JNK1 activation mediates C5b-9-induced P0 mRNA instability and P0 gene expression in Schwann cells

Journal of the Peripheral Nervous System : JPNS
Stefan DavidC L Koski

Abstract

The protein zero (P0) glycoprotein is an important component of compact peripheral nerve myelin produced by the glial cells of the mammalian peripheral nervous system. P0 mRNA expression is reduced following exposure of Schwann cells to sublytic C5b-9, the terminal activation complex of the complement cascade. Sublytic complement treatment decreased P0 mRNA by 81% within 6 h and required C5b-9 assembly. C5b-9 induced a threefold increase in both JNK1 activity and c-jun mRNA within 20 and 30 min, respectively, compared with cells treated with either human serum depleted of complement component C7 (C7dHS) or medium alone. Sublytic C5b-9 stimulation, in the presence of the transcription inhibitor Actinomycin D, decreased P0 mRNA expression by 52%, indicating that mRNA was selectively destabilized. This effect was prevented by pretreatment with L-JNK inhibitor 1 (L-JNKI1). To study a potential inhibition of P0 gene transcription, we transfected Schwann cells with a P0 promoter-firefly luciferase construct. Sublytic C5b-9 stimulation of the transfected cells decreased luciferase activity by 82% at 6 h, and this effect was prevented by pretreatment with L-JNKI1 inhibitor. Our results indicate that the ability of C5b-9 in vitro to aff...Continue Reading

References

Jan 1, 1979·Proceedings of the National Academy of Sciences of the United States of America·J E Bottenstein, G H Sato
Sep 1, 1991·Journal of Neurocytology·S MorrisonD Kirkham
Jul 1, 1989·Neuropathology and Applied Neurobiology·D A CompstonB Jasani
Sep 1, 1987·Brain Research·T E FeasbyM Neilson
Jul 26, 1996·Science·M JaegleD Meijer
Jul 19, 1996·The Journal of Biological Chemistry·L R CollinsJ H Brown
Dec 1, 1996·Current Opinion in Cell Biology·T S Zorick, G Lemke
Feb 1, 1997·Journal of Molecular Neuroscience : MN·R H Quarles
Oct 23, 1997·Current Opinion in Neurology·S S Scherer
Aug 1, 1997·Molecular Neurobiology·R J Colello, U Pott
Dec 13, 1997·The Journal of Infectious Diseases·C L Koski
Apr 30, 1998·Current Opinion in Cell Biology·Y T Ip, R J Davis
Jul 22, 1998·Microscopy Research and Technique·M Jaegle, D Meijer
Apr 29, 1999·Brain Pathology·R Mirsky, K R Jessen
Dec 3, 1999·Journal of Neurochemistry·S M Dashiell, C L Koski
Nov 9, 2000·The Journal of Immunology : Official Journal of the American Association of Immunologists·S NatafS R Barnum
Aug 8, 2001·The Journal of Immunology : Official Journal of the American Association of Immunologists·L SoaneM L Shin
Sep 12, 2001·The International Journal of Biochemistry & Cell Biology·R K Barr, M A Bogoyevitch
Oct 11, 2001·American Journal of Physiology. Renal Physiology·T TakanoL Aoudjit
Dec 26, 2001·Molecular and Cellular Neurosciences·D M MenichellaM E Shy
Dec 26, 2001·The Journal of Immunology : Official Journal of the American Association of Immunologists·Richard J MeadB Paul Morgan
Jan 16, 2002·Current Opinion in Genetics & Development·Claire R Weston, Roger J Davis
Jun 29, 2002·Science·Claire R WestonRoger J Davis
Jul 2, 2002·Journal of Anatomy·K R Jessen, R Mirsky
Aug 24, 2002·The Journal of Immunology : Official Journal of the American Association of Immunologists·Hongwei PengAndrey V Cybulsky
Jan 7, 2003·Neurochemical Research·Joseph Eichberg
Nov 14, 2003·Proceedings of the National Academy of Sciences of the United States of America·Junji YamauchiEric M Shooter
Jan 24, 2004·Experimental and Molecular Pathology·Florin NiculescuHorea Rus
Feb 6, 2004·The Journal of Cell Biology·David B ParkinsonKristjan R Jessen

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Citations

Apr 18, 2014·Journal of Clinical Immunology·Nevena TzekovaPatrick Küry
Aug 2, 2008·Molecular Immunology·V RamagliaF Baas
Sep 18, 2007·Journal of the Peripheral Nervous System : JPNS·Guido CavalettiGiovanni Tredici
Aug 8, 2009·Progress in Brain Research·V Ramaglia, F Baas
May 4, 2021·Frontiers in Cell and Developmental Biology·Yiqiang ZhiDan Xu

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