Inoh Kazuhiko, Muramatsu Hisako, Ochiai Keiko, Torii Shuhei, Muramatsu Takashi
Department of Biochemistry, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Biochem Biophys Res Commun. 2004 Apr 23;317(1):108-13. doi: 10.1016/j.bbrc.2004.03.015.
Midkine is a heparin-binding cytokine or growth factor and promotes the migration of inflammatory leukocytes. Upon partial hepatectomy, adhesion of the intestine was less severe in midkine-deficient mice than in wild-type mice. In a newly developed assay, in which the omentum adhered to the injured peritoneal wall, the incidence of adhesion in the deficient mice was reduced to 20% of that in the wild-type mice. Administration of midkine to the deficient mice increased the frequency of adhesion. The area of adhesion was also reduced to 8.3% in the deficient mice. The extent of migration of macrophages and neutrophils in the omentum around the adhesive region was reduced in the deficient mice. Therefore, midkine was concluded to play important roles in the formation of intraperitoneal adhesions, at least partly by promoting the migration of macrophages and neutrophils to the omentum.
中期因子是一种肝素结合细胞因子或生长因子，可促进炎性白细胞的迁移。在部分肝切除术后，中期因子缺陷小鼠的肠粘连程度比野生型小鼠轻。在一项新开发的检测中，大网膜粘附于受损的腹膜壁，缺陷小鼠的粘连发生率降至野生型小鼠的20%。给缺陷小鼠注射中期因子会增加粘连频率。缺陷小鼠的粘连面积也降至8.3%。缺陷小鼠中，粘连区域周围大网膜内巨噬细胞和中性粒细胞的迁移程度降低。因此，得出结论，中期因子在腹膜粘连形成中起重要作用，至少部分是通过促进巨噬细胞和中性粒细胞向大网膜迁移来实现的。
