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本文引用的文献

1
Limb ischemia after iliac ligation in aged mice stimulates angiogenesis without arteriogenesis.老年小鼠髂动脉结扎后肢体缺血会刺激血管生成但不会刺激动脉生成。
J Vasc Surg. 2009 Feb;49(2):464-73. doi: 10.1016/j.jvs.2008.08.077. Epub 2008 Nov 22.
2
Isolation of a slowly adhering cell fraction containing stem cells from murine skeletal muscle by the preplate technique.采用预板层技术从小鼠骨骼肌中分离出含干细胞的缓慢黏附细胞组分。
Nat Protoc. 2008;3(9):1501-9. doi: 10.1038/nprot.2008.142.
3
AT1 receptor inhibition prevents astrocyte degeneration and restores vascular growth in oxygen-induced retinopathy.血管紧张素Ⅱ1型受体抑制可预防氧诱导性视网膜病变中的星形胶质细胞变性并恢复血管生长。
Glia. 2008 Aug 1;56(10):1076-90. doi: 10.1002/glia.20680.
4
Urokinase gene transfer augments angiogenesis in ischemic skeletal and myocardial muscle.尿激酶基因转移可增强缺血骨骼肌和心肌的血管生成。
Mol Ther. 2007 Nov;15(11):1939-46. doi: 10.1038/sj.mt.6300262. Epub 2007 Jul 24.
5
The chemokine system in arteriogenesis and hind limb ischemia.动脉生成与后肢缺血中的趋化因子系统。
J Vasc Surg. 2007 Jun;45 Suppl A(Suppl A):A48-56. doi: 10.1016/j.jvs.2007.02.030.
6
Tumors induce a subset of inflammatory monocytes with immunosuppressive activity on CD8+ T cells.肿瘤诱导出一部分对CD8+ T细胞具有免疫抑制活性的炎性单核细胞。
J Clin Invest. 2006 Oct;116(10):2777-90. doi: 10.1172/JCI28828.
7
Integrin alpha4beta1 promotes monocyte trafficking and angiogenesis in tumors.整合素α4β1促进肿瘤中的单核细胞运输和血管生成。
Cancer Res. 2006 Feb 15;66(4):2146-52. doi: 10.1158/0008-5472.CAN-05-2704.
8
Myeloid suppressor cells in cancer: recruitment, phenotype, properties, and mechanisms of immune suppression.癌症中的髓系抑制细胞:募集、表型、特性及免疫抑制机制
Semin Cancer Biol. 2006 Feb;16(1):53-65. doi: 10.1016/j.semcancer.2005.07.005. Epub 2005 Sep 15.
9
Differential necrosis despite similar perfusion in mouse strains after ischemia.缺血后小鼠品系中尽管灌注相似但仍存在差异性坏死。
J Surg Res. 2005 Dec;129(2):242-50. doi: 10.1016/j.jss.2005.06.013. Epub 2005 Jul 27.
10
Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis.荷瘤宿主中髓系免疫抑制细胞Gr⁺CD11b⁺的扩增直接促进肿瘤血管生成。
Cancer Cell. 2004 Oct;6(4):409-21. doi: 10.1016/j.ccr.2004.08.031.

肌源性 Gr1(dim)CD11b(+) 细胞增强缺血性后肢小鼠模型中的血管新生。

Muscle-derived Gr1(dim)CD11b(+) cells enhance neovascularization in an ischemic hind limb mouse model.

机构信息

Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, 46202, USA.

出版信息

Blood. 2010 Sep 2;116(9):1623-6. doi: 10.1182/blood-2009-08-237040. Epub 2010 Jun 1.

DOI:10.1182/blood-2009-08-237040
PMID:20516368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2938848/
Abstract

Gr1(+)CD11b(+) cells are characterized as myeloid-derived suppressor cells potentially involved in angiogenesis. We demonstrate that Gr1(+)CD11b(+) cells isolated from ischemic muscle in a hind-limb ischemic C57BL/6 mouse model play a role in vessel formation after ischemic injury. Gr1(dim)CD11b(+) cells, a subpopulation of Gr1(+)CD11b(+) cells, within skeletal muscle were increased in context of ischemia. Strikingly, astrocyte-plexus formed from muscle-derived Gr1(dim)CD11b(+) cells in Matrigel culture, followed by formation of isolectin and von Willebrand Factor-expressing cells, similar to that reported for angiogenesis in retina. When isolated muscle-derived Gr1(dim)CD11b(+) cells were injected into ischemic muscles, recovery of blood flow was significantly enhanced and these cells were incorporated into vessel walls. This suggests that Gr1(dim)CD11b(+) cells are recruited into ischemic regions after ischemia and may be involved in angiogenesis by their capacity to generate vascular cells.

摘要

Gr1(+)CD11b(+) 细胞被认为是髓系来源的抑制性细胞,可能参与血管生成。我们证明,从小鼠后肢缺血模型缺血肌肉中分离出的 Gr1(+)CD11b(+)细胞在缺血损伤后参与血管形成。Gr1(dim)CD11b(+) 细胞是 Gr1(+)CD11b(+)细胞的一个亚群,在缺血情况下骨骼肌中增加。引人注目的是,源自肌肉来源的 Gr1(dim)CD11b(+)细胞在 Matrigel 培养物中形成星形胶质细胞丛,随后形成异凝集素和血管性血友病因子表达细胞,类似于视网膜血管生成的情况。当分离的肌肉来源的 Gr1(dim)CD11b(+)细胞被注射到缺血肌肉中时,血流恢复明显增强,这些细胞被整合到血管壁中。这表明 Gr1(dim)CD11b(+)细胞在缺血后被募集到缺血区域,并可能通过生成血管细胞的能力参与血管生成。