Only in Titles

           Search results for: Bovine Fibroblast surface protein   

paperclip

#28647625   2017/06/25 Save this To Up

Thermoresponsive poly(glycidyl ether) brushes on gold: Surface engineering parameters and their implication for cell sheet fabrication.

Thermoresponsive polymer coatings, optimized for cell adhesion and thermally-triggered cell detachment, allow the fabrication of confluent cell sheets with intact extracellular matrix. However, rational design guidelines for such coatings are rare, since temperature-triggered cell adhesion and detachment from thermoresponsive surfaces are mechanistically not well understood. Herein, we investigated the impact of molecular weight (2, 9, 24kDa), grafting density (0.04-1.4 chains nm(-2)), morphology, and roughness of well-characterized thermoresponsive poly(glycidyl ether) brushes on the cell response at 37 and 20°C. NIH 3T3 mouse fibroblasts served as a model cell line for adhesion, proliferation, and cell sheet detachment. The cell response was correlated with serum protein adsorption from cell culture medium containing 10% fetal bovine serum. Intact cell sheets could be harvested from all the studied poly(glycidyl ether) coated surfaces, irrespective of the molecular weight, provided that the morphology of the coating was homogenous and the surface was fully shielded by the hydrated brush. The degree of chain overlap was estimated by the ratio of twice the polymer's Flory radius in a theta solvent to its interchain distance, which should be located in the strongly overlapping brush regime (2 Rf/l>1.4). In contrast, dense PNIPAM (2.5kDa) control monolayers did not induce protein adsorption from cell culture medium at 37°C and, as a result, did not allow a significant cell adhesion. These structural design parameters of functional poly(glycidyl ether) coatings on gold will contribute to future engineering of these thermoresponsive coatings on more common, cell culture relevant substrates.

2432 related Products with: Thermoresponsive poly(glycidyl ether) brushes on gold: Surface engineering parameters and their implication for cell sheet fabrication.

Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media Cellufine Formyl , 10 ml Cellufine Formyl Media Cellufine Formyl Media (S)-(+)-Benzyl Glycidyl E Rabbit Anti-cellulase Pol Rabbit Anti-Cell death in Multiple lung carcinoma (

Related Pathways

  •  
  • No related Items
paperclip

#28642037   2017/06/23 Save this To Up

Testosterone regulates 3T3-L1 pre-adipocyte differentiation and epididymal fat accumulation in mice through modulating macrophage polarization.

Low testosterone levels are strongly related to obesity in males. The balance between the classically M1 and alternatively M2 polarized macrophages also plays a critical role in obesity. It is not clear whether testosterone regulates macrophage polarization and then affects adipocyte differentiation. In this report, we demonstrate that testosterone strengthens interleukin (IL) -4-induced M2 polarization and inhibits lipopolysaccharide (LPS)-induced M1 polarization, but has no direct effect on adipocyte differentiation. Cellular signaling studies indicate that testosterone regulates macrophage polarization through the inhibitory regulative G-protein (Gαi) mainly, rather than via androgen receptors, and phosphorylation of Akt. Moreover, testosterone inhibits pre-adipocyte differentiation induced by M1 macrophage medium. Lowering of serum testosterone in mice by injecting a luteinizing hormone receptor (LHR) peptide increases epididymal white adipose tissue. Testosterone supplementation reverses this effect. Therefore, our findings indicate that testosterone inhibits pre-adipocyte differentiation by switching macrophages to M2 polarization through the Gαi and Akt signaling pathways.

2623 related Products with: Testosterone regulates 3T3-L1 pre-adipocyte differentiation and epididymal fat accumulation in mice through modulating macrophage polarization.

Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Gro g Macrophage In Macrophage Colony Stimula Macrophage Colony Stimula Mouse Macrophage Inflamma Mouse Macrophage Inflamma Mouse Macrophage Inflamma Mouse Macrophage Inflamma

Related Pathways

paperclip

#28537766   2017/05/24 Save this To Up

Pirfenidone Induces G1 Arrest in Human Tenon's Fibroblasts In Vitro Involving AKT and MAPK Signaling Pathways.

To investigate the underlying mechanism by which pirfenidone blocks the transition from the G1 to S phase in primary human Tenon's fibroblasts.

2412 related Products with: Pirfenidone Induces G1 Arrest in Human Tenon's Fibroblasts In Vitro Involving AKT and MAPK Signaling Pathways.

MID1 interacting G12-like AKT PKB Signaling Phospho GPCR Signaling to MAPK ER AKT1 & MAPK14 Protein Pro AKT1 & MAPKAPK2 Protein P PathwayReady™ PI3 K Akt Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Interferon-a Receptor Typ Goat Anti-Human Synaptota Goat Anti-Human STK39 SPA Goat Anti-Human SPHK1, (i

Related Pathways

  •  
  • No related Items
paperclip

#28489410   2017/05/10 Save this To Up

Strategically Designing a Pumpless Microfluidic Device on an "Inert" Polypropylene Substrate with Potential Application in Biosensing and Diagnostics.

This study is an attempt to make a step forward to implement the very immature concept of pumpless transportation of liquid into a real miniaturized device or lab-on-chip (LOC) on a plastic substrate. "Inert" plastic materials such as polypropylene (PP) are used in a variety of biomedical applications but their surface engineering is very challenging. Here, it was demonstrated that with a facile innovative wettability patterning route using fluorosilanized UV-independent TiO2 nanoparticle coating it is possible to create wedge-shaped open microfluidic tracks on inert solid surfaces for low-cost biomedical devices (lab-on-plastic). For the future miniaturization and integration of the tracks into a device, a variety of characterization techniques were used to not only systematically study the surface patterning chemistry and topography but also to have a clear knowledge of its biological interactions and performance. The effect of such surface architecture on the biological performance was studied in terms of static/dynamic protein (bovine serum albumin) adsorption, bacterial (Staphylococcus aureus and Staphylococcus epidermidis) adhesion, cell viability (using HeLa and MCF-7 cancer cell lines as well as noncancerous human fibroblast cells), and cell patterning (Murine embryonic fibroblasts). Strategies are discussed for incorporating such a confined track into a diagnostic device in which its sensing portion is based on protein, microorganism, or cells. Finally, for the proof-of-principle of biosensing application, the well-known high-affinity molecular couple of BSA-antiBSA as a biological model was employed.

1222 related Products with: Strategically Designing a Pumpless Microfluidic Device on an "Inert" Polypropylene Substrate with Potential Application in Biosensing and Diagnostics.

Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A Th1 Th2 Th17 (Human) Anti Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A Th1 Th2 Th17 (Human) Anti HIV 2 env gp36 recombinan Anti HTLV I gp46 Clone 65 MONOBODIES (Monoclonal An Integrin β1 (CD29) Antib

Related Pathways

paperclip

#28451903   2017/04/28 Save this To Up

A single L288I substitution in the fusion protein of bovine parainfluenza virus type 3 enhances virus growth in semi-suitable cell lines.

The bovine parainfluenza virus type 3 BN-CE vaccine strain was obtained by serial passage of the BN-1 strain in chicken embryonic fibroblasts (CEF). We previously identified a substitution (L288I) in the fusion (F) protein between the two strains. To examine the effect of the substitution on CEF adaptation and attenuation, we generated a recombinant BN-1 strain with the L288I substitution in the F protein (F(L288I)-EGFP). F(L288I)-EGFP replicated more efficiently than a recombinant BN-1 strain (wt-EGFP) in semi-suitable cell lines, suggesting that the L288I substitution was established in the BN-1 strain during the process of adaptation in CEF.

2333 related Products with: A single L288I substitution in the fusion protein of bovine parainfluenza virus type 3 enhances virus growth in semi-suitable cell lines.

Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Native Parainfluenza Viru Rabbit Anti-Cell death in Anti-Infectious Pancreati Anti-Infectious Pancreati

Related Pathways

paperclip

#28380519   2017/04/05 Save this To Up

Evidence that gene expression of ovarian follicular tight junction proteins is regulated in vivo and in vitro in cattle.

Tight junctions (TJ) are common paracellular sealing structures that control the transport of water, ions, and macromolecules across cell layers. Because the role of TJ in bovine follicular development is unknown, we investigated the developmental and hormonal regulation of the transmembrane TJ protein, occludin (OCLN), and the cytoplasmic TJ proteins, TJ protein 1 (TJP1) and cingulin (CGN) in bovine granulosa cells (GC) and theca cells (TC). For this purpose, bovine GC and TC were isolated from large (>8 mm) and/or small (1 to 5 mm) follicles and either extracted for real-time PCR (qPCR) or cultured in vitro. The abundances of both and mRNA were greater ( < 0.05) in TC than GC, whereas the mRNA abundance was greater ( < 0.05) in GC than TC. The abundance of mRNA in both GC and TC was greater ( < 0.05) in small follicles compared with large follicles, whereas the GC of large follicles had less ( < 0.05) mRNA abundance than the GC of small follicles. The abundance of mRNA in GC or TC did not differ ( > 0.10) among follicle sizes. In vitro treatment with various growth factors known to affect ovarian folliculogenesis indicated that , , and were hormonally regulated. Fibroblast growth factor 9 (FGF9) decreased ( < 0.05) the and mRNA abundances. Tumor necrosis factor α (TNFα) and vascular endothelial growth factor A (VEGFA) increased ( < 0.05) the mRNA abundance but decreased ( < 0.05) the mRNA abundance. Dexamethasone (DEX) increased ( < 0.05) and mRNA abundances. Epidermal growth factor (EGF) decreased ( < 0.05) and dihydrotestosterone (DHT) increased ( < 0.05) the abundances of , , and mRNA. We propose that the downregulation of OCLN and other TJ proteins during follicular development could reduce barrier function, thereby participating in increasing follicle size by allowing for an increase in the volume of follicular fluid as well as by allowing additional serum factors into the follicular fluid that potentially may directly impact GC functions. The results of the current study indicate the following in cattle: 1) gene expression of TJ proteins (i.e., , , and ) differs between GC and TC and changes with follicle size, and 2) autocrine, paracrine, and endocrine regulators, such as FGF9, EGF, DHT, TNFα, and glucocorticoids, modulate , , and mRNA abundance in TC in vitro.

1771 related Products with: Evidence that gene expression of ovarian follicular tight junction proteins is regulated in vivo and in vitro in cattle.

DNA (cytosine 5) methyltr Recombinant Influenza HA Recombinant Influenza HA Recombinant Influenza HA Native Influenza HA (A So Native Influenza HA (A So Native Influenza HA (A So Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon

Related Pathways

paperclip

#28367764   2017/04/03 Save this To Up

Formononetin, an isoflavone, activates AMP-activated protein kinase/β-catenin signalling to inhibit adipogenesis and rescues C57BL/6 mice from high-fat diet-induced obesity and bone loss.

Balance between adipocyte and osteoblast differentiation is the key link of disease progression in obesity and osteoporosis. We have previously reported that formononetin (FNT), an isoflavone extracted from Butea monosperma, stimulates osteoblast formation and protects against postmenopausal bone loss. The inverse relationship between osteoblasts and adipocytes prompted us to analyse the effect of FNT on adipogenesis and in vivo bone loss, triggered by high-fat diet (HFD)-induced obesity. The anti-obesity effect and mechanism of action of FNT was determined in 3T3-L1 cells and HFD-induced obese male mice. Our findings show that FNT suppresses the adipogenic differentiation of 3T3-L1 fibroblasts, through down-regulation of key adipogenic markers such as PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and sterol regulatory element-binding protein (SREBP) and inhibits intracellular TAG accumulation. Increased intracellular reactive oxygen species levels and AMP-activated protein kinase (AMPK) activation accompanied by stabilisation of β-catenin were attributed to the anti-adipogenic action of FNT. In vivo, 12 weeks of FNT treatment inhibited the development of obesity in mice by attenuating HFD-induced body weight gain and visceral fat accumulation. The anti-obesity effect of FNT results from increased energy expenditure. FNT also protects against HFD-induced dyslipidaemia and rescues deterioration of trabecular bone volume by increasing bone formation and decreasing bone resorbtion caused by HFD. FNT's rescuing action against obesity-induced osteoporosis commenced at the level of progenitors, as bone marrow progenitor cells, obtained from the HFD mice group supplemented with FNT, showed increased osteogenic and decreased adipogenic potentials. Our findings suggest that FNT inhibits adipogenesis through AMPK/β-catenin signal transduction pathways and protects against HFD-induced obesity and bone loss.

2618 related Products with: Formononetin, an isoflavone, activates AMP-activated protein kinase/β-catenin signalling to inhibit adipogenesis and rescues C57BL/6 mice from high-fat diet-induced obesity and bone loss.

Rabbit Anti-Rat Androgen Androgen Receptor (Ab 650 17β-Acetoxy-2α-bromo-5 3-O-Acetyl 5,14-Androstad 3-O-Acetyl-17-O-tert-buty 3β-O-Acetyl-androsta-5,1 Androsta-1,4,6-triene-3,1 (3β)-Androsta-5,16-diene Rabbit Anti-G protein alp 19 Hydroxy 4 androstene 3 4 Androstene 3,17 dione C Recombinant Human Androge

Related Pathways

  •  
  • No related Items
paperclip

#28337939   2017/03/24 Save this To Up

Bidirectional apical-basal traffic of the cation-independent mannose-6-phosphate receptor in brain endothelial cells.

Brain capillary endothelium mediates the exchange of nutrients between blood and brain parenchyma. This barrier function of the brain capillaries also limits passage of pharmaceuticals from blood to brain, which hinders treatment of several neurological disorders. Receptor-mediated transport has been suggested as a potential pharmaceutical delivery route across the brain endothelium, e.g. reports have shown that the transferrin receptor (TfR) facilitates transcytosis of TfR antibodies, but it is not known whether this recycling receptor itself traffics from apical to basal membrane in the process. Here, we elucidate the endosomal trafficking of the retrograde transported cation-independent mannose-6-phosphate receptor (MPR300) in primary cultures of brain endothelial cells (BECs) of porcine and bovine origin. Receptor expression and localisation of MPR300 in the endo-lysosomal system and trafficking of internalised receptor are analysed. We also demonstrate that MPR300 can undergo bidirectional apical-basal trafficking in primary BECs in co-culture with astrocytes. This is, to our knowledge, the first detailed study of retrograde transported receptor trafficking in BECs, and the study demonstrates that MPR300 can be transported from the luminal to abluminal membrane and reverse. Such trafficking of MPR300 suggests that retrograde transported receptors in general may provide a mechanism for transport of pharmaceuticals into the brain.

2635 related Products with: Bidirectional apical-basal traffic of the cation-independent mannose-6-phosphate receptor in brain endothelial cells.

Human Brain Microvascular GFP Expressing Human Brai Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Mouse Brain Microvascular GFP Expressing Mouse Brai anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Interferon-a Receptor Typ

Related Pathways

paperclip

#28325841   2017/03/22 Save this To Up

An inducible amphipathic helix within the intrinsically disordered C terminus can participate in membrane curvature generation by peripherin-2/rds.

Peripherin-2/rds is required for biogenesis of vertebrate photoreceptor outer segment organelles. Its localization at the high-curvature rim domains of outer segment disk membranes suggests that it may act to shape these structures; however, the molecular function of this protein is not yet resolved. Here, we apply biochemical, biophysical, and imaging techniques to elucidate the role(s) played by the protein's intrinsically disordered C-terminal domain and an incipient amphipathic α-helix contained within it. We investigated a deletion mutant lacking only this α-helix in stable cell lines and Xenopus laevis photoreceptors. We also studied a soluble form of the full-length ∼7-kDa cytoplasmic C terminus in cultured cells and purified from Escherichia coli The α-helical motif was not required for protein biosynthesis, tetrameric subunit assembly, tetramer polymerization, localization at disk rims, interaction with GARP2, or the generation of membrane curvature. Interestingly, however, loss of the helical motif up-regulated membrane curvature generation in cellulo, introducing the possibility that it may regulate this activity in photoreceptors. Furthermore, the incipient α-helix (within the purified soluble C terminus) partitioned into membranes only when its acidic residues were neutralized by protonation. This suggests that within the context of full-length peripherin-2/rds, partitioning would most likely occur at a bilayer interfacial region, potentially adjacent to the protein's transmembrane domains. In sum, this study significantly strengthens the evidence that peripherin-2/rds functions directly to shape the high-curvature rim domains of the outer segment disk and suggests that the protein's C terminus may modulate membrane curvature-generating activity present in other protein domains.

2647 related Products with: An inducible amphipathic helix within the intrinsically disordered C terminus can participate in membrane curvature generation by peripherin-2/rds.

Rabbit Anti-SARS-Associat Breast cancer membrane pr Cancer Apoptosis Phospho- Nuclear Membrane Receptor Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Apoptosis (Human) Antibod Atherosclerosis (Human) A Atherosclerosis (Mouse) A Chemokine (Human) Antibod Cytokine (Human) Antibody

Related Pathways

  •  
  • No related Items
paperclip

#28270508   2017/03/08 Save this To Up

Discoidin domain receptor 2 mediates collagen-induced activation of membrane-type 1 matrix metalloproteinase in human fibroblasts.

Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a membrane-bound MMP that is highly expressed in cells with invading capacity, including fibroblasts and invasive cancer cells. However, pathways of MT1-MMP up-regulation are not clearly understood. A potential physiological stimulus for MT1-MMP expression is fibrillar collagen, and it has been shown that it up-regulates both MT1-MMP gene and functions in various cell types. However, the mechanisms of collagen-mediated MT1-MMP activation and its physiological relevance are not known. In this study, we identified discoidin domain receptor 2 (DDR2) as a crucial receptor that mediates this process in human fibroblasts. Knocking down DDR2, but not the β1 integrin subunit, a common subunit for all collagen-binding integrins, inhibited the collagen-induced MT1-MMP-dependent activation of pro-MMP-2 and up-regulation of MT1-MMP at the gene and protein levels. Interestingly, DDR2 knockdown or pharmacological inhibition of DDR2 also inhibited the MT1-MMP-dependent cellular degradation of collagen film, suggesting that cell-surface collagen degradation by MT1-MMP involves DDR2-mediated collagen signaling. This DDR2-mediated mechanism is only present in non-transformed mesenchymal cells as collagen-induced MT1-MMP activation in HT1080 fibrosarcoma cells and MT1-MMP function in MDA-MB231 breast cancer cells were not affected by DDR kinase inhibition. DDR2 activation was found to be noticeably more effective when cells were stimulated by collagen without the non-helical telopeptide region compared with intact collagen fibrils. Furthermore, DDR2-dependent MT1-MMP activation by cartilage was found to be more efficient when the tissue was partially damaged. These data suggest that DDR2 is a microenvironment sensor that regulates fibroblast migration in a collagen-rich environment.

1332 related Products with: Discoidin domain receptor 2 mediates collagen-induced activation of membrane-type 1 matrix metalloproteinase in human fibroblasts.

Goat Anti-Human Serotonin Anti AGO2 Human, Monoclon Human Interleukin-16 IL-1 Human Interleukin-17E (IL Human Epstein-Barr Virus Human Interleukin-1-alpha Human Interleukin-10 IL-1 Human Interleukin-11 IL-1 Human Interleukin-13 IL-1 Human Interleukin-15 IL-1 Human Interleukin-19 IL-1 Human Interleukin-21 IL-2

Related Pathways