Distribution and Expression of RhoA in Rat Retina after Optic Nerve Injury

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Abstract

Background: RhoA is a small guanosine triphosphatase which participates in signaling pathways of axonal repellents or inhibitors. However, the distribution and expression of RhoA in the rat retina after optic nerve injury has not been elucidated yet. Objectives: To study the distribution and expression of RhoA in the rat retina after optic nerve injury. Methods: Immunohistochemistry was used to determine the distribution of RhoA in rat retina after optic nerve injury. The expression of RhoA was analyzed by Western blot. Results: In normal retina and the retina 1 day after optic nerve injury, RhoA was distributed in the retinal ganglion cell (RGC) layer. Three days after optic nerve injury, it existed in RGCs and the inner plexiform layer. However, 7 days after surgery its immunoreactivity was abundant not only in the RGC and inner plexiform layers but also in the inner nuclear and outer plexiform layers. Western blot analysis showed that the expression of RhoA increased significantly in the retina after optic nerve injury in comparison with normal retina. Conclusion: Theseresults indicate that the distribution and expression of RhoA were extended and enhanced after optic nerve injury, and that RhoA plays an important role in optic nerve regeneration.

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Most cited references 11

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Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein.

T GrandPré, F. Nakamura, T Vartanian … (2000)

Adult mammalian axon regeneration is generally successful in the peripheral nervous system (PNS) but is dismally poor in the central nervous system (CNS). However, many classes of CNS axons can extend for long distances in peripheral nerve grafts. A comparison of myelin from the CNS and the PNS has revealed that CNS white matter is selectively inhibitory for axonal outgrowth. Several components of CNS white matter, NI35, NI250(Nogo) and MAG, that have inhibitory activity for axon extension have been described. The IN-1 antibody, which recognizes NI35 and NI250(Nogo), allows moderate degrees of axonal regeneration and functional recovery after spinal cord injury. Here we identify Nogo as a member of the Reticulon family, Reticulon 4-A. Nogo is expressed by oligodendrocytes but not by Schwann cells, and associates primarily with the endoplasmic reticulum. A 66-residue lumenal/extracellular domain inhibits axonal extension and collapses dorsal root ganglion growth cones. In contrast to Nogo, Reticulon 1 and 3 are not expressed by oligodendrocytes, and the 66-residue lumenal/extracellular domains from Reticulon 1, 2 and 3 do not inhibit axonal regeneration. These data provide a molecular basis to assess the contribution of Nogo to the failure of axonal regeneration in the adult CNS.

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Identification of myelin-associated glycoprotein as a major myelin-derived inhibitor of neurite growth.

L McKerracher, S. David, D.L. Jackson … (1994)

Contact-dependent axon growth inhibitory activity is present in CNS myelin, but the inhibitory proteins have not been fully characterized. We report here that at least two peaks of inhibitory activity can be separated by fractionating solubilized CNS myelin proteins by DEAE chromatography. A major peak of inhibitory activity corresponded to the elution profile of myelin-associated glycoprotein (MAG). Immunodepletion of MAG from these inhibitory fractions removed neurite growth inhibition, whereas recombinant MAG (ectodomain) was a potent inhibitor of neurite outgrowth. Immunodepletion of MAG from total extracts of CNS myelin restored neurite growth up to 63% of control levels. These results establish that MAG is a significant, and possibly the major, inhibitor in CNS myelin; this has broad implications for axonal regeneration in the injured mammalian CNS.

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Nogo and axon regeneration.

Martin Schwab (2004)

Nogo-A is one of several neurite growth inhibitory components present in oligodendrocytes and CNS myelin membranes. Nogo has a crucial role in restricting axonal regeneration and compensatory fibre growth in the injured adult mammalian CNS. Recent studies have shown that in vivo applications of Nogo neutralizing antibodies, peptides blocking the Nogo receptor subunit NgR, or blockers of the postreceptor components Rho-A and ROCK induce long-distance axonal regeneration and compensatory sprouting, accompanied by an impressive enhancement of functional recovery, in the rat and mouse spinal cord.

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Author and article information

Journal

Journal ID (publisher-id): ORE

Journal ID (nlm-ta): Ophthalmic Res

Journal ID (doi): 10.1159/issn.0030-3747

Title: Ophthalmic Research

Publisher: S. Karger AG

ISSN (Print): 0030-3747

ISSN (Electronic): 1423-0259

Publication date Subscription-year: 2007

Publication date (Print): June 2007

Publication date (Electronic): 25 May 2007

Volume: 39

Issue: 3

Pages: 174-178

Affiliations

^aDepartment of Ophthalmology, Southwest Hospital, Third Military Medical University, Chongqing, and ^bThe Hospital of the Chinese People’s Armed Police Forces No. 8650, Jingzhong City, China

Article

Publisher ID: 103237 Other ID: Ophthalmic Res 2007;39:174–178

DOI: 10.1159/000103237

PubMed ID: 17534117

SO-VID: 97647810-c838-4b8e-90dc-d2ca2d05d1b6

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 10 July 2006

Date accepted : 19 December 2006

Page count

Figures: 2, References: 21, Pages: 5

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