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首页> 外文期刊>Stem Cell Research & Therapy >Conditioned medium from bone marrow-derived mesenchymal stem cells inhibits vascular calcification through blockade of the BMP2–Smad1/5/8 signaling pathway
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Conditioned medium from bone marrow-derived mesenchymal stem cells inhibits vascular calcification through blockade of the BMP2–Smad1/5/8 signaling pathway

机译：骨髓源间充质干细胞的条件培养基通过阻断BMP2–Smad1 / 5/8信号通路抑制血管钙化

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Arterial calcification is associated with cardiovascular disease as a complication of advanced atherosclerosis and is a significant contributor to cardiovascular morbidity and mortality. Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) plays an important role in arterial calcification and is characterized by cellular necrosis, inflammation, and lipoprotein and phospholipid complexes, especially in atherosclerotic calcification. The conditioned medium from bone marrow-derived mesenchymal stem cells (MSC-CM) is well known as a rich source of autologous cytokines and is universally used for tissue regeneration in current clinical medicine. Here, we demonstrate that MSC-CM inhibits beta-glycerophosphate (β-GP)-induced vascular calcification through blockade of the bone morphogenetic protein-2 (BMP2)–Smad1/5/8 signaling pathway. VSMC calcification was induced by β-GP followed by treatment with MSC-CM. Mineral deposition was assessed by Alizarin Red S staining. Intracellular calcium content was determined colorimetrically by the o-cresolphthalein complexone method and alkaline phosphatase (ALP) activity was measured by the para-nitrophenyl phosphate method. Expression of BMP2, BMPR1A, BMPR1B, BMPR2, msh homeobox?2 (Msx2), Runt-related transcription factor 2 (Runx2), and osteocalcin (OC), representative osteoblastic markers, was assessed using real-time polymerase chain reaction analysis while the protein expression of BMP2, Runx2, and phosphorylated Smad1/5/8 was detected by western blot analysis. Our data demonstrated that MSC-CM inhibits osteoblastic differentiation and mineralization of VSMCs as evidenced by decreased calcium content, ALP activity, and decreased expression of BMP-2, Runx2, Msx2, and OC. MSC-CM suppressed the expression of phosphorylated Smad1/5/8 and the β-GP-induced translocation from the cytoplasm to the nucleus. Further study demonstrated that human recombinant BMP-2 overcame the suppression of VSMC calcification by MSC-CM. MSC-CM may act as a novel therapy for VSMC calcification by mediating the BMP2–Smad1/5/8 signaling pathway
机译：动脉钙化与心血管疾病有关，是晚期动脉粥样硬化的并发症，并且是心血管发病率和死亡率的重要因素。血管平滑肌细胞（VSMC）的成骨细胞分化在动脉钙化中起重要作用，其特征是细胞坏死，炎症以及脂蛋白和磷脂复合物，特别是在动脉粥样硬化钙化中。众所周知，来自骨髓间充质干细胞（MSC-CM）的条件培养基是自体细胞因子的丰富来源，并且在当前的临床医学中普遍用于组织再生。在这里，我们证明了MSC-CM通过阻断骨形态发生蛋白2（BMP2）–Smad1 / 5/8信号通路来抑制β-甘油磷酸（β-GP）诱导的血管钙化。 β-GP诱导VSMC钙化，然后用MSC-CM处理。矿物沉积通过茜素红S染色评估。用邻甲酚酞配合物比色法测定细胞内钙含量，用对硝基苯磷酸酯法测定碱性磷酸酶（ALP）的活性。使用实时聚合酶链反应分析评估BMP2，BMPR1A，BMPR1B，BMPR2，msh homeobox？2（Msx2），Runt相关转录因子2（Runx2）和骨钙蛋白（OC）的表达，这些表达是成骨细胞标志物。 Western印迹分析检测BMP2，Runx2和磷酸化Smad1 / 5/8的蛋白表达。我们的数据表明，MSC-CM抑制VSMC的成骨细胞分化和矿化，这可以通过降低钙含量，ALP活性以及降低BMP-2，Runx2，Msx2和OC的表达来证明。 MSC-CM抑制了磷酸化Smad1 / 5/8的表达和β-GP诱导的从细胞质到细胞核的转运。进一步的研究表明，人重组BMP-2克服了MSC-CM对VSMC钙化的抑制作用。 MSC-CM可能通过介导BMP2-Smad1 / 5/8信号通路而成为VSMC钙化的新疗法

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