期刊文献+

M-CSF促进RAW 264.7细胞MMP-9的分泌及其可能机制 被引量:6

Wpiegulation of macrophage colony-stimulating factor on protease secretion in RAW 264.7 cell and its possible mechanism
下载PDF
导出
摘要 目的探讨巨噬细胞集落刺激因子(MCSF)致动脉粥样硬化的作用是否与其影响基质金属蛋白酶(MMP)表达和活性改变有关及其可能机制。方法应用明胶酶图分析方法观察MCSF和(或)PD98059对体外培养的RAW264.7细胞MMP9活性的影响;Westerblot检测MCSF和(或)PD98059对体外培养的RAW264.7细胞pERK1/2表达的影响。结果MCSF能增强RAW264.7细胞MMP9的活性,并呈一定的剂量依赖性;同时MCSF也呈时间、浓度依赖性促进pERK1/2的表达;PD98059不仅阻断了ERK1/2的磷酸化,而且也降低了MMP9的活性。结论MCSF可诱导RAW264.7细胞MMP9的活性增加,其机制可能与MCSF激活MAPKERK1/2通路有关。 Aim To study the effect of Macrophage colony-stimulating factor(M-CSF) on MMP-9 in RAW 264. 7 cell and explore the relationship between atherosclerosis caused by M-CSF and the activity of MMP-9. Methods Gelatin zymography analysis was used to investigate the effect of M-CSF and PI)98059 on the activity of MMP-9 in cultured RAW 264. 7 cell. Western blot was used to study the effect of M-CSF and PD98059 on the express of p-ERK1/2 in cultured RAW 264. 7 cell. Results The enzyme activity of MMP-9 was significantly increased after 24-hour M- CSF treatment. Meanwhile, M-CSF upregulated the expression of p-ERK1/2. Pre-treatment with PD98059 blocked partly the increased expression of p-ERK1/2 and the activity of MMP-9 induced by M-CSF. Conclusion M-CSF can induce the secretion of MMP9 in RAW 264. 7 cell, which may be mediated by the phosphorylation of ERK1/2.
出处 《中国药理学通报》 CAS CSCD 北大核心 2006年第8期947-951,共5页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助课题(No30470719)
关键词 巨噬细胞集落刺激因子 基质金属蛋白酶 细胞外信号调节激酶1/2 动脉粥样硬化 巨噬细胞 macrophage colony-stimulating factor MMP ERK1/2 atherosclerosis RAW 264. 7
  • 相关文献

参考文献22

  • 1Galis Z S,Sukhova G K,Lark M W,et al.Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques[J].J Clin Invest,1994,94:2493-503.
  • 2Brown D L,Hibbs M S,Kearney M,et al.Identification of 92-kD gelatinase in human coronary atherosclerotic lesions:association of active enzyme synthesis with unstable angina[J].Circulation,1995,91:2125 -31.
  • 3Loftus I M,Naylor A R,Goodall S.Increased matrix metalloproteinase-9 activity in unstable carotid plaques.A potential role in acute plaque disruption[J].Stroke,2000,31(1):40 -7.
  • 4Ferroni P,Basili S,Martini F,et al.Serum metalloproteinase 9 levels in patients with coronary artery disease:a novel marker of inflammation[J].J Investig Med,2003,51 (5):295-300.
  • 5Jones C B,Sane D C,Herrington D M.Matrix metalloproteinases:a review of theirstructure and role in acute coronary syndrome[J].Cardiovasc Res,2003,59 (4):812-23.
  • 6Pang Z J.Effect of macrophage colony stimulating factor overexpression on oxidative injury/resistance of RAW264.7 cells[J].Clin Exp Med,2003,3(1):20-6.
  • 7Mozes G,Mohacsi F,Gloviozki P,et al.Adenovirus-mediated gene transfer of macrophage colony stimulating factor to the arterial wall in vivo[J].Arterioscler Thromb Vasc Biol,1998,18:1157 -63.
  • 8Hojo Y,Ikeda U,Takahashi M,et al.Increased levels of monocyte-related cytokines in patients with unstable angina[J].Atherosclerosis,2002,161 (2):403-8.
  • 9Rallidis L S,Zolindaki M G,Manioudaki H S,et al.Prognostic value of C-reactive protein,fibrinogen,interleukin-6,and macrophage colony stimulating factor in severe unstable angina[J].Clin Cardiol,2002,25(11):505-10.
  • 10Rallidis L S,Zolindaki M G,Pentzeridis P C,et al.Raised concentrations of macrophage colony stimulating factor in severe unstable angina beyond the acute phase are strongly predictive of long term outcome[J].Heart,2004,90(1):25 -9.

二级参考文献11

  • 1Zempo N, Koyama N,Richard DK et al. Regulation of vascular smooth muscle cell migration and proliferation in vitro and in injured rat arteries by a synthetic matrix metalloproteinase inhibitor. Arterioscler, Throm Vasc Biol,1996;16(1):28~33
  • 2Bunkenburg B,Amelsvoort T,Rogg H et al. Receptor-mediated effects of angiotensin Ⅱ on growth of vascular smooth muscle cells from spontaneously hypertensive rats. Hypertension,1992;20(6):746~54
  • 3Pauly RR, Passaniti A, Bilato C et al. Migration of cultured vascular smooth muscle cells through a basement membrane barrier requires type Ⅳ collagenase activity and is inhibited by cellular differentiation. Circ Res,1994;75(1):41~54
  • 4文允镒. 高血压时的血管改变及其机制. 见:孙宁玲,徐成斌主编. 今日高血压,第1版,北京:中国医药科技出版社,2000:49-50
  • 5Gibbons GH,Dzau VJ. The emerging concept of vascular remodeling.N Engl J Med,1994;330(20):1431~8
  • 6Saito S, Frank GD, Motley ED et al. Metalloproteinase inhibitor blocks angiotensin Ⅱ-induced migration through inhibition of epidermal growth factor receptor transactivation. Biochem Biophys Res Commun, 2002;294(5):1023~9
  • 7Matsubara H. Pathophysiological role of angiotensin Ⅱ type 2 receptor in cardiovascular and renal disease. Circ Res, 1998;83(12):1182~91
  • 8Tsutsumi Y,Matsubara H,Masaki H et al. Angiotensin Ⅱ type 2 receptor overexpression activates the vascular kinin system and causes vasodilation. J Clin Invest, 1999;104(7):925~35
  • 9Li JS, Sharifi AM, Schiffrin EL. Effect of AT1 angiotensin-receptor blockade on structure and function of small arteries in SHR. J Cardiovasc Pharmacol, 1997;30(1):75~83
  • 10卢韶华,张农,张秀荣,吴浩,方磊,生玮,张月娥,许祖德.大鼠肺纤维化模型间质成纤维细胞和肺泡巨噬细胞基质金属蛋白酶2及膜型基质金属蛋白酶mRNA的表达[J].中华结核和呼吸杂志,2001,24(9):527-530. 被引量:18

同被引文献96

引证文献6

二级引证文献32

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部