CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice.
CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice.
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DOI：
10.1093/cvr/cvt155
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发表时间：
2013-10-01
影响因子：
10.8
通讯作者：
Shapiro LH
中科院分区：
文献类型：
--
作者：
Pereira FE;Cronin C;Ghosh M;Zhou SY;Agosto M;Subramani J;Wang R;Shen JB;Schacke W;Liang B;Yang TH;McAulliffe B;Liang BT;Shapiro LH
确定CD13作为一种粘附分子在体内炎症细胞运输至损伤部位中的作用及其在永久性冠状动脉闭塞致心肌梗死后伤口愈合中的功能。永久性结扎后7天，CD13基因敲除（CD13KO）小鼠的心脏显示出心功能显著降低，表明在缺乏CD13的情况下，愈合受损。从机制上讲，CD13KO梗死显示小的内皮内衬管腔结构增加，但灌注没有增加，这与缺乏CD13的血管生成缺陷相反。CD13KO小鼠心肌细胞显示正常的基础收缩功能，消除了心肌细胞功能障碍作为不良重构的机制。相反，CD13KO梗死的免疫组织化学和流式细胞术分析显示，浸润的造血细胞（包括单核细胞、巨噬细胞、树突状细胞和T细胞）减少了65%，这表明CD13粘附在炎症运输中起着关键作用。因此，CD13KO梗死也含有较少的肌成纤维细胞，这与炎症减少导致的成纤维细胞分化衰减一致，从而导致不良的重构。在缺血心脏中，虽然代偿机制明显减轻了潜在的血管生成缺陷，但CD13对于炎症细胞的适当运输至关重要，炎症细胞是启动和维持修复反应所必需的，从而促进最佳的梗死后愈合。
To determine the role of CD13 as an adhesion molecule in trafficking of inflammatory cells to the site of injury in vivo and its function in wound healing following myocardial infarction induced by permanent coronary artery occlusion. Seven days post-permanent ligation, hearts from CD13 knockout (CD13KO) mice showed significant reductions in cardiac function, suggesting impaired healing in the absence of CD13. Mechanistically, CD13KO infarcts showed an increase in small, endothelial-lined luminal structures, but no increase in perfusion, arguing against an angiogenic defect in the absence of CD13. Cardiac myocytes of CD13KO mice showed normal basal contractile function, eliminating myocyte dysfunction as a mechanism of adverse remodelling. Conversely, immunohistochemical and flow cytometric analysis of CD13KO infarcts demonstrated a dramatic 65% reduction in infiltrating haematopoietic cells, including monocytes, macrophages, dendritic, and T cells, suggesting a critical role for CD13 adhesion in inflammatory trafficking. Accordingly, CD13KO infarcts also contained fewer myofibroblasts, consistent with attenuation of fibroblast differentiation resulting from the reduced inflammation, leading to adverse remodelling. In the ischaemic heart, while compensatory mechanisms apparently relieve potential angiogenic defects, CD13 is essential for proper trafficking of the inflammatory cells necessary to prime and sustain the reparative response, thus promoting optimal post-infarction healing.
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DOI：
10.1016/j.biocel.2006.11.005
发表时间：
2007-01-01
影响因子：
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作者：
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发表时间：
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影响因子：
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