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  • Growth factors induce monocyte binding to vascular smooth muscle cells: implications for monocyte retention in atherosclerosis. 15140748

    Adhesive interactions between monocytes and vascular smooth muscle cells (VSMC) may contribute to subendothelial monocyte-macrophage retention in atherosclerosis. We investigated the effects of angiotensin II (ANG II) and platelet-derived growth factor (PDGF)-BB on VSMC-monocyte interactions. Treatment of human aortic VSMC (HVSMC) with ANG II or PDGF-BB significantly increased binding to human monocytic THP-1 cells and to peripheral blood monocytes. This was inhibited by antibodies to monocyte beta(1)- and beta(2)-integrins. The binding was also attenuated by blocking VSMC arachidonic acid (AA) metabolism by inhibitors of 12/15-lipoxygenase (12/15-LO) or cyclooxygenase-2 (COX-2). Conversely, binding was enhanced by overexpression of 12/15-LO or COX-2. Direct treatment of HVSMC with AA or its metabolites also increased binding. Furthermore, VSMC derived from 12/15-LO knockout mice displayed reduced binding to mouse monocytic cells relative to genetic control mice. Using specific signal transduction inhibitors, we demonstrated the involvement of Src, phosphoinositide 3-kinase, and MAPKs in ANG II- or PDGF-BB-induced binding. Interestingly, after coculture with HVSMC, THP-1 cell surface expression of the scavenger receptor CD36 was increased. These results show for the first time that growth factors may play additional roles in atherosclerosis by increasing monocyte binding to VSMC via AA metabolism and key signaling pathways. This can lead to monocyte subendothelial retention, CD36 expression, and foam cell formation.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Skeletal growth factors regulate the synthesis of insulin-like growth factor binding protein-5 in bone cell cultures. 7537737

    Skeletal cells secrete insulin-like growth factors (IGFs) I and II and six known IGF binding proteins (IGFBPs). IGFBP-5 stimulates bone formation, and its synthesis correlates with changes in osteoblast cell growth. We tested the effects of basic fibroblast growth factor (bFGF), transforming growth factor beta 1 (TGF beta 1), and platelet-derived growth factor (PDGF) BB on IGFBP-5 expression in cultures of osteoblast-enriched cells from 22-day-old fetal rat calvariae (Ob cells). Treatment of Ob cells with bFGF, TGF beta 1, and PDGF BB caused a time- and dose-dependent decrease in IGFBP-5 mRNA levels and inhibited IGFBP-5 polypeptide levels in the extracellular matrix. The effects of bFGF, TGF beta 1, and PDGF BB on IGFBP-5 transcripts were independent of cell division and were observed in the presence and absence of hydroxyurea. bFGF, TGF beta 1, and PDGF BB did not modify the decay of IGFBP-5 mRNA in transcriptionally arrested Ob cells, and they inhibited IGFBP-5 heterogeneous nuclear RNA and the rate of IGFBP-5 transcription. In conclusion, bFGF, TGF beta 1, and PDGF BB inhibit IGFBP-5 expression in Ob cells independently of their mitogenic activity and through mechanisms that involve decreased transcription.
    Document Type:
    Reference
    Product Catalog Number:
    06-110

  • Growth factors that repress myoblast differentiation sustain phosphorylation of a specific site on histone H1. 7678408

    A monoclonal antibody (12D11) is presented that binds an epitope on histone H1 only when it is phosphorylated. Skeletal myoblasts, which are cultured in high mitogen medium to induce proliferation and inhibit differentiation, contain histone H1 reactive with monoclonal antibody 12D11, whereas differentiated myocytes and adult skeletal muscle do not. Phosphorylation of H1 at the 12D11 epitope, as assessed by antibody binding, is also induced and maintained in myoblasts cultured in low mitogen medium supplemented with transforming growth factor beta, which blocks differentiation but allows the cells to withdraw from the cell cycle (Olson, E., Sternberg, E., Hu, J., Spizz, G., and Wilcox, C. (1986) J. Cell Biol. 103, 1799-1805; Massague, J., Cheipetz, S., Endo, T., and Nadal-Ginard, B. (1986) Proc. Natl. Acad. Sci. U.S.A. 83, 8206-8210). These observations suggest that phosphorylation of histone H1 at the 12D11 epitope is associated with the negative regulation of myoblast differentiation by growth factors.
    Document Type:
    Reference
    Product Catalog Number:
    05-1324
    Product Catalog Name:
    Anti-phospho-Histone H1 Antibody, clone 12D11

  • Hemopoietic growth factors with the exception of interleukin-4 activate the p38 mitogen-activated protein kinase pathway. 9013568

    The mammalian mitogen-activated protein (MAP) kinase homologue p38 has been shown to be activated by pro-inflammatory cytokines as well as physical and chemical stresses. We now show that a variety of hemopoietic growth factors, including Steel locus factor, colony stimulating factor-1, granulocyte/macrophage-colony stimulating factor, and interleukin-3, activate p38 MAP kinase and the downstream kinase MAPKAP kinase-2. Furthermore, although these growth factors activate both p38 MAP kinase and Erk MAP kinases, we demonstrate using a specific inhibitor of p38 MAP kinase, SB 203580, that p38 MAP kinase activity was required for MAP kinase-activated protein kinase-2 activation. Conversely p38 MAP kinase was shown not to be required for in vivo activation of p90(rsk), known to be downstream of the Erk MAP kinases. Interleukin-4 was unique among the hemopoietic growth factors we examined in failing to induce activation of either p38 MAP kinase or MAP kinase-activated protein kinase-2. These findings demonstrate that the activation of p38 MAP kinase is involved not only in responses to stresses but also in signaling by growth factors that regulate the normal development and function of cells of the immune system.
    Document Type:
    Reference
    Product Catalog Number:
    06-668

  • Growth factors and stromal matrix proteins associated with mammographic densities. 11303594

    Extensive radiologically dense breast tissue is associated with a marked increase in breast cancer risk. To explore the biological basis for this association, we have examined the association of growth factors and stromal matrix proteins in breast tissue with mammographic densities. Ninety-two formalin-fixed paraffin blocks of breast tissues surrounding benign lesions were obtained, half from breasts with little or no density and half from breasts with extensive density, matched for age at biopsy. Sections were stained for cell nuclei, total collagen, the stromal matrix regulatory protein tissue metalloproteinase-3 (TIMP-3), and the growth factors, transforming growth factor-alpha and insulin-like growth factor (IGF-I). The area of immunoreactive staining was measured using quantitative microscopy. Breast tissue from subjects with extensive densities had a greater nuclear area (P = 0.007), as well as larger stained areas of total collagen (P = 0.003), TIMP-3 (P = 0.08), and IGF-I (P = 0.02) when compared with subjects with little breast density. Differences were greater for subjects less than 50 years of age. These data indicate that increased tissue cellularity, greater amounts of collagen, and increased IGF-I and TIMP-3 expression are found in tissue from mammographically dense breasts and suggest mechanisms that may mediate the associated increased risk of breast cancer.
    Document Type:
    Reference
    Product Catalog Number:
    05-172
    Product Catalog Name:
    Anti-IGF-I Antibody, clone Sm1.2

  • Growth factors and steroid mediated regulation of cytoskeletal protein expression in serum-deprived primary astrocyte cultures. 18612815

    In this research we aimed to investigate the interactions between growth factors (GFs) and dexamethasone (DEX) on cytoskeletal proteins GFAP and vimentin (VIM) expression under different experimental conditions. Condition I: 24 h pretreatment with bFGF, subsequent 72 h switching in serum-free medium (SFM) and final addition of GFs, alone or by two in the last 24 h, after a prolonged (60 h) DEX treatment. Condition II: 36 h pretreatment with DEX (with bFGF in the last 24 h), followed by SFM for 60 h and final addition for 24 h with growth factors alone or two of them together. Western blot analysis data showed a marked GFAP expression in cultures submitted to Condition I comparing results to untreated or treated controls. VIM expression was instead significantly reduced after GFs addition in the last 24 h of 60 h DEX treatment, respect to control DEX-pretreated ones. Referring data to untreated controls, VIM expression was significantly enhanced after GFs addition. GFAP showed also a significant increase in astrocytes submitted to Condition II, respect to untreated or treated control cultures. VIM expression was up and down regulated under Condition II. Collectively, our findings evidence an interactive dialogue between GFs and DEX in astroglial cultures, co-pretreated with DEX and bFGF, regulating cytoskeletal network under stressful conditions.
    Document Type:
    Reference
    Product Catalog Number:
    MAB3400
    Product Catalog Name:
    Anti-Vimentin Antibody, clone V9

  • Glial growth factors are alternatively spliced erbB2 ligands expressed in the nervous system. 8096067

    Glial growth factors, proteins that are mitogenic for Schwann cells, and several ligands for the p185erbB2 receptor, are products of the same gene. Alternative splicing of the messenger RNA generates an array of putative membrane-attached, intracellular and secreted signalling proteins, at least some of which are expressed in the developing spinal cord and brain. These factors are probably important in the development and regeneration of the nervous system.
    Document Type:
    Reference
    Product Catalog Number:
    06-229
    Product Catalog Name:
    Anti-phospho-erbB-2/HER-2 (Tyr1248) Antibody

  • Chondroitinase and growth factors enhance activation and oligodendrocyte differentiation of endogenous neural precursor cells after spinal cord injury. 22629425

    The adult spinal cord harbours a population of multipotent neural precursor cells (NPCs) with the ability to replace oligodendrocytes. However, despite this capacity, proliferation and endogenous remyelination is severely limited after spinal cord injury (SCI). In the post-traumatic microenvironment following SCI, endogenous spinal NPCs mainly differentiate into astrocytes which could contribute to astrogliosis that exacerbate the outcomes of SCI. These findings emphasize a key role for the post-SCI niche in modulating the behaviour of spinal NPCs after SCI. We recently reported that chondroitin sulphate proteoglycans (CSPGs) in the glial scar restrict the outcomes of NPC transplantation in SCI by reducing the survival, migration and integration of engrafted NPCs within the injured spinal cord. These inhibitory effects were attenuated by administration of chondroitinase (ChABC) prior to NPC transplantation. Here, in a rat model of compressive SCI, we show that perturbing CSPGs by ChABC in combination with sustained infusion of growth factors (EGF, bFGF and PDGF-AA) optimize the activation and oligodendroglial differentiation of spinal NPCs after injury. Four days following SCI, we intrathecally delivered ChABC and/or GFs for seven days. We performed BrdU incorporation to label proliferating cells during the treatment period after SCI. This strategy increased the proliferation of spinal NPCs, reduced the generation of new astrocytes and promoted their differentiation along an oligodendroglial lineage, a prerequisite for remyelination. Furthermore, ChABC and GF treatments enhanced the response of non-neural cells by increasing the generation of new vascular endothelial cells and decreasing the number of proliferating macrophages/microglia after SCI. In conclusions, our data strongly suggest that optimization of the behaviour of endogenous spinal NPCs after SCI is critical not only to promote endogenous oligodendrocyte replacement, but also to reverse the otherwise detrimental effects of their activation into astrocytes which could negatively influence the repair process after SCI.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Scaffolds containing growth factors and extracellular matrix induce hepatocyte proliferation and cell migration in normal and regenerating rat liver. 21126791

    Intrahepatic drug delivery from implantable scaffolds is being developed as a strategy to modulate growth and enhance regeneration at the time of liver resection. In this study we examine the effects of scaffolds containing hepatocyte growth factor, epidermal growth factor, fibroblast growth factor 1, fibroblast growth factor 2, and liver-derived extracellular matrix (L-ECM) when implanted into normal and partially hepatectomized rat livers.
    Document Type:
    Reference
    Product Catalog Number:
    AP180B
    Product Catalog Name:
    Donkey Anti-Goat IgG Antibody, biotin-SP conjugate, Species Adsorbed