Potential role for antiangiogenic proteins in the myocardial infarction repair process
Potential role for antiangiogenic proteins in the myocardial infarction repair process
复制标题
DOI：
10.1016/j.jss.2003.06.001
复制
发表时间：
2004-01-01
影响因子：
2.2
通讯作者：
Schwarz, MA
中科院分区：
文献类型：
--
作者：
Thompson, JL;Ryan, JA;Schwarz, MA
客观的。尽管血管生成蛋白已被确定为急性心肌梗塞后心肌血运重建的正调节剂，但关于抗血管生成蛋白在心肌血运重建中的作用知之甚少。我们探索了内皮单核细胞激活多肽 (EMAP) II 的时空分布，以确定抗血管生成蛋白是否在梗塞后心肌组织的修复中发挥作用。方法。利用大鼠心肌梗塞模型来检查 6 周内的 EMAP II 分布（原位杂交）和蛋白质表达（Western 分析）。结果。在基线时，EMAP II 蛋白和 mRNA 的表达量最低，转录产物主要位于正常大鼠心肌的血管周围基质区域。心肌梗塞后六小时，EMAP II 将其分布从血管周围基质转变为入侵的炎症细胞群。这与 EMAP II 蛋白的 2 倍增加 (P < 0.0009) 及其转录主要定位于梗塞区域相关。 EMAP II 蛋白表达在梗塞后的几周内保持升高，转录仅限于梗塞区域，并且在梗塞区域周围的活脉管系统中注意到 EMAP II 转录产物显着减少。心肌梗塞后六周，EMAP II 蛋白升高至高于对照，将其转录位置从炎症细胞群改变为位于相对无血管疤痕组织中的成纤维细胞，并恢复其在存活的梗塞周围组织中的血管周围基质分布。结论。因此，这种抗血管生成蛋白的时空分布表明负性血管调节剂可能在急性心肌梗塞后的血运重建过程中发挥作用。 (C) 2004 Elsevier Inc. 保留所有权利。
Objective. Although angiogenic proteins have been identified as positive modulators of myocardial revascularization following acute myocardial infarction, little if anything is known regarding the role that antiangiogenic proteins have in myocardial revascularization. We explored the temporospatial distribution of endothelial-monocyte activating polypeptide (EMAP) II to determine whether antiangiogenic proteins have a role in the repair of myocardial tissue following infarction.Methods. A rat model of myocardial infarction was utilized to examine EMAP II distribution (in situ hybridization) and protein expression (Western analysis) over a 6-week period.Results. At baseline, EMAP II protein and mRNA are minimally expressed with transcription products localizing predominately to the perivascular stroma region in the normal rat myocardium. Six hours following myocardial infarction, EMAP II changes its distribution from the perivascular stroma to an invading inflammatory cell population. This is associated with a 2-fold (P < 0.0009) increase in EMAP II protein and its transcription primarily localized to the infarct region. EMAP II protein expression remains elevated throughout the weeks following the infarction with transcription limited to the infarct region and a notable decrease in EMAP II transcription products noted in the viable vasculature surrounding the infarct zone. Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue.Conclusion. Thus, the temporospatial distribution of this antiangiogenic protein suggests that negative vascular modulators may have a function in the revascularization process following acute myocardial infarction. (C) 2004 Elsevier Inc. All rights reserved.