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  • Distinct patterns of expression of fibroblast growth factors and their receptors in human atheroma and nonatherosclerotic arteries. Association of acidic FGF with plaque ... 7693761

    Because fibroblast growth factors (FGFs) modulate important functions of endothelial cells (EC) and smooth muscle cells (SMC), we studied FGF expression in human vascular cells and control or atherosclerotic arteries. All cells and arteries contained acidic (a) FGF and basic (b) FGF mRNA. Northern analysis detected aFGF mRNA only in one of five control arteries but in all five atheroma tested, while levels of bFGF mRNA did not differ among control (n = 3) vs. plaque specimens (n = 6). Immunolocalization revealed abundant bFGF protein in control vessels (n = 10), but little in plaques (n = 14). In contrast, atheroma (n = 14), but not control arteries (n = 10), consistently exhibited immunoreactive aFGF, notably in neovascularized and macrophage-rich regions of plaque. Because macrophages colocalized with aFGF, we tested human monocytoid THP-1 cells and demonstrated accumulation of aFGF mRNA during PMA-induced differentiation. We also examined the expression of mRNA encoding FGF receptors (FGFRs). All cells and arteries contained FGFR-1 mRNA. Only SMC and control vessels had FGFR-2 mRNA, while EC and some arteries contained FGFR-4 mRNA. The relative lack of bFGF in plaques vs. normal arteries suggests that this growth factor may not contribute to cell proliferation in advanced atherosclerosis. However, aFGF produced by plaque macrophages may stimulate the growth of microvessels during human atherogenesis.
    Document Type:
    Reference
    Product Catalog Number:
    05-117
    Product Catalog Name:
    Anti-FGF-2/basic FGF (neutralizing) Antibody, clone bFM-1

  • Mechanical injury increases bFGF and CNTF mRNA expression in the mouse retina. 9268592

    We characterized the survival-factor response of the normal mouse retina to mechanical injury by examining the expression of mRNAs for basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), and their receptors, FGF receptor-1 (FGFR-1) and CNTF receptor alpha (CNTFR-alpha). The retina was injured by making an incision through the choroid and retinal pigment epithelium that penetrated the subretinal space of each eye of an adult BALB/c mouse. Retinas were taken 6 hr, 12 hr, 1, 2, 4, 7, 10 and 16 days post-injury. Control animals were without injury. Northern blot analysis was performed to determine bFGF, CNTF and their receptor mRNA levels. A significant increase in bFGF and CNTF mRNAs was observed after injury, along with an increase in glial fibrillary acidic protein (GFAP) expression. More than 2-fold of upregulation of bFGF mRNA was seen as early as 6 hr after injury. This increase reached a maximum of more than 5-fold at day 2 post-injury and then declined slowly, and was still about 2.5-fold of the control level by day 16. Expression of CNTF showed a small increase of about 1.6-fold at 6 hr after injury. The upregulation reached a peak level of about 2.7-fold at day 4 after injury, then declined to control level by day 16. There was only a very small increase in FGFR-1 at 6, 12 and 24 hr after injury, and no significant increases in FGFR-1 at time points longer than 1 day post-injury. Expression of GFAP followed a time course similar to that of bFGF. We conclude that mechanical injury induces bFGF, CNTF, and GFAP expression in the mouse retina with time courses similar to the upregulation of these molecules in rat retina. Compared to the upregulation in rat retina, however, the injury-induced upregulation of bFGF and GFAP is much less in the mouse retina. In addition, there was only a very small induction of FGFR-1 expression in the mouse retina. These findings may explain, at least in part, the lack of injury-induced photoreceptor protection in the mouse retina.
    Document Type:
    Reference
    Product Catalog Number:
    AB1770

  • Astrocyte activation by fibroblast growth factor-1 and motor neuron apoptosis: implications for amyotrophic lateral sclerosis. 15773903

    Fibroblast growth factor-1 (FGF1 or acidic FGF) is highly expressed in motor neurons. FGF-1 is released from cells by oxidative stress, which might occur from SOD-1 aberrant function in amyotrophic lateral sclerosis (ALS). Although FGF-1 is known to be neuroprotective after spinal cord injury or axotomy, we found that FGF-1 could activate spinal cord astrocytes in a manner that decreased motor neuron survival in co-cultures. FGF-1 induced accumulation of the FGF receptor 1 (FGFR1) in astrocyte nuclei and potently stimulated nerve growth factor (NGF) expression and secretion. The FGFR1 tyrosine kinase inhibitor PD166866 prevented these effects. Previously, we have shown that NGF secretion by reactive astrocytes induces motor neuron apoptosis through a p75(NTR)-dependent mechanism. Embryonic motor neurons co-cultured on the top of astrocytes exhibiting activated FGFR1 underwent apoptosis, which was prevented by PD166866 or by adding either anti-NGF or anti-p75(NTR) neutralizing antibodies. In the degenerating spinal cord of mice carrying the ALS mutation G93A of Cu, Zn superoxide dismutase, FGF-1 was no longer localized only in the cytosol of motor neurons, while FGFR1 accumulated in the nuclei of reactive astrocytes. These results suggest that FGF-1 released by oxidative stress from motor neurons might have a role in activating astrocytes, which could in turn initiate motor neuron apoptosis in ALS through a p75(NTR)-dependent mechanism.
    Document Type:
    Reference
    Product Catalog Number:
    AB1526SP
    Product Catalog Name:
    Anti-Nerve Growth Factor-β Antibody