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

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[#CSB-EL017709MO] Mouse platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Mouse, Sample Type serum, plasma


CSB-EL017709MO | Mouse platelet-derived growth factor beta polypeptide (simian sarcoma viral (v-sis) oncogene homolog) (PDGFB) ELISA kit, Species Mouse, Sample Type serum, plasma, 96T
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(1) Stress forces first lineage differentiation of mouse Embryonic Stem Cells, validation of a high throughput screen for toxicant stress.[TOP]

Pubmed ID :30328800
Publication Date : //
Mouse Embryonic Stem Cells (mESC) are unique in their self-renewal and pluripotency. Hypothetically, mESCs model gestational stress effects or stresses of in vitro fertilization/assisted reproductive technologies or drug/environmental exposures that endanger embryos. Testing mESCs stress responses should diminish and expedite in vivo embryo screening. Transgenic mESCs for green fluorescent protein (GFP) reporters of differ-entiation use the promoter for platelet-derived growth factor receptor (Pdgfr)a driving GFP expression to moni-tor hyperosmotic stress-forced mESC proliferation decrease (stunting), and differentiation increase that further stunts mESC population growth. In differentiating mESCs Pdgfra marks the first lineage extraembryonic primi-tive endoderm (ExEndo), Hyperosmotic stress forces mESC differentiation gain (Pdgfra-GFP) in monolayer or 3D embryoid bodies. Despite culture with potency-maintaining LIF, stress forces ExEndo as assayed using mi-croplate readers and validated by co-expression of Pdgfra-GFP, Disabled 2 (Dab2) and laminin by immunofluo-rescence and GFP protein and Dab2 by immunoblot. In agreement with previous reports, Rex1 and Oct4 loss was inversely proportional to increased Pdgfra-GFP mESC after treatment with high hyperosmotic sorbitol de-spite LIF. The increase in subpopulations of Pdgfra-GFP+ cells>background at ~23% was similar to the previ-ously reported ~25% increase in Rex1-RFP negative subpopulation at matched high sorbitol doses. By micro-plate reader there is a ~7-11fold increase in GFP at the a high submorbid and a morbid dose despite LIF, com-pared with LIF alone. By flow cytometry the subpopulation of Pdgfra-GFP+ cells>background increases ~8-16fold at these doses. Taken together the microplate, flow cytometry, immunoblot, and immunofluorescence data suggest that RA or hyperosmotic stress force dose-dependent differentiation whether LIF is present or not and this is negatively correlated with and possibly compensates for stress-forced diminished ESC population expansion and potency loss.

Authors : Li Quanwen, Louden Erica, Zhou Jordan, Drewlo Sascha, Dai Jing, Puscheck Elizabeth Ella, Chen Kang, Rappolee Daniel A,

(2) Conditional deletion of platelet derived growth factor receptor alpha (Pdgfra) in urorectal mesenchyme causes mesenchyme apoptosis and urorectal developmental anomalies in mice.[TOP]

Pubmed ID :30323271
Publication Date : //
In mammals, urorectal development starts at early embryonic stage, defective urorectal development results in anorectal malformations, which are common congenital developmental defects of the anus and the urethra in newborns. The etiology and embryology of the defects are still largely unknown. Platelet-derived growth factor receptor alpha (Pdgfra) is a cell surface receptor tyrosine kinase, upon binding to its ligands (Pdgfa-d), mediates intracellular signaling and regulates embryonic development. The expression of Pdgfra is tightly regulated in the developing urorectal mesenchyme, and its dysregulation is associated with urorectal defects in animals with urorectal defects. Knockout of Pdgfra induces early embryo lethality which precludes investigation of Pdgfra in urorectal development. To address the temporal requirement of Pdgfra in urorectal development, we conditionally deleted Pdgfra in Pdgfra-expressing tissues using a tamoxifen inducible Cre-loxP approach in mice, examined the urorectal development in Pdgfra conditional knockout (Pdgfra-cKO) embryos. We showed that conditional deletion of Pdgfra in Pdgfra-expressing tissues at E10-E11 caused cloaca septation defect, anteriorly displaced anus, defective urogenital folds development and abnormal urethra tubularization in both male and female mice. Furthermore, we showed that Pdgfra was required for the survival of urorectal mesenchyme, deletion of Pdgfra caused apoptosis in the peri-cloacal, the peri-urethra and the urorectal septum mesenchyme of Pdgfra-cKO mutants, associated with an induction of p53, Ndrg1 and activation of caspase-3 in Pdgfra-cKO embryos. In conclusion, Pdgfra is required for the development and survival of the urorectal mesenchyme in embryo, dysregulated Pdgfra signaling induced urorectal defects in mice resembling human congenital diseases of anorectal malformations and hypospadias. Perturbation of PDGFRA signaling may contribute to anorectal malformations and hypospadias in human.

Authors : Qian Chen, Wu Zhongluan, Ng Roy Chun-Laam, Garcia-Barceló Maria-Mercè, Yuan Zheng-Wei, Wong Kenneth Kak Yuen, Tam Paul Kwong Hang, Lui Vincent Chi Hang,

(3) Novel effect of sildenafil on hair growth.[TOP]

Pubmed ID :30292404
Publication Date : //
Sildenafil, a phosphodiesterase 5 (PDE5) inhibitor, is known to increase the intracellular level of cyclic guanosine monophosphate (cGMP), which causes vasodilation. However, the effect of sildenafil on human hair follicles (hHFs) is unknown.

Authors : Choi Hye-In, Kang Bo-Mi, Jang Jeehee, Hwang Sungjoo Tommy, Kwon Ohsang,

(4) An on-site preparable, novel bone-grafting complex consisting of human platelet-rich fibrin and porous particles made of a recombinant collagen-like protein.[TOP]

Pubmed ID :30270545
Publication Date : //
Platelet-rich fibrin (PRF) is widely used in regenerative medicine. Nonetheless, major issues include its controversial effects on bone regeneration and a lack of quality-assured glass tubes required for coagulation. We used porous particles (FBG) comprising a recombinant RGD motif-enriched collagen I-like protein to activate the coagulation pathway and examined the effects of the resulting PRF-FBG complex on bone regeneration. Human whole-blood samples were mixed with FBG in plastic tubes and centrifuged to prepare a PRF-FBG complex. Platelet-derived growth factor-BB (PDGF-BB) levels and cell growth activity were determined by ELISA and a bioassay using osteoblasts. Bone regenerative activity was assessed using a mouse model of calvarial bone defect. FBG facilitated PRF-like matrix formation during centrifugation. In this PRF-FBG complex, the microstructure of fibrin fibers was similar to that of PRF prepared conventionally in glass tubes. PDGF-BB levels and mitogenic action were not significantly influenced by FBG. In the bone defect model, although PRF did not exert any significant positive effects on its own, in combination with FBG, it synergistically stimulated new bone formation. This study demonstrated that incorporation of FBG into whole-blood samples induces PRF formation without the aid of glass tubes. The resulting PRF-FBG complex could be a promising bone grafting material in clinical settings. © 2018 Wiley Periodicals, Inc. J. Biomed. Mater. Res. Part B, 2018.

Authors : Tsukioka Tsuneyuki, Hiratsuka Takahiro, Nakamura Masayuki, Watanabe Taisuke, Kitamura Yutaka, Isobe Kazushige, Okudera Toshimitsu, Okudera Hajime, Azuma Akihiko, Uematsu Kohya, Nakata Koh, Kawase Tomoyuki,

(5) Copper Transporter ATP7A Interacts with IQGAP1, a Rac1 Binding Scaffold Protein: Role in PDGF-induced VSMC Migration and Vascular Remodeling.[TOP]

Pubmed ID :30257103
Publication Date : //
Vascular smooth muscle cell (VSMC) migration contributes to neointimal formation after vascular injury. We previously demonstrated that copper (Cu) transporter ATP7A is involved in PDGF-induced VSMC migration in Cu- and Rac1-dependent manner. Underlying mechanism is still unknown. Here we show that ATP7A interacts with IQGAP1, a Rac1- and receptor tyrosine kinase-binding scaffold proteins, which mediates PDGF-induced VSMC migration and vascular remodeling. In cultured rat aortic SMCs, PDGF stimulation rapidly promoted ATP7A association with IQGAP1 and Rac1, and their translocation to lipid rafts and leading edge. Co-transfection assay revealed that ATP7A directly bound to N-terminal domain of IQGAP1. Functionally, either ATP7A or IQGAP1 depletion using siRNA significantly inhibited PDGF-induced VSMC migration without additive effects, suggesting that IQGAP1 and ATP7A are in the same axis to promote migration. Furthermore, IQGAP1 siRNA blocked PDGF-induced ATP7A association with Rac1 as well as their translocation to leading edge while PDGF-induced IQGAP1 translocation was not affected by ATP7A siRNA or Cu chelator. Overexpression of mutant IQGAP1 lacking Rac1 binding site prevented PDGF-induced translocation of Rac1, but not ATP7A, to the leading edge, thereby inhibiting lamellipodia formation and VSMC migration. In vivo, ATP7A colocalized with IQGAP1 at neointimal VSMC in mice wire injury model, while neointimal formation and extracellular matrix deposition induced by vascular injury were inhibited in ATP7A mutant mice with reduced Cu transporter function. In summary, IQGAP1 functions as ATP7A and Rac1 binding scaffold protein to organize PDGF-dependent ATP7A translocation to the lamellipodial leading edge, thereby promoting VSMC migration and vascular remodeling.

Authors : Ashino Takashi, Kohno Takashi, Sudhahar Varadarajan, Ash Dipankar, Ushio-Fukai Masuko, Fukai Tohru,

(6) Endothelial cell activation on 3D-matrices derived from PDGF-BB-stimulated fibroblasts is mediated by Snail1.[TOP]

Pubmed ID :30250018
Publication Date : //
Carcinomas, such as colon cancer, initiate their invasion by rescuing the innate plasticity of both epithelial cells and stromal cells. Although Snail is a transcriptional factor involved in the Epithelial-Mesenchymal Transition, in recent years, many studies have also identified the major role of Snail in the activation of Cancer-Associated Fibroblast (CAF) cells and the remodeling of the extracellular matrix. In CAFs, Platelet-derived growth factor (PDGF) receptor signaling is a major functional determinant. High expression of both SNAI1 and PDGF receptors is associated with poor prognosis in cancer patients, but the mechanism(s) that underlie these connections are not understood. In this study, we demonstrate that PDGF-activated fibroblasts stimulate extracellular matrix (ECM) fiber remodeling and deposition. Furthermore, we describe how SNAI1, through the FAK pathway, is a necessary factor for ECM fiber organization. The parallel-oriented fibers are used by endothelial cells as "tracks", facilitating their activation and the creation of tubular structures mimicking in vivo capillary formation. Accordingly, Snail1 expression in fibroblasts was required for the co-adjuvant effect of these cells on matrix remodeling and neoangiogenesis when co-xenografted in nude mice. Finally, in tumor samples from colorectal cancer patients a direct association between stromal SNAI1 expression and the endothelial marker CD34 was observed. In summary, our results advance the understanding of PDGF/SNAI1-activated CAFs in matrix remodeling and angiogenesis stimulation.

Authors : Herrera Alberto, Herrera Mercedes, Guerra-Perez Natalia, Galindo-Pumariño Cristina, Larriba María Jesús, García-Barberán Vanesa, Gil Beatriz, Giménez-Moyano Sara, Ferreiro-Monteagudo Reyes, Veguillas Pilar, Candia Antonio, Peña Raúl, Pinto Jesús, García-Bermejo Mª Laura, Muñoz Alberto, García de Herreros Antonio, Bonilla Félix, Carrato Alfredo, Peña Cristina,

(7) MiR-218 regulated cardiomyocyte differentiation and migration in mouse embryonic stem cells by targeting PDGFRα.[TOP]

Pubmed ID :30246400
Publication Date : //
MicroRNAs (miRNAs) have been identified as key players in cardiogenesis and heart pathophysiological processes. However, many miRNAs are still not recognized for their roles in cardiomyocytes differentiation. In this study, we evaluated the effects of microRNA-218 (miR-218) in cardiomyocyte differentiation of the mouse embryonic stem cells (ESCs) in vitro. The percentage of the beating embryoid bodies (EBs) in miR-218 mimic-treated cells was reduced to 32% compared with miR-218 mimic negative control (56%) on day 5 + 3. The amplitude of the intracellular Ca transients in the cardiomyocytes derived from ESCs was reduced upon miR-218 overexpression, followed by the decreased calcium-related proteins and cell junction proteins expressions. Besides, miR-218 expression in ESCs was related to the directional spreading ability of EBs during differentiation. The increased expression of miR-218 could promote the migration of ESCs in vitro, while the decreased expression of miR-218 could inhibit the migration by the transwell experiment. Meanwhile, miR-218 could regulate cell migration-related proteins Cdc42 and Rac1. Platelet-derived growth factor receptor α (PDGFRα) was further confirmed to be a direct target of miR-218 both physically and functionally by dual-luciferase reporter assay. Our data further described that overexpression of PDGFRα rescued the miR-218-mediated inhibition of cardiomyocyte differentiation and restored the miR-218-mediated promotion of cell migration. In conclusion, miR-218 was demonstrated to exert an inhibitory function and promoted cell migration via targeting PDGFRα during cardiomyocyte differentiation from ESCs. The current study revealed the role of miR-218 and may provide an important hint for cardiomyocyte differentiation of ESCs and induced pluripotent stem cells.

Authors : Xu Tingting, Liu Nuoya, Shao Ying, Huang Yujie, Zhu Danyan,

(8) Nck1 Deficiency Impairs Adipogenesis by Activation of PDGFRα in Preadipocytes.[TOP]

Pubmed ID :30240612
Publication Date : //
Obesity results from an excessive expansion of white adipose tissue (WAT), which is still poorly understood from an etiologic-mechanistic perspective. Here, we report that Nck1, a Src homology domain-containing adaptor, is upregulated during WAT expansion and in vitro adipogenesis. In agreement, Nck1 mRNA correlates positively with peroxisome proliferator-activated receptor (PPAR) γ and adiponectin mRNAs in the WAT of obese humans, whereas Nck1-deficient mice display smaller WAT depots with reduced number of adipocyte precursors and accumulation of extracellular matrix. Furthermore, silencing Nck1 in 3T3-L1 preadipocytes increases the proliferation and expression of genes encoding collagen, whereas it decreases the expression of adipogenic markers and impairs adipogenesis. Silencing Nck1 in 3T3-L1 preadipocytes also promotes the expression of platelet-derived growth factor (PDGF)-A and platelet-derived growth factor receptor (PDGFR) α activation and signaling. Preventing PDGFRα activation using imatinib, or through PDGF-A or PDGFRα deficiency, inhibits collagen expression in Nck1-deficient preadipocytes. Finally, imatinib rescues differentiation of Nck1-deficient preadipocytes. Altogether, our findings reveal that Nck1 modulates WAT development through PDGFRα-dependent remodeling of preadipocytes.

Authors : Haider Nida, Dusseault Julie, Larose Louise,

(9) Excess vascular endothelial growth factor-A disrupts pericyte recruitment during blood vessel formation.[TOP]

Pubmed ID :30238211
Publication Date : //
Pericyte investment into new blood vessels is essential for vascular development such that mis-regulation within this phase of vessel formation can contribute to numerous pathologies including arteriovenous and cerebrovascular malformations. It is critical therefore to illuminate how angiogenic signaling pathways intersect to regulate pericyte migration and investment. Here, we disrupted vascular endothelial growth factor-A (VEGF-A) signaling in ex vivo and in vitro models of sprouting angiogenesis, and found pericyte coverage to be compromised during VEGF-A perturbations. Pericytes had little to no expression of VEGF receptors, suggesting VEGF-A signaling defects affect endothelial cells directly but pericytes indirectly. Live imaging of ex vivo angiogenesis in mouse embryonic skin revealed limited pericyte migration during exposure to exogenous VEGF-A. During VEGF-A gain-of-function conditions, pericytes and endothelial cells displayed abnormal transcriptional changes within the platelet-derived growth factor-B (PDGF-B) and Notch pathways. To further test potential crosstalk between these pathways in pericytes, we stimulated embryonic pericytes with Notch ligands Delta-like 4 (Dll4) and Jagged-1 (Jag1) and found induction of Notch pathway activity but no changes in PDGF Receptor-β (Pdgfrβ) expression. In contrast, PDGFRβ protein levels decreased with mis-regulated VEGF-A activity, observed in the effects on full-length PDGFRβ and a truncated PDGFRβ isoform generated by proteolytic cleavage or potentially by mRNA splicing. Overall, these observations support a model in which, during the initial stages of vascular development, pericyte distribution and coverage are indirectly affected by endothelial cell VEGF-A signaling and the downstream regulation of PDGF-B-PDGFRβ dynamics, without substantial involvement of pericyte Notch signaling during these early stages.

Authors : Darden Jordan, Payne Laura Beth, Zhao Huaning, Chappell John C,

(10) Phenotype of Vascular Smooth Muscle Cells (VSMCs) Is Regulated by miR-29b by Targeting Sirtuin 1.[TOP]

Pubmed ID :30231015
Publication Date : //
BACKGROUND Phenotypic switch of vascular smooth muscle cells (VSMCs) participates in the etiology of various vascular diseases. It has been proved that microRNAs (miRNAs) serve as crucial regulators of functions of VSMCs. This study aimed to discover how miR-29b regulates the transformation of VSMCs phenotypes in mice. MATERIAL AND METHODS Primary VSMCs of aorta in mice were cultured in DMEM medium. A series of experiments involving transfection of oligonucleotides in cultured VSMCs, quantitative reverse transcription PCR (qRT-PCR), luciferase reporter assay, and Western blotting analysis were performed in this study. RESULTS We found that in VSMCs cultured in presence of stimulator, platelet-derived growth factor-BB (PDGF-BB), miR-29b was upregulated significantly and expressions of VSMC-phenotype-related genes (α-SMA, calponin, and SM-MHC) were regulated by miR-29b. Moreover, through downregulation of sirtuin 1 (SIRT1), miR-29b affects phenotypic transformation of VSMCs. Luciferase report assay identified a significant increase of SIRT1 3'-UTR activity in treatment with miR-29b inhibitor, which, however, was reversed in the presence of miR-29b mimic. Suppression of miR-29b reversed the activation of NF-κB induced by PDGF-BB in VSMCs. CONCLUSIONS We concluded that miR-29b is an important regulator in the PDGF-BB-mediated VSMC phenotypic transition by targeting SIRT1. Interventions aimed at miR-29b may be promising in treating numerous proliferative vascular disorders.

Authors : Sun Qian-Ru, Zhang Xiong, Fang Kun,