Identification and regulation of differentiation In bone marrow -derived vascular progenitor cells

骨髓源性血管祖细胞分化的鉴定和调控

• 批准号: 13557061
• 负责人: HIRATA Yasunobu
• 金额: $ 7.42万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-13557061/
• 关键词: neointima; arteriosclerosis; stem cell; bone marrow; VSMC; LacZ; 成体幹細胞; 新生内膜I; 欠陥平滑筋; LacZ

We have suggested that bone marrow-derived progenitor cells may contribute to the pathogenesis of vascular diseases. On the other hand, It was reported that bone marrow cells do not participate substantially in vascular remodeling in other experimental systems. in this study, three distinct types of mechanical vascular injuries were induced in the same mouse whose bone marrow had been reconstituted with that of GFP or LacZ mice. All injuries are known to cause smooth muscle cell (SMC) hyperplasia. At 4 weeks after wire-mediated endovascular injury, a significant number of the neointlmal and medial cells derived from bone marrow. In contrast, marker-positive cells were seldom detected in the lesion induced by perivascular cuff replacement. There were only a few bone marrow-derived cells in the neointima after ligation of the common carotid artery. These results indicate that the origin of Intimal cells is diverse and that contribution of bone marrow-derived cells to neointlmal hyperpiasia depends on the type of model.

我们已经提出，骨髓来源的祖细胞可能有助于血管疾病的发病机理。另一方面，据报道，骨髓细胞在其他实验系统中没有基本参与血管重塑。在这项研究中，在同一小鼠中诱导了三种不同类型的机械血管损伤，其骨髓已与GFP或LACZ小鼠的骨髓重构。已知所有损伤都会引起平滑肌细胞（SMC）增生。电线介导的内血管内损伤后4周，大量的新生细胞和内侧细胞来自骨髓。相反，在血管周围袖口置换诱导的病变中很少检测到标记阳性细胞。普通颈动脉连接后，新内膜中只有几个骨髓衍生的细胞。这些结果表明，内膜细胞的起源是多种多样的，并且骨髓衍生的细胞对新肿瘤性超症的贡献取决于模型的类型。

项目成果

Sata M, Hirata Y, et al.: "Acute and chronic smooth muscle cell apoptosis after mechanical vascular injury can occur independently of the fas-death pahtway"Arterioscler Thromb Vasc Biol. 21. 1733-1737 (2001)

Sata M、Hirata Y 等人：“机械性血管损伤后的急性和慢性平滑肌细胞凋亡可以独立于 fas-死亡途径发生”Arterioscler Thromb Vasc Biol。

Abe M, Sata M, Nishimatsu H, Nagata D, Suzuki E, Terauchi Y, Kadowaki T, Matsuo H, Hirata Y, Nagai R: "Adrenomedullin augments collateral development in response to acute ischemia."Biochem Biophys Res Commun. 306. 10-15 (2003)

Abe M、Sata M、Nishimatsu H、Nagata D、Suzuki E、Terauchi Y、Kadowaki T、Matsuo H、Hirata Y、Nagai R：“肾上腺髓质素增强侧枝发育以应对急性缺血。”Biochem Biophys Res Commun。

Saiura A, Hirata Y, et al.: "Tranilast inhibits transplant-associated coronary arteriosclerosis in a murine model of cardiac transplantation"Eur J Pharmacol. 433. 163-168 (2001)

Saiura A、Hirata Y 等人：“曲尼司特在小鼠心脏移植模型中抑制移植相关的冠状动脉硬化”Eur J Pharmacol。

Suzuki E, Hirata Y. et al.: "Angiotensin II induces myocyte enhancer factor 2-and calcineurin/nuclear factor of activated T cell-dependent transcriptional activation in vascular myocytes"Circ.Res.. 90. 1004-1011 (2002)

Suzuki E、Hirata Y.等人：“血管紧张素 II 诱导血管肌细胞中激活的 T 细胞依赖性转录激活的肌细胞增强因子 2-和钙调神经磷酸酶/核因子”Circ.Res.. 90. 1004-1011 (2002)

Satonaka H, Hirata Y 他: "Calcineurin promotes the expression of monocyte chemoattractant protein-1 in vascular myocytes and mediates vascular inflammation."Circ Res. (in press). (2004)

Satonaka H、Hirata Y 等人：“钙调磷酸酶促进血管肌细胞中单核细胞趋化蛋白-1 的表达并介导血管炎症。”Circ Res（出版中）。