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猪主动脉器官培养中内膜细胞增殖的内皮刺激作用

Endothelial stimulation of intimal cell proliferation in a porcine aortic organ culture.

作者信息

Koo E W, Gotlieb A I

机构信息

Department of Pathology, Banting and Best Diabetes Centre, University of Toronto, Toronto General Hospital, Ontario, Canada.

出版信息

Am J Pathol. 1989 Mar;134(3):497-503.

PMID:2923181
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1879525/
Abstract

A porcine thoracic aortic organ culture system was used to study the interaction between endothelial cells (EC) and the underlying intimal smooth muscle cells (SMC). The presence of EC in organ cultures was confirmed by the ability of luminal cells to incorporate acetylated-LDL. It was found that incubation of nondenuded organ cultures in 5% fetal bovine serum for 7 days resulted in a significant increase in the mean number of intimal SMC (41.5 +/- 0.9) compared with organ cultures in which the endothelium was removed at the beginning of the experiment (denuded, 15.2 +/- 0.8). Incubation of the latter for 7 days in conditioned medium collected from nondenuded organ cultures also resulted in a significant increase in the mean number of intimal SMC (30.2 +/- 2.2). Incubation of aortic medial SMC cultures in the conditioned medium also enhanced SMC growth. Autoradiography studies at each day of the 7 days showed that intimal SMC proliferation was similar in both nondenuded and denuded organ cultures when the latter was incubated in the conditioned medium. These data suggests that in this model the secretion of a soluble mediator by dysfunctioning, injured, or proliferating endothelial cells stimulates intimal cell proliferation either directly or indirectly.

摘要

使用猪胸主动脉器官培养系统来研究内皮细胞(EC)与下层内膜平滑肌细胞(SMC)之间的相互作用。通过管腔细胞摄取乙酰化低密度脂蛋白的能力来确认器官培养物中EC的存在。结果发现,与在实验开始时去除内皮的器官培养物(去内皮,15.2±0.8)相比,将未去内皮的器官培养物在5%胎牛血清中孵育7天,内膜SMC的平均数量显著增加(41.5±0.9)。将后者在从未去内皮的器官培养物收集的条件培养基中孵育7天,内膜SMC的平均数量也显著增加(30.2±2.2)。将主动脉中膜SMC培养物在条件培养基中孵育也增强了SMC的生长。在7天中的每一天进行的放射自显影研究表明,当将去内皮的器官培养物在条件培养基中孵育时,其内膜SMC增殖与未去内皮的器官培养物相似。这些数据表明,在该模型中,功能失调、受损或增殖的内皮细胞分泌的可溶性介质直接或间接刺激内膜细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/b6eca42f9722/amjpathol00123-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/185ad3e8b8fd/amjpathol00123-0020-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/fc3000ba0578/amjpathol00123-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/b6eca42f9722/amjpathol00123-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/185ad3e8b8fd/amjpathol00123-0020-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/fc3000ba0578/amjpathol00123-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9135/1879525/b6eca42f9722/amjpathol00123-0022-a.jpg

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VLA-4 and lymphocyte trafficking in immune-inflammatory states: novel therapeutic approaches in allograft arteriopathy.VLA - 4与免疫炎症状态下的淋巴细胞迁移:同种异体移植血管病的新型治疗方法
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