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Originally published In Press as doi:10.1074/jbc.M300205200 on April 14, 2003

J. Biol. Chem., Vol. 278, Issue 25, 22555-22562, June 20, 2003
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PP2A Activation by {beta}2-Adrenergic Receptor Agonists

NOVEL REGULATORY MECHANISM OF KERATINOCYTE MIGRATION*

Christine E. Pullar, Jin Chen and R. Rivkah Isseroff {ddagger}

From the Department of Dermatology, University of California, Davis, Davis, California 95616

Understanding the mechanisms that regulate cell migration is important for devising novel therapies to control metastasis or enhance wound healing. Previously, we demonstrated that {beta}2-adrenergic receptor ({beta}2-AR) activation in keratinocytes inhibited their migration by decreasing the phosphorylation of a critical promigratory signaling component, the extracellular signal-related kinase (ERK). Here we demonstrate that {beta}2-AR-induced inhibition of migration is mediated by the activation of the serine/threonine phosphatase PP2A. Pretreating human keratinocytes with the PP2A inhibitor, okadaic acid, prevented the {beta}2-AR-induced inhibition of migration, either as isolated cells or as a confluent sheet of cells repairing an in vitro "wound" and also prevented the {beta}2-AR-induced reduction in ERK phosphorylation. Similar results were obtained with human corneal epithelial cells. In keratinocytes, immunoprecipitation studies revealed that {beta}2-AR activation resulted in the rapid association of {beta}2-AR with PP2A as well as a 37% increase in association of PP2A with ERK2. Finally, {beta}2-AR activation resulted in a rapid and transient 2-fold increase in PP2A activity. Thus, we provide the first evidence that {beta}2-AR activation in keratinocytes modulates migration via a novel pathway utilizing PP2A to alter the promigratory signaling cascade. Exploiting this pathway may result in novel therapeutic approaches for control of epithelial cell migration.

Received for publication, January 8, 2003 , and in revised form, March 20, 2003.

* This work was supported in part by National Institutes of Health Grant AR 44518 (to R. R. I.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

{ddagger} To whom correspondence should be addressed: University of California, Davis, Dept. of Dermatology, TB192, One Shields Ave., Davis, CA 95616. Tel.: 530-752-9767; Fax: 530-752-9766; E-mail: rrisseroff{at}ucdavis.edu.


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