Effect of postconditioning on dynamic expression of tenascin-C and left ventricular remodeling after myocardial ischemia and reperfusion.
Effect of postconditioning on dynamic expression of tenascin-C and left ventricular remodeling after myocardial ischemia and reperfusion.
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DOI：
10.1186/s13550-015-0100-8
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发表时间：
2015
期刊：
影响因子：
3.2
通讯作者：
Kinuya S
中科院分区：
文献类型：
--
作者：
Taki J;Inaki A;Wakabayashi H;Matsunari I;Imanaka-Yoshida K;Ogawa K;Hiroe M;Shiba K;Yoshida T;Kinuya S
Tenascin-C （TNC）是一种细胞外基质糖蛋白，在与活跃组织重塑相关的不同区域短暂表达。本研究旨在利用125i标记的抗TNC抗体（125I-TNC-Ab），探讨缺血后适应（PC）对缺血再灌注大鼠心肌TNC表达和心室重构的影响。对照组大鼠27只，左冠状动脉（LCA）闭塞30 min，再灌注1、3、7、14天。再灌注后立即行PC （n = 27）。在研究时，注射125I-TNC-Ab （1.0 - 2.5 MBq）。6 ~ 9 h后，在LCA再闭塞后立即静脉注射99mTc-MIBI (100 ~ 200 MBq)，以验证危险区域，1 min后处死大鼠。双示踪放射自显影术评估125I-TNC-Ab摄取和危险面积。两组再灌注2 M后行超声心动图检查心室重构情况。对照大鼠再灌注后1天125I-TNC-Ab摄取比为3.73±0.71，第3天升高（4.65±0.87），第7天（2.91±0.55,P < 0.005，第3天）和第14天（2.01±0.17,P < 0.005，第1天和第3天）显著降低。在1 ~ 14天的再灌注期间，PC降低了125I-TNC-Ab的摄取；1天2.59±0.59,P < 0.05:在3天,3.10±0.42 P < 0.005:在7天1.93±0.37,P < 0.05:在14天1.40±0.07,P < 0.001。超声心动图显示，PC降低了心室舒张末期和收缩期尺寸（分别为1.00±0.06 cm至0.83±0.14 cm （P < 0.05）和0.90±0.15 cm至0.62±0.19 cm (P < 0.05)），阻止了心室分数缩短百分率的下降（10.5±3.7至28.2±10.7,P < 0.005）。这些数据表明，125I-TNC-Ab成像可以通过可视化TNC表达来监测心肌损伤、随后的修复过程以及其对PC等新型治疗干预措施的反应。
Tenascin-C (TNC), an extracellular matrix glycoprotein, is expressed transiently in distinct areas in association with active tissue remodeling. This study aimed to explore how ischemic postconditioning (PC) affects myocardial expression of TNC and ventricular remodeling using 125I-labeled anti-TNC antibody (125I-TNC-Ab) in a rat model of ischemia and reperfusion. In control rats (n = 27), the left coronary artery (LCA) was occluded for 30 min followed by reperfusion for 1, 3, 7, and 14 days. PC (n = 27) was performed just after the reperfusion. At the time of the study, 125I-TNC-Ab (1.0 to 2.5 MBq) was injected. Six to 9 h later, to verify the area at risk, 99mTc-MIBI (100 to 200 MBq) was injected intravenously just after the LCA reocclusion, with the rats sacrificed 1 min later. Dual tracer autoradiography was performed to assess 125I-TNC-Ab uptake and area at risk. To examine the ventricular remodeling, echocardiography was performed 2 M after reperfusion in both groups. In control rats, 125I-TNC-Ab uptake ratio at 1 day after reperfusion was 3.73 ± 0.71 and increased at 3 days (4.65 ± 0.87), followed by a significant reduction at 7 days (2.91 ± 0.55, P < 0.005 vs 3 days) and14 days (2.01 ± 0.17, P < 0.005 vs 1 and 3 days). PC attenuated the 125I-TNC-Ab uptake throughout the reperfusion time from 1 to 14 days; 2.59 ± 0.59 at 1 day, P < 0.05: 3.10 ± 0.42 at 3 days, P < 0.005: 1.93 ± 0.37 at 7 days, P < 0.05: 1.40 ± 0.07 at 14 days, P < 0.001. In echocardiography, PC reduced the ventricular end-diastolic and systolic dimensions (1.00 ± 0.06 cm to 0.83 ± 0.14 cm (P < 0.05) and 0.90 ± 0.15 cm to 0.62 ± 0.19 cm (P < 0.05), respectively) and prevented a decline of ventricular percentage fractional shortening (10.5 ± 3.7 to 28.2 ± 10.7, P < 0.005). These data indicate that 125I-TNC-Ab imaging may be a way to monitor myocardial injury, the subsequent repair process, and its response to novel therapeutic interventions like PC by visualizing TNC expression.
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