In Vitro Modulation of Microglia Motility by Glioma Cells Is Mediated by Hepatocyte Growth Factor/Scatter Factor

In Vitro Modulation of Microglia Motility by Glioma Cells Is Mediated by Hepatocyte Growth... AbstractOBJECTIVEConsidered as immune effector cells of the central nervous system, microglia represent a major component of the inflammatory cells found in malignant gliomas. Although their role in brain tumor biology is unclear, accumulation of microglia in malignant brain tumors may be mediated through active secretion of cytokines by glioma cells. Because hepatocyte growth factor/scatter factor (HGF/SF) has been shown to modulate glioma motility through an autocrine mechanism, and because microglia have been reported to express the HGF/SF receptor Met, we hypothesized that microglia recruitment by gliomas may also occur through the secretion of HGF/SF.METHODSThe effect of glioma cells in augmenting BV-2 murine microglia motility was studied by using an in vitro Boyden chamber migration assay. To determine the chemokines involved in microglia migration, neutralizing monoclonal antibodies against monocyte chemotactic protein-1 and HGF/SF were tested. Immunoblotting was used to check for the expression of HGF/SF by glioma cells, and the expression of Met by BV-2 cells was examined by flow cytometry.RESULTSBV-2 migration was noted within 7 hours of incubation with both human (U251 MG and U373 MG) and murine (GL261) glioma cell lines. This migration corresponded to HGF/SF secretion by glioma cells and was completely inhibited by neutralizing monoclonal antibody against HGF/SF, but not monocyte chemotactic protein-1. Exposure of BV-2 cells to recombinant HGF/SF, but not monocyte chemotactic protein-1, resulted in their migration and down-regulation of Met in a dose-dependent fashion.CONCLUSIONHGF/SF, which plays a role in glioma motility and mitogenesis, may also act as a chemokine for microglia and may be responsible for the microglia infiltration in malignant gliomas. This active recruitment of microglia may play an important role in glioma biology. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurosurgery Oxford University Press

In Vitro Modulation of Microglia Motility by Glioma Cells Is Mediated by Hepatocyte Growth Factor/Scatter Factor

In Vitro Modulation of Microglia Motility by Glioma Cells Is Mediated by Hepatocyte Growth Factor/Scatter Factor

EXPERIMENTAL STUDIES In Vitro Modulation of Microglia Motility by Glioma Cells Is Mediated by Hepatocyte Growth Factor/Scatter Factor Behnam Badie, M .D ., Jill Schartner, B.S., Jessica Klaver, Jessica Vorpahl Neuro-oncology Laboratory, Department of Neurological Surgery, University of W isconsin School of Medicine, Madison, W isconsin OBJECTIVE: C o n s id e re d as i m m u n e e f fe c t o r cells o f th e c e n tra l nervous system, m ic ro g lia rep re se n t a m a jo r c o m p o n e n t of the in fla m m a to r y cells fo u n d in m a lig n a n t gliomas. A lth o u g h t h e ir ro le in b ra in t u m o r b io lo g y is u n c le a r, accumulation o f m ic r o g lia in m a lig n a n t b ra in tu m o rs m a y be m e d ia te d th ro u g h a c tiv e secretio n o f cyto k in es by g lio m a cells. Because h e p a t o c y t e g r o w t h f a c t o r /s c a t t e r fa c to r (H G F /S F ) has been s h o w n to m o d u la t e g lio m a m o t ility th ro u g h an autocrine m e c h a n is m , a n d because m ic ro g lia have been r e p o r te d to express th e H G F /S F r e c e p t o r M e t , w e hypothesized th a t m ic r o g lia r e c r u i t m e n t by gliom as m a y also o c c u r th ro u g h th e s e c re tio n o f H G F /S F . METFIODS: T h e e ffe c t o f g lio m a cells in a u g m e n tin g B V -2 m u r in e m ic ro g lia m o t ility w as studied by using a n in v itr o Boyden cham ber m ig ra tio n assay. T o d e te rm in e the chemokines involved in m icroglia m igration, neutralizing m on oclo n al antibodies against m o n o c y te c h e m o ta c tic protein-1 and H G F /S F w e r e tested. Im m u n o b lo ttin g was used to check for the expression o f H G F /S F by g lio m a cells, and the expression o f M e t by B V-2 cells was exam in ed by flo w cyto m etry. RESULTS: B V -2 m i g r a t i o n w a s n o t e d w i t h i n 7 h o u rs o f i n c u b a t io n w i t h b o t h h u m a n ( U 2 5 1 M G a n d U 3 7 3 M G ) a n d murine ( G L 2 6 1 ) g l i o m a c...
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Publisher
Oxford University Press
Copyright
© Published by Oxford University Press.
ISSN
0148-396X
eISSN
1524-4040
D.O.I.
10.1097/00006123-199905000-00075
Publisher site
See Article on Publisher Site

Abstract

AbstractOBJECTIVEConsidered as immune effector cells of the central nervous system, microglia represent a major component of the inflammatory cells found in malignant gliomas. Although their role in brain tumor biology is unclear, accumulation of microglia in malignant brain tumors may be mediated through active secretion of cytokines by glioma cells. Because hepatocyte growth factor/scatter factor (HGF/SF) has been shown to modulate glioma motility through an autocrine mechanism, and because microglia have been reported to express the HGF/SF receptor Met, we hypothesized that microglia recruitment by gliomas may also occur through the secretion of HGF/SF.METHODSThe effect of glioma cells in augmenting BV-2 murine microglia motility was studied by using an in vitro Boyden chamber migration assay. To determine the chemokines involved in microglia migration, neutralizing monoclonal antibodies against monocyte chemotactic protein-1 and HGF/SF were tested. Immunoblotting was used to check for the expression of HGF/SF by glioma cells, and the expression of Met by BV-2 cells was examined by flow cytometry.RESULTSBV-2 migration was noted within 7 hours of incubation with both human (U251 MG and U373 MG) and murine (GL261) glioma cell lines. This migration corresponded to HGF/SF secretion by glioma cells and was completely inhibited by neutralizing monoclonal antibody against HGF/SF, but not monocyte chemotactic protein-1. Exposure of BV-2 cells to recombinant HGF/SF, but not monocyte chemotactic protein-1, resulted in their migration and down-regulation of Met in a dose-dependent fashion.CONCLUSIONHGF/SF, which plays a role in glioma motility and mitogenesis, may also act as a chemokine for microglia and may be responsible for the microglia infiltration in malignant gliomas. This active recruitment of microglia may play an important role in glioma biology.

Journal

NeurosurgeryOxford University Press

Published: May 1, 1999

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