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Published January 1, 1995 | Published
Journal Article Open

An Anti-CD9 Monoclonal Antibody Promotes Adhesion and Induces Proliferation of Schwann Cells in vitro

Abstract

We have recently found that CD9, a cell surface glycoprotein involved in intercellular signaling in hematopoietic cells, is also expressed by neurons and glia in the peripheral nervous system. Antibody perturbation experiments were conducted to examine the function of CD9 in neural cells. Three anti-CD9 monoclonal antibodies (mAbs) (ROCA1, ROCA2, B2C11) were tested for their ability to promote adhesion of several Schwann cell lines (S-16, RN22, JS1), primary Schwann cells and PC12 cells. Only B2C11 promotes adhesion in all cells tested. Although ROCA2 immunolabels living cells strongly, it had no effect on the adhesion of any of these cells. In addition, ROCA1 and several positive- staining, control mAbs also had no effect. Another mAb, 192-IgG, directed against the low affinity NGF receptor, also promotes the adhesion of S-16, PC12, and primary Schwann cells. In addition to adhesion, contact of S-16 Schwann cells with B2C11 specifically induces morphological changes and robust proliferation. None of the other mAbs, including 192-IgG, induce proliferation of S-16 cells. These results provide evidence that CD9 may be involved in signaling, activation and growth regulation of cells in the nervous system.

Additional Information

© 1995 Society for Neuroscience. For the first six months after publication SfN's license will be exclusive. Beginning six months after publication the Work will be made freely available to the public on SfN's website to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). Received Mar. 29, 1994; revised June 13, 1994; accepted July 12, 1994. We thank Dr. Richard Quarles for the S-16 cells, Dr. David Anderson for the RN22, JSI, and PC12 cells; Doreen McDowell for media preparation; and Drs. Joshua Sanes, Zaven Kaprielian, Karen Allendoerfer; and Kyung-Ok Cho for their constructive comments on the manuscript. This work was supported by an NINDS grant to P.H.P. and an American Heart Association Research Fellowship and an NIH Training Grant fellowship to M.H.

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