Perfusion defect size predicts engraftment but not early retention of intra-myocardially injected cardiosphere-derived cells after acute myocardial infarction.
Perfusion defect size predicts engraftment but not early retention of intra-myocardially injected cardiosphere-derived cells after acute myocardial infarction.
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DOI：
10.1007/s00395-011-0197-5
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发表时间：
2011-11
影响因子：
9.5
通讯作者：
Bengel FM
中科院分区：
文献类型：
--
作者：
Lautamäki R;Terrovitis J;Bonios M;Yu J;Tsui BM;Abraham MR;Bengel FM
治疗性细胞的保留和植入是心肌再生的关键。潜在的机制，包括组织灌流的作用，还不是很清楚。在Wistar京都大鼠的实验性心肌梗死后，心肌内注射同基因的心肌球源性细胞(CDCs)。CDCs用[18F]-FDG(n=7)标记，用于1h滞留的定量；或用钠碘转运体基因(NIS；n=108)标记，用于报告成像检测24 h的植入。同时进行脑血流灌注成像。FDG组和NIS组心肌梗死面积分别为LV的37±9.9%和38±10.9%。所有动物的细胞信号均位于梗死区边缘。心肌梗死面积与1h CDC滞留无明显相关性(r=0.65；−=0.11)。然而，梗死范围与24小时植入显著相关(r=0.75；P=0.03)。注射部位的残余灌注量与细胞滞留/植入无关。更大的梗塞与CDC植入的改善有关。这一观察结果鼓励进一步研究缺血损伤后的微环境条件及其在治疗细胞存活中的作用。
Therapeutic cell retention and engraftment are critical for myocardial regeneration. Underlying mechanisms, including the role of tissue perfusion, are not well understood. In Wistar Kyoto rats, syngeneic cardiosphere-derived cells (CDCs) were injected intramyocardially, after experimental myocardial infarction. CDCs were labeled with [18F]-FDG (n = 7), for quantification of 1-h retention, or with sodium-iodide-symporter gene (NIS; n = 8), for detection of 24-h engraftment by reporter imaging. Perfusion was imaged simultaneously. Infarct size was 37 ± 9 and 38 ± 9% of LV in FDG and NIS groups. Cell signal was located in the infarct border zone in all animals. No significant relationship was observed between infarct size and 1-h CDC retention (r = −0.65; P = 0.11). However, infarct size correlated significantly with 24-h engraftment (r = 0.75; P = 0.03). Residual perfusion at the injection site was not related to cell retention/engraftment. Larger infarcts are associated with improved CDC engraftment. This observation encourages further investigation of microenvironmental conditions after ischemic damage and their role in therapeutic cell survival.
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