Volume 272, Number 44, Issue of October 31, 1997 pp. 27987-27993
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Role of Egr-1 Gene Expression in B Cell Receptor-induced Apoptosis in an Immature B Cell Lymphoma

(Received for publication, March 10, 1997, and in revised form, June 3, 1997)

Subramanian Muthukkumar ^§ , Seong-Su Han ^§ , Sumathi Muthukkumar , Vivek M. Rangnekar and Subbarao Bondada ^§

From the  Department of Microbiology and Immunology, the ^§ Sanders Brown Research Center on Aging, and the  Department of Surgery, Division of Urology, University of Kentucky, Lexington, Kentucky 40536

Ligation of B cell receptor (BCR) on BKS-2, an immature B cell lymphoma by anti-IgM antibodies (Ab) caused apoptosis. Here we report that signaling through B cell receptor in wild type BKS-2 cells down-regulated the expression of Egr-1, a zinc finger-containing transcription factor. A reduction in the level of Egr-1 mRNA could be demonstrated as early as 30 min after the ligation of BCR on BKS-2 cells. Immunocytochemical and Western blot analysis revealed that the expression of EGR-1 protein was also inhibited by anti-IgM treatment. Antisense oligonucleotides to Egr-1 caused growth inhibition and apoptosis in BKS-2 cells, suggesting that expression of Egr-1 is important for the survival of these B lymphoma cells. In contrast to wild type BKS-2 cells, the mutant 1.B5 cell line, which is refractory to B cell receptor-mediated growth-inhibitory signals, showed an increased expression of Egr-1 upon treatment with anti-IgM. These results implicate a role for Egr-1 in blocking B cell receptor-mediated apoptosis in immature B cells.

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