caa a22 4500 475748387 CHVBK 20180406123520.0 cr unu---uuuuu 170329e20000701xx s 000 0 eng 10.1023/A:1006623905019 doi (NATIONALLICENCE)springer-10.1023/A:1006623905019 A Unique Monoclonal Antibody mNI-11 Rapidly Enhances Spread Formation in Human Umbilical Vein Endothelial Cells [Elektronische Daten] [Nobunao Ikewaki, Hidekazu Tamauchi, Akira Yamada, Norimasa Mori, Hiromichi Yamao, Hiroshi Inoue, Hidetoshi Inoko] We previously reported a novel monoclonal antibody (MAb), designated mNI-11, recognizing an adhesion-associated antigen distinct from any previously reported ones. In this article, this adhesion-associated antigen with a molecular weight of about 97 kDa was found to be strongly expressed on human umbilical vein endothelial cells (HUVECs) by fluorescence-activated cell sorter (FACS) analysis. Expression of this antigen on HUVECs was slightly increased in response to the exposure to tumor necrosis factor-α (TNF-α) or phorbol myristate acetate (PMA). As a biological function exerted by this antigen, it was of great interest that immobilized mNI-11 directly and rapidly enhanced the spread formation of HUVECs, whereas MAbs binding other adhesion-associated antigens such as mNI-58A (anti-CD11a), L130 (anti-CD18), L133.1 (anti-CD31), L178 (anti-CD44), L25.3 (anti-CD49d), or LB-2 (anti-CD54) did not carry such activity under the same conditions. The HUVECs spread formation enhanced by mNI-11 was completely blocked in the presence of a microfilament formation inhibitor, cytochalasin D (CyD), a Ca2+-calmodulin inhibitor, W-7, EDTA, and was partially blocked by a microtubule formation inhibitor, nocodazole, a protein kinase C (PKC) inhibitor, H-7, and a protein synthesis inhibitor, cycloheximide (CHX). However, a protein tyrosine kinase (PTK) inhibitor, genistein, did not affect the spread formation under the same conditions. Taken together, it was suggested that the spread formation of HUVECs enhanced by mNI-11 was mainly associated with the influx of Ca2+ and microfilament reorganization. In addition, the novel property associated with mNI-11 to enhance the spread formation of HUVECs was possibly mediated through its reaction against a unique epitope on HUVECs. Plenum Publishing Corporation, 2000 Human umbilical vein endothelial cells (HUVECs) nationallicence mNI-11 nationallicence monoclonal antibody nationallicence spread formation nationallicence Ikewaki Nobunao aut Tamauchi Hidekazu aut Yamada Akira aut Mori Norimasa aut Yamao Hiromichi aut Inoue Hiroshi aut Inoko Hidetoshi aut Journal of Clinical Immunology Kluwer Academic Publishers-Plenum Publishers 20/4(2000-07-01), 317-324 0271-9142 20:4<317 2000 20 10875 https://doi.org/10.1023/A:1006623905019 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1006623905019 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ikewaki Nobunao aut NATIONALLICENCE 700 1- Tamauchi Hidekazu aut NATIONALLICENCE 700 1- Yamada Akira aut NATIONALLICENCE 700 1- Mori Norimasa aut NATIONALLICENCE 700 1- Yamao Hiromichi aut NATIONALLICENCE 700 1- Inoue Hiroshi aut NATIONALLICENCE 700 1- Inoko Hidetoshi aut NATIONALLICENCE 773 0- Journal of Clinical Immunology Kluwer Academic Publishers-Plenum Publishers 20/4(2000-07-01), 317-324 0271-9142 20:4<317 2000 20 10875 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer