Interleukin-2 is present in human blood vessels and released in biologically active form by heparanase.
Interleukin-2 is present in human blood vessels and released in biologically active form by heparanase.
复制标题
DOI：
10.1038/icb.2011.45
复制
发表时间：
2012-02
影响因子：
4
通讯作者：
Wrenshall, Lucile E.
中科院分区：
文献类型：
--
作者：
Miller, John D.;Clabaugh, Suzanne E.;Smith, Deandra R.;Stevens, R. Brian;Wrenshall, Lucile E.
白细胞介素-2是一种多方面的细胞因子，具有免疫刺激和免疫抑制特性。我们的实验室最近证明，IL-2的可用性调节，在一定程度上，与串珠素，硫酸乙酰肝素蛋白聚糖。鉴于串珠素在血管中的丰度，我们询问IL-2是否存在于血管壁中。我们的研究结果表明，IL-2与人动脉壁内的内皮细胞和平滑肌细胞相关。该IL-2通过乙酰肝素酶释放，促进IL-2依赖性细胞系的增殖。鉴于人动脉中存在IL-2，我们询问IL-2缺陷小鼠的大血管是否正常。IL-2缺陷小鼠的动脉表现出平滑肌细胞的损失，表明IL-2可能有助于它们的存活。总的来说，这些结果表明IL-2在血管生物学中的未被认识的作用，并且对免疫和心血管系统都具有重要意义。
Interleukin-2 is a multifaceted cytokine with both immunostimulatory and immunosuppressive properties. Our laboratory recently demonstrated that the availability of IL-2 is regulated, in part, by association with perlecan, a heparan sulfate proteoglycan. Given the abundance of perlecan in blood vessels, we asked whether IL-2 is present in vessel walls. Our results indicate that IL-2 is associated with endothelial and smooth muscle cells within the human arterial wall. This IL-2 is released by heparanase, and promotes the proliferation of an IL-2 dependent cell line. Given the presence of IL-2 in human arteries, we asked whether the large vessels of IL-2 deficient mice were normal. The aortas of IL-2 deficient mice exhibited a loss of smooth muscle cells, suggesting that IL-2 may contribute to their survival. In their entirety, these results suggest a here-to-fore unrecognized role of IL-2 in vascular biology, and have significant implications for both the immune and cardiovascular systems.
登录
查看更多内容
影响因子：
5
作者：
Kradin, RL;Xia, WJ;Pinto, C
通讯作者：
Pinto, C
影响因子：
5.3
作者：
Nabata, T;Fukuo, K;Ogihara, T
通讯作者：
Ogihara, T
在动脉粥样硬化之前和开发过程中淋巴细胞募集到主动脉壁是部分依赖性L-选择蛋白。
DOI：
10.1084/jem.20052205
发表时间：
2006-05-15
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
通讯作者：
--
DOI：
10.1161/01.atv.0000063109.94810.ee
发表时间：
2003-04-01
影响因子：
8.7
作者：
Kinsella, MG;Tran, PK;Wight, TN
通讯作者：
Wight, TN
影响因子：
5.7
作者：
Miyamoto, Shin'ichi;Nakamura, Michio;Ochiai, Atsushi
通讯作者：
Ochiai, Atsushi