Expression of SDMF and atherosclerosis

SDMF的表达与动脉粥样硬化

• 批准号: 09671026
• 负责人: MORISAKI Nobuhiro
• 金额: $ 1.98万
• 依托单位: Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671026/
• 关键词: smooth muscle cells; SDMF; pheno type; migration; Autocrine; otherosclerosis; オートクリレ

1. in vivo expression of SDMF : Rats were subjected to baloon catheter injury and SDMF mRNA was examined by the northern blot analysis. SDMF was not expressed in the arteries before injury, but expressed in them 14 days after injury. Moreover, in situ hybridization staining revealed that SDMF mRNA was expressed in the arteries not before injury but 14 days after injury. SDMF was selectively expressed in the thickened intima but not in the media of the arteries 14 days after injury. The expression pattern was similar to that of type I collagen.2. regulation of SDMF gene : Cultured rat smooth muscle cells were used. Serum depletion from the culture medium stimulated SDMF mRNA expression by the northern blot analysis time-dependently from 12-48h. Next, serum depleted smooth muscle cells were stimulated by serum. On the first day, SDMF mRNA expression markedly decreased, then with increased cell density, SDMF mRNA expression increased, suggesting that cell density affects expression of SDMF gene. Finally, of various cytokines tested, only TGF-beta stimulated expression of SDMF.

1. SDMF在体内的表达：采用northern blot法检测大鼠气囊导管损伤后SDMF mRNA的表达。SDMF在损伤前未在动脉中表达，但在损伤后14 d有表达。此外，原位杂交染色显示，SDMF mRNA在损伤前而非损伤后14天在动脉中表达。损伤后14天，SDMF在增厚的内膜中选择性表达，而在动脉中不表达。表达模式与I型胶原相似。SDMF基因调控：采用培养的大鼠平滑肌细胞。通过northern blot分析，培养基中血清缺失刺激SDMF mRNA表达的时间依赖于12-48h。然后，用血清刺激血清耗竭的平滑肌细胞。第1天SDMF mRNA表达量明显降低，随着细胞密度的增加，SDMF mRNA表达量增加，提示细胞密度影响SDMF基因的表达。最后，在测试的各种细胞因子中，只有tgf - β刺激SDMF的表达。

项目成果

Morisaki N et al: "Angisgenic interaction between retina EC and PC from normal unddiabetic rabbits, and phenotype changes of diabetic cells" Cell Mol Biol. in press.

Morisaki N 等人：“正常非糖尿病兔视网膜 EC 和 PC 之间的血管生成相互作用，以及糖尿病细胞的表型变化”Cell Mol Biol。

Kanzaki T, Morisaki N et al: "Role of latent TGF-β binding protein in vascular remodeling" Biocheur Biophys Res Commun. 246. 26-30 (1998)

Kanzaki T、Morisaki N 等人：“潜在 TGF-β 结合蛋白在血管重塑中的作用”Biocheur Biophys Res Commun. 246. 26-30 (1998)。

Ikeda M, …, Morisaki N et al: "Natriuretic peptidl family as a novel antimigration factor of vascular smooth muscle cells" Arterloscler Thromb Vasc Biol. 17. 731-736 (1997)

Ikeda M, …, Morisaki N 等人：“钠尿肽家族作为血管平滑肌细胞的新型抗迁移因子”Arterloscler Thromb Vasc Biol。

Morisaki N et al.: "Angiogenic intera ction between retlnal EC and PC from mormal and diabetic rabbits, and phenotype chanyes of diabetic cell." Cell Mol Biol. (in press).

Morisaki N 等人：“正常兔子和糖尿病兔子的视网膜 EC 和 PC 之间的血管生成相互作用，以及糖尿病细胞的表型变化。”

Higashi T, …, Morisaki N et al.: "The receptor for advanced glycation and products mediates the chemotaxis of rabbit smooth muscle cells" Diabetes. 46. 463-472 (1997)

Higashi T, …, Morisaki N 等人：“晚期糖化受体及其产物介导兔平滑肌细胞的趋化性”糖尿病。 46. 463-472 (1997)