Kim Mi-Kyoung, Kim Sang Doo, Lee Ha Young, Lee Sun Young, Shim Jae Woong, Yun Jeanho, Kim Jong-Min, Min Do Sik, Yoo Young Hyun, Bae Yoe-Sik
Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
FEBS Lett. 2008 Oct 15;582(23-24):3379-84. doi: 10.1016/j.febslet.2008.09.023. Epub 2008 Sep 18.
The collagen-binding motif (CBM) peptide, a cleavage product of osteopontin (OPN), stimulated intracellular calcium increase in human neutrophils. CBM peptide-stimulated calcium was inhibited by pertussis toxin (PTX), suggesting the influence of PTX-sensitive G-proteins. In addition CBM peptide stimulated the chemotactic migration of human neutrophils and human monocytes. CBM peptide-induced neutrophil chemotaxis was completely inhibited by PTX, once again indicating the influence of Gi proteins. CBM peptide was also found to induce mitogen activated protein kinase activation. CBM peptide-induced neutrophil chemotaxis was mediated by p38 kinase as well as an extracellular signal-regulated protein kinase. Taken together, the results suggest that a cleavage product of OPN, CBM peptide, initiates immune responses by inducing neutrophil trafficking via certain PTX-sensitive cell surface receptors.
骨桥蛋白（OPN）的裂解产物——胶原结合基序（CBM）肽，可刺激人中性粒细胞内的钙离子增加。百日咳毒素（PTX）可抑制CBM肽刺激引起的钙离子增加，提示PTX敏感型G蛋白的影响。此外，CBM肽可刺激人中性粒细胞和人单核细胞的趋化迁移。PTX可完全抑制CBM肽诱导的中性粒细胞趋化，再次表明Gi蛋白的影响。还发现CBM肽可诱导丝裂原活化蛋白激酶激活。CBM肽诱导的中性粒细胞趋化由p38激酶以及细胞外信号调节蛋白激酶介导。综上所述，结果表明OPN的裂解产物CBM肽通过某些PTX敏感型细胞表面受体诱导中性粒细胞迁移，从而引发免疫反应。
