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Originally published In Press as doi:10.1074/jbc.M007492200 on October 26, 2000

J. Biol. Chem., Vol. 276, Issue 3, 2132-2138, January 19, 2001
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Intracellular Calcium Mobilization Induces Immediate Early Gene pip92 via Src and Mitogen-activated Protein Kinase in Immortalized Hippocampal Cells*

Kwang Chul ChungDagger §, Jee Young SungDagger §, Wooin AhnDagger , Hyewhon Rhim||, Tae Hwan Oh**, Min Goo LeeDagger , and Young Soo AhnDagger §

From the Dagger  Department of Pharmacology and § Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Korea, || Biomedical Research Center, Korea Institute of Science and Technology, Seoul 130-650, Korea, and ** Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Regulation of intracellular calcium levels plays a central role in cell survival, proliferation, and differentiation. A cell-permeable, tumor-promoting thapsigargin elevates the intracellular calcium levels by inhibiting endoplasmic reticulum Ca2+-ATPase. The Src-tyrosine kinase family is involved in a broad range of cellular responses ranging from cell growth and cytoskeletal rearrangement to differentiation. The immediate early gene pip92 is induced in neuronal cell death as well as cell growth and differentiation. To resolve the molecular mechanism of cell growth by intracellular calcium mobilization, we have examined the effect of thapsigargin and subsequent intracellular calcium influx on pip92 expression in immortalized rat hippocampal H19-7 cells. An increase of intracellular calcium ion levels induced by thapsigargin stimulated the expression of pip92 in H19-7 cells. Transient transfection of the cells with kinase-inactive mitogen-activated protein kinase kinase (MEK) and Src kinase or pretreatment with the chemical MEK inhibitor PD98059 significantly inhibited pip92 expression induced by thapsigargin. When constitutively active v-Src or MEK was overexpressed, the transcriptional activity of the pip92 gene was markedly increased. Dominant inhibitory Raf-1 blocked the transcriptional activity of pip92 induced by thapsigargin. The transcription factor Elk1 is activated during thapsigargin-induced pip92 expression. Taken together, these results suggest that an increase of intracellular calcium ion levels by thapsigargin stimulates the pip92 expression via Raf-MEK-extracellular signal-regulated protein kinase- as well as Src kinase-dependent signaling pathways.

* This work was supported by Korea Institute of Science & Technology Evaluation and Planning (KISTEP) Brain Science Research Grant 98-J04-02-01-A-08 (to K. C. C.), a Yonsei University College of Medicine faculty research grant for 1998 (to K. C. C.), and the Korea Institute of Science and Technology (KIST) Frontier Project (to T. H. O.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Pharmacology, Yonsei University College of Medicine, Shinchon-Dong 134, Seodaemun-Gu, Seoul 120-752, Korea. Tel.: 82-2-361-5229; Fax: 82-2-313-1894; E-mail: kchung@yumc.yonsei.ac.kr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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