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Basic Fibroblast Growth (basic + fibroblast_growth)

Distribution by Scientific Domains
Medical Sciences60%

Terms modified by Basic Fibroblast Growth

  • basic fibroblast growth factor
    		•

    Selected Abstracts

    Hyaluronate-heparin conjugate gels for the delivery of basic fibroblast growth factor (FGF-2)

    JOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 1 2002
    Lin-Shu Liu
    Abstract The stability and activity of recombinant growth factors administered locally for the repair of damaged tissue can be directly influenced by the physical structure and chemical composition of the delivery matrix. This study describes a novel basic fibroblast growth factor-2 (FGF-2) delivery system synthesized by the conjugation of a structure-stabilizing polymer, hyaluronate (HA), with a sulfated glycosaminoglycan, heparin (HP), that has inherent specific binding sites for members of the FGF family. The biopolymers were formed via stable amine or labile imine bonds by coupling amine-modified HA with oxidized heparin. The addition of recombinant human FGF-2 resulted in the rapid binding of FGF-2 to the heparin segment of the hyaluronate-heparin (HAHP) conjugate. The FGF-2 was released in vitro from the imine-bonded (HAHPi) gels in the form of FGF-2-heparin complexes through the hydrolysis of the imine bonds. In contrast, the release of growth factor from the more stable amine-bonded (HAHPa) gels required treatment with free heparin or enzymatic digestion of the hyaluronate segment. Functional analysis of the released FGF-2 showed that the HAHP conjugate gels increased both the stability and activity of the growth factor. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 62: 128,135, 2002 [source]

    Specificity of the second messenger pathways involved in basic fibroblast growth factor-induced survival and neurite growth in chick ciliary ganglion neurons

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 13 2009
    Alessandra Gilardino
    Abstract Basic fibroblast growth factor (bFGF) exerts multiple neurotrophic actions on cultured neurons from the ciliary ganglion of chick embryo, among them promotion of neuronal survival and of neurite outgrowth. To understand the specificity of the signal transduction cascades involved in the control of these processes, we used pharmacological inhibitors of the three main effectors known to act downstream of the bFGF receptor (FGFR): phospholipase C, (PLC,), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3-K). Neuronal survival was assessed at 24 and 48 hr; neurite growth was analyzed both on dissociated neurons and on explants of whole ganglia. Our data show that only the PI3-K pathway is involved in the survival-promoting effect of bFGF; on the other hand, all three effectors converge on the enhancement of neurite outgrowth, both on isolated neurons and in whole ganglia. © 2009 Wiley-Liss, Inc. [source]

    Cytokines, matrix metalloproteases, angiogenic and growth factors in tears of normal subjects and vernal keratoconjunctivitis patients

    ALLERGY, Issue 5 2009
    A. Leonardi
    Background:, To detect the presence of multiple mediators and growth factors in tears of vernal keratoconjunctivitis (VKC) patients with active disease using stationary phase antibody arrays. Methods:, Tears were collected from 12 normal subjects (CT) and 24 active VKC patients. Tears were centrifuged and successively probed using three microwell plate arrays specific for: (i) cytokines: interleukin (IL)-2, IL-4, IL-5, IL-8, IL-10, IL-12, IL-13, interferon-, and tumour necrosis factor-,; (ii) growth factors: basic fibroblast growth factor (bFGF), platelet-derived growth factor, thrombopoietin, angiopoietin-2, vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), keratocyte growth factor, tissue inhibitor of metalloprotease (TIMP)-1 and heparin-binding epithelial growth factor (HB-EGF) and (iii) matrix metalloprotease (MMP)-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-10, MMP-13, TIMP-1 and TIMP-2. Results:, Interleukin-8 signals were detected in all CT and highly detected in all VKC samples. The Th2-type cytokines, IL-4, IL-5 and IL-10 were detected only in tears of VKC patients. Signals for bFGF, HB-EGF, VEGF and HGF were detected in 41,87% of VKC samples and in few CT samples. Only TIMP-1 and TIMP-2 were found in all normal and patient tear samples, whereas MMP-1, MMP-2, MMP-3, MMP-9 and MMP-10 were highly present in all VKC samples. Conclusions:, Stationary phase antibody array methodology was useful for the screening of various cytokines, growth factors and MMPs in tears. These analyses identified in tears of VKC patients previously unreported factors including MMP-3 and MMP-10 and multiple proteases, growth factors and cytokines, which may all play an important role in the pathogenesis of conjunctival inflammation. [source]

    Potent inhibition of in vivo angiogenesis and tumor growth by a novel cyclooxygenase-2 inhibitor, enoic acanthoic acid

    CANCER SCIENCE, Issue 12 2007
    Hye Jin Jung
    Recent studies have shown that cyclooxygenase-2 is crucially involved in angiogenesis. In fact, several specific cyclooxygenase-2 inhibitors suppress angiogenesis in vivo, suggesting that cyclooxygenase-2 is a promising target for the treatment of angiogenesis-related diseases. In the present study we investigate the activity of a new cyclooxygenase-2 inhibitor, enoic acanthoic acid (EAA), which was synthesized from the known natural cyclooxygenase-2 inhibitor, acanthoic acid (AA). The demonstration of a high correlation between EAA- and celecoxib-induced gene expression signatures in microarray experiments validated the specificity of EAA on cyclooxygenase-2. In angiogenesis assays, EAA potently inhibited basic fibroblast growth factor-induced invasion and tube formation of bovine aortic endothelial cells in vitro. Moreover, this inhibitor prevented both neovascularization of the chorioallantoic membrane of growing chick embryo and basic fibroblast growth factor-induced mouse corneal angiogenesis in vivo. EAA also significantly suppressed the growth of bladder tumors in a mouse model, showing better antitumor activity than celecoxib. Furthermore, gelatin zymogram analysis revealed that EAA potently inhibited the activities of matrix metalloproteinase 2 and 9. These results clearly demonstrate that EAA is a promising agent for the prevention and treatment of angiogenesis-related diseases including cancer. (Cancer Sci 2007; 98: 1943,1948) [source]

    Betulinic Acid Inhibits Growth Factor-induced in vitro Angiogenesis via the Modulation of Mitochondrial Function in Endothelial Cells

    CANCER SCIENCE, Issue 4 2002
    Ho Jeong Kwon
    Betulinic acid (BetA), a pentacyclic triterpene, is a selective apoptosis-inducing agent that works directly in mitochondria. Recent study has revealed that BetA inhibits in vitro enzymatic activity of aminopeptidase N (APN, EC 3.4.11.2), which is known to play an important role in angiogenesis, but the anti-angiogenic activity of BetA has not been reported yet. Data presented here show that BetA potently inhibited basic fibroblast growth factor (bFGF)-induced invasion and tube formation of bovine aortic endothelial cells (BAECs) at a concentration which had no effect on the cell viability. To access whether the anti-angiogenic nature of BetA originates from its inhibitory action against aminopeptidase N (APN) activity, the effect of BetA on APN was investigated. Surprisingly, BetA did not inhibit in vivo APN activity in endothelial cells or APN-positive tumor cells. On the other hand, BetA significantly decreased the mitochondrial reducing potential, and treatment with mitochondrial permeability transition (MPT) inhibitors attenuated BetA-induced inhibition of endothelial cell invasion. These results imply that anti-angiogenic activity of BetA occurs through a modulation of mitochondrial function rather than APN activity in endothelial cells. [source]