Tani Mariko, Tanaka Sarasa, Oeda Chihiro, Azumi Yuichi, Kawamura Hiromi, Sakaue Motoyoshi, Ito Mikiko
Graduate School of Human Science and Environment, University of Hyogo, 1-1-12 Shinzaike-Honcho, Himeji, Hyogo 670-0092, Japan.
School of Human Science and Environment, University of Hyogo, 1-1-12 Shinzaike-Honcho, Himeji, Hyogo 670-0092, Japan.
J Clin Biochem Nutr. 2021 Jan;68(1):23-31. doi: 10.3164/jcbn.19-114. Epub 2020 Jul 10.
Vascular calcification is major source of cardiovascular disease in patients with chronic kidney disease. Hyperphosphatemia leads to increased intracellular phosphorus influx, which leads to an increase in osteoblast-like cells in vascular smooth muscle cell. PiT-1 transports phosphate in vascular smooth muscle cell. However, the mechanism of vascular calcification is not completely understood. This study investigated candidate phosphorus-related molecules other than PiT-1. We hypothesized that phosphorus-related molecules belonging to the solute-carrier (SLC) superfamily would be involved in vascular calcification. As a result of DNA microarray analysis, we focused on SLC37A2 and showed that mRNA expression of these cells increased on calcified aotic smooth muscle cells (AoSMC). SLC37A2 has been reported to transport both glucose-6-phosphate/phosphate and phosphate/phosphate exchanges. analysis showed that SLC37A2 expression was not affected by inflammation on AoSMC. The expression of SLC37A2 mRNA and protein increased in calcified AoSMC. analysis showed that SLC37A2 mRNA expression in the aorta of chronic kidney disease rats was correlated with osteogenic marker genes. Furthermore, SLC37A2 was expressed at the vascular calcification area in chronic kidney disease rats. As a result, we showed that SLC37A2 is one of the molecules that increase with vascular calcification and .
血管钙化是慢性肾脏病患者心血管疾病的主要来源。高磷血症导致细胞内磷流入增加，进而导致血管平滑肌细胞中类成骨细胞增加。PiT-1在血管平滑肌细胞中转运磷酸盐。然而，血管钙化的机制尚未完全明确。本研究调查了除PiT-1之外的候选磷相关分子。我们假设属于溶质载体（SLC）超家族的磷相关分子会参与血管钙化。通过DNA微阵列分析，我们聚焦于SLC37A2，并发现这些细胞的mRNA表达在钙化的主动脉平滑肌细胞（AoSMC）中增加。据报道，SLC37A2可转运葡萄糖-6-磷酸/磷酸盐和磷酸盐/磷酸盐交换。分析表明，炎症对AoSMC上SLC37A2的表达没有影响。钙化的AoSMC中SLC37A2 mRNA和蛋白的表达增加。分析表明，慢性肾脏病大鼠主动脉中SLC37A2 mRNA表达与成骨标记基因相关。此外，SLC37A2在慢性肾脏病大鼠的血管钙化区域表达。结果，我们表明SLC37A2是随着血管钙化而增加的分子之一。
