Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Ekström, Per

doi:10.1002/jnr.490420107

Cited by 7 publications

(3 citation statements)

References 47 publications

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“…In this respect the developmental stage of the cells does not seem to be important. Our data are consistent with those reported by Ekström (1995), who found that increased levels of cAMP inhibited proliferation of non-neuronal cells in the frog sciatic nerve. We obtained further support for a suppressive effect of cAMP using HA 1004, a potent inhibitor of protein kinase A (PKA) (Hidaka et al, 1984).…”

Section: Discussionsupporting

confidence: 93%

Regulation of Schwann cell proliferation in cultured segments of the adult rat sciatic nerve

Svenningsen

Kanje

1998

J. Neurosci. Res.

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Schwann cell proliferation was studied in cultured segments of the rat sciatic nerve by measurement of [3H] thymidine incorporation or through bromodeoxyuridine-(BrdU)-labelling and immunocytochemistry. The aim was to delineate mechanisms involved in the injury-induced proliferative response of Schwann cells. Removal of extracellular Ca2+ by addition of EGTA to the culture medium suppressed [3H] thymidine incorporation as did the calmodulin inhibitor 48/80. The Ca2+ ionophore A23187 increased incorporation. Staurosporin, an inhibitor of protein kinase C (PKC), suppressed [3H] thymidine incorporation while phorbol-12-myristate-13-acetate (PMA) enhanced incorporation. Manipulation of the cAMP system showed that increased cAMP levels inhibited proliferation. Inhibition of protein kinase A by HA 1004 increased the incorporation of [3H] thymidine. Immunostaining for BrdU and glial specific markers together with morphological evaluation of myelin association showed that proliferation occurred in Schwann cells. The results are consistent with a model in which Schwann cell proliferation is enhanced by Ca2+ through activation of calmodulin-dependent and/or PKCdependent mechanisms. Inhibition is achieved through the cAMP system. Together, these results show that Schwann cells regulate proliferation differently in an integrated environment, e.g. the nerve structure, than in isolation as primary monocultures.

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Section: Discussionsupporting

confidence: 93%

Regulation of Schwann cell proliferation in cultured segments of the adult rat sciatic nerve

Svenningsen

Kanje

1998

J. Neurosci. Res.

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“…These models differ, primarily, in how the mechanical stimulus is applied to the cultured tissue and, secondarily, by what type of tissue is cultured and what cellular parameters are measured. Other models have been developed to study the response of peripheral nervous system tissue to trauma (e.g., Edbladh et al, 1994;Ekstrom, 1995a) as well as the response of nonmammalian nervous sytems to traumatic injury (e.g., Ekstrom, 1995b;Krause et al, 1994;Yawo and Kuno, 1985). Pioneering work by several investigators performed with cultures of chick neurons is not addressed in this review; however, the interested reader is directed to the following references (Bird, 1978;Levi and Meyer, 1945;Shaw and Bray, 1977;Sole, 1980).…”

Section: Introductionmentioning

confidence: 99%

In VitroCentral Nervous System Models of Mechanically Induced Trauma: A Review

Morrison¹,

Saatman²,

Meaney³

et al. 1998

Journal of Neurotrauma

180

121

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Injury is one of the leading causes of death among all people below the age of 45 years. In the United States, traumatic brain injury (TBI) and spinal cord injury (SCI) together are responsible for an estimated 90,000 disabled persons annually. To improve treatment of the patient and thereby decrease the associated mortality, morbidity, and cost, several in vivo models of central nervous system (CNS) injury have been developed and characterized over the past two decades. To complement the ability of these in vivo models to reproduce the sequelae of human CNS injury, in vitro models of neuronal injury have also been developed. Despite the inherent simplifications of these in vitro systems, many aspects of the posttraumatic sequelae are faithfully reproduced in cultured cells, including ultrastructural changes, ionic derangements, alterations in electrophysiology, and free radical generation. This review presents a number of these in vitro systems, detailing the mechanical stimuli, the types of tissue injured, and the in vivo injury conditions most closely reproduced by the models. The data generated with these systems is then compared and contrasted with data from in vivo models of CNS injury. We believe that in vitro models of mechanical injury will continue to be a valuable tool to study the cellular consequences and evaluate the potential therapeutic strategies for the treatment of traumatic injury of the CNS.

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“…The decline in cAMP levels due to PDE upregulation following injury may be a necessary step in allowing the proliferation of SCs that occurs following injury. Ekstrom (1995) demonstrated that elevated cAMP levels prevent SC proliferation after injury to the frog sciatic nerve, perhaps through cAMP dependent kinase inhibition of mitogen-activated protein kinases (Graves et aI., 1993;Sevetson et aI., 1993).…”

mentioning

confidence: 99%

Cell Biology and Pathology of Myelin

1997

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Cell biology and pathology of myelln evolving biological concepts and therapeutic approaches I edited by Bernhard H.J. Juurlink •. ,. let a1.l.p. cm. --(Alschul symposia ser ies ; v. 4) Includes bibllographical references and index. No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher v vi Preface dresses the cellular and molecular control over a glial cell's expression of the myelinating phenotype. The final part of the volume discusses evolving therapeutic approaches in the treatment of demyelinating/dysmyelinating diseases and for promotion of functional recovery after spinal cord injury. After reading the chapters in this volume, the reader will agree that over the last decade we have come a long way in unraveling the cell-cell interactions that govern gene expression involved in myelination and axonal growth. Understanding the mechanisms that govern these cell-cell interactions is opening the path to the development of rational and effective neurotherapies in the area of demyelinating/dysmyelinating diseases and spinal cord injuries.The symposium, using seed monies from the Altschul Trust Fund, could not have been held without the generous financial support of the following funding agencies and corporations

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Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

Cited by 7 publications

References 47 publications

Regulation of Schwann cell proliferation in cultured segments of the adult rat sciatic nerve

Regulation of Schwann cell proliferation in cultured segments of the adult rat sciatic nerve

In VitroCentral Nervous System Models of Mechanically Induced Trauma: A Review

Cell Biology and Pathology of Myelin

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