Bone marrow-derived cells do not repair endothelium in a mouse model of chronic endothelial cell dysfunction.
Bone marrow-derived cells do not repair endothelium in a mouse model of chronic endothelial cell dysfunction.
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DOI：
10.1093/cvr/cvp215
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发表时间：
2009-11-01
影响因子：
10.8
通讯作者：
Orlic D
中科院分区：
文献类型：
--
作者：
Perry TE;Song M;Despres DJ;Kim SM;San H;Yu ZX;Raghavachari N;Schnermann J;Cannon RO 3rd;Orlic D
骨髓来源的内皮祖细胞（EPCs）在循环中替代受损的血管内皮。我们评估了一种假设，即健康动物骨髓移植可以恢复年轻内皮型一氧化氮合酶缺陷（eNOS - / -）小鼠的正常动脉内皮并预防高血压。在第6天、第14天或第28天，对eNOS−/−小鼠进行放射或布苏芬诱导的脑基消融，然后移植由C57BL/6J小鼠增强的绿色荧光蛋白阳性（EGFP+）细胞组成的脑基移植。骨髓移植后4个月外周血细胞嵌合率均大于85%。对心脏、肾脏和肝脏的分子分析显示，在所有治疗组中均存在低水平嵌合，与残留的循环EGFP+血细胞一致。当用共聚焦显微镜检查脑移植的eNOS- / -小鼠的主动脉、冠状动脉、肾、肝和脾动脉时，在任何治疗组的这些血管中都没有检测到EGFP或eNOS阳性内皮细胞。同样，遥测也没有检测到血压的降低。因此，使用几种不同的治疗方案，在我们的测量中没有观察到差异。在慢性血管疾病的enos缺陷小鼠模型或出生后生长的野生型小鼠中，我们没有发现脑脊髓瘤衍生的内皮细胞更新的证据。因此，慢性功能失调的内皮和内皮稳态的更新可能依赖于常驻血管祖细胞。
Bone marrow (BM)-derived endothelial progenitor cells (EPCs) in the circulation replace damaged vascular endothelium. We assessed the hypothesis that a BM transplant from healthy animals would restore normal arterial endothelium and prevent hypertension in young endothelial nitric oxide synthase-deficient (eNOS−/−) mice. Radiation or busulfan-induced BM ablation in eNOS−/− mice on day 6, day 14, or day 28 was followed by a BM transplant consisting of enhanced green fluorescent protein positive (EGFP+) cells from C57BL/6J mice. Peripheral blood cell chimerism was always greater than 85% at 4 months after BM transplant. Molecular assays of heart, kidney, and liver revealed low-level chimerism in all treatment groups, consistent with residual circulating EGFP+ blood cells. When aorta, coronary, renal, hepatic, and splenic arteries in BM-transplanted eNOS−/− mice were examined by confocal microscopy, there were no EGFP- or eNOS-positive endothelial cells detected in these vessels in any of the treatment groups. Likewise, telemetry did not detect any reduction in blood pressure. Thus, no differences were observed in our measurements using several different treatment protocols. We found no evidence for BM-derived EPC renewal of endothelium in this eNOS-deficient mouse model of a chronic vascular disease or in wild-type mice during postnatal growth. Hence, renewal of chronic dysfunctional endothelium and endothelial homeostasis may be dependent on resident vascular progenitor cells.
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影响因子：
4.6
作者：
Zengin, E;Chalajour, F;Erg端n, S
通讯作者：
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