcome in feline histiocytic disorders, and characterize the expression of PDGFRβ and KIT in order to identify potential treatment targets. Morphologically diagnosed feline histiocytic tumours were reviewed and characterized by immunohistochemistry (IHC). Five cases of feline progressive histiocytosis (FPH), eight histiocytic sarcomas (HS) and two haemophagocytic histiocytic sarcomas (HaeHS) were confirmed. PDGFRβ was variably positive in most histiocytic cases, while KIT was negative in all. Clinical presentation, treatment and outcome were also evaluated. Partial responses were recorded in measurable disease with tyrosine kinase inhibitors and lomustine, and radiotherapy achieved long-term control in some cases. Survival times were shortest in HaeHS and disseminated disease. PDGFRβ, but not KIT, may represent a therapeutic target in feline histiocytic disorders but more studies are needed to investigate other potential treatment targets.

Authors : Treggiari E, Ressel L, Polton G A, Benoit J, Desmas I, Blackwood L,