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骨髓细胞可修复大鼠吸烟导致的肺气肿。

Bone marrow cells repair cigarette smoke-induced emphysema in rats.

机构信息

Dept. of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan Univ. School of Medicine, Suwon 440-746, South Korea.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2011 Sep;301(3):L255-66. doi: 10.1152/ajplung.00253.2010. Epub 2011 May 27.

DOI:10.1152/ajplung.00253.2010
PMID:21622846
Abstract

The therapeutic potential of stem cells in chronic obstructive pulmonary disease is not well known although stem cell therapy is effective in models of other pulmonary diseases. We tested the capacities of bone marrow cells (BMCs), mesenchymal stem cells (MSCs), and conditioned media of MSCs (MSC-CM) to repair cigarette smoke-induced emphysema. Inbred female Lewis rats were exposed to cigarette smoke for 6 mo and then received BMCs, MSCs, or MSC-CM from male Lewis rats. For 2 mo after injection, the BMC treatment gradually alleviated the cigarette smoke-induced emphysema and restored the increased mean linear intercept. The BMC treatment significantly increased cell proliferation and the number of small pulmonary vessels, reduced apoptotic cell death, attenuated the mean pulmonary arterial pressure, and inhibited muscularization in small pulmonary vessels. However, only a few male donor cells were detected from 1 day to 1 mo after BMC administration. The MSCs and cell-free MSC-CM also induced the repair of emphysema and increased the number of small pulmonary vessels. Our data show that BMC, MSCs, and MSC-CM treatment repaired cigarette smoke-induced emphysema. The repair activity of these treatments is consistent with a paracrine effect rather than stem cell engraftment because most of the donor cells disappeared and because cell-free MSC-CM also induced the repair.

摘要

干细胞在慢性阻塞性肺疾病中的治疗潜力尚不清楚,尽管干细胞疗法在其他肺部疾病模型中是有效的。我们测试了骨髓细胞(BMCs)、间充质干细胞(MSCs)和 MSC 条件培养基(MSC-CM)修复香烟烟雾引起的肺气肿的能力。同窝雌性 Lewis 大鼠暴露于香烟烟雾中 6 个月,然后接受来自雄性 Lewis 大鼠的 BMCs、MSCs 或 MSC-CM。注射后 2 个月,BMC 治疗逐渐缓解了香烟烟雾引起的肺气肿,并恢复了增加的平均线性截距。BMC 治疗显著增加了细胞增殖和小肺血管数量,减少了细胞凋亡死亡,降低了平均肺动脉压,并抑制了小肺血管的肌化。然而,在 BMC 给药后 1 天至 1 个月内,仅检测到少数雄性供体细胞。MSCs 和无细胞 MSC-CM 也诱导了肺气肿的修复,并增加了小肺血管的数量。我们的数据表明,BMC、MSCs 和 MSC-CM 治疗修复了香烟烟雾引起的肺气肿。这些治疗的修复活性与旁分泌作用一致,而不是与干细胞移植一致,因为大多数供体细胞消失,并且无细胞 MSC-CM 也诱导了修复。

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