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灌注缺损大小可预测移植,但不能预测急性心肌梗死后心肌内注射心脏球源性细胞的早期保留。

Perfusion defect size predicts engraftment but not early retention of intra-myocardially injected cardiosphere-derived cells after acute myocardial infarction.

机构信息

Division of Nuclear Medicine, Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.

出版信息

Basic Res Cardiol. 2011 Nov;106(6):1379-86. doi: 10.1007/s00395-011-0197-5. Epub 2011 Jun 25.

DOI:10.1007/s00395-011-0197-5
PMID:21706191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3228962/
Abstract

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 [(18)F]-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.

摘要

治疗性细胞保留和植入对于心肌再生至关重要。但基础机制,包括组织灌注的作用,尚不清楚。在 Wistar Kyoto 大鼠中,实验性心肌梗死后将同种异体心脏球源性细胞(CDCs)注射到心肌内。用 [(18)F]-FDG(n=7)标记 CDCs,以定量检测 1 小时的保留率,或用钠碘转运体基因(NIS;n=8)标记,以通过报告基因成像检测 24 小时的植入。同时进行灌注成像。梗死面积在 FDG 和 NIS 组分别为 LV 的 37±9%和 38±9%。在所有动物中,细胞信号都位于梗死交界区。梗死面积与 1 小时 CDC 保留之间未观察到显著相关性(r=-0.65;P=0.11)。然而,梗死面积与 24 小时的植入显著相关(r=0.75;P=0.03)。注射部位的残留灌注与细胞保留/植入无关。较大的梗死与改善的 CDC 植入相关。这一观察结果鼓励进一步研究缺血性损伤后的微环境条件及其在治疗性细胞存活中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/990ee2b33ef6/395_2011_197_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/64866e0f888c/395_2011_197_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/1537e6d71602/395_2011_197_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/3ae22fd4831b/395_2011_197_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/990ee2b33ef6/395_2011_197_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/64866e0f888c/395_2011_197_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/1537e6d71602/395_2011_197_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/3ae22fd4831b/395_2011_197_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d327/3228962/990ee2b33ef6/395_2011_197_Fig4_HTML.jpg

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