Ishiguro K, Kadomatsu K, Kojima T, Muramatsu H, Nakamura E, Ito M, Nagasaka T, Kobayashi H, Kusugami K, Saito H, Muramatsu T
Department of Biochemistry, Nagoya University School of Medicine, Showa-ku, Nagoya, Aichi, Japan.
Dev Dyn. 2000 Dec;219(4):539-44. doi: 10.1002/1097-0177(2000)9999:9999<::AID-DVDY1081>3.0.CO;2-K.
Syndecan-4 is a transmembrane protein bearing heparan sulfate chains, involved in anticoagulation and focal adhesion formation. Here, we revealed that syndecan-4 was expressed in the fetal vessels in the placental labyrinth by in situ hybridization and immunohistochemical staining. At 17.5 gestational days, the area of degenerated fetal vessels in the placental labyrinth was more diffuse and larger in Synd4(-/-) embryos than wild-type controls. Calcium and fibrin(ogen) depositions in the degenerated vessels were also more extensive and more severe in the placentas of Synd4(-/-) embryos. These findings suggest that syndecan-4 deficiency impairs the fetal vessels in the placenta, probably due to a deficit in the anticoagulation mechanism. This article is the first report demonstrating that among a large number of core proteins of heparan sulfate proteoglycans, a defect of a single core protein caused impaired anticoagulation in a specific site.
Syndecan-4是一种带有硫酸乙酰肝素链的跨膜蛋白,参与抗凝和粘着斑形成。在此,我们通过原位杂交和免疫组织化学染色揭示,syndecan-4在胎盘迷路的胎儿血管中表达。在妊娠17.5天时,Synd4(-/-)胚胎胎盘迷路中退化胎儿血管的面积比野生型对照更弥散且更大。Synd4(-/-)胚胎胎盘退化血管中的钙和纤维蛋白(原)沉积也更广泛且更严重。这些发现表明,syndecan-4缺乏会损害胎盘内的胎儿血管,可能是由于抗凝机制存在缺陷。本文是首次报道,在大量硫酸乙酰肝素蛋白聚糖的核心蛋白中,单一核心蛋白的缺陷会导致特定部位的抗凝功能受损。