PNAS：人类干细胞成功治愈猴子的帕金森症
生物谷报道：一项新的研究显示，只注射一次神经干细胞就能明显改善猴子的帕金森症症状。这项研究为用干细胞治疗人类的同种疾病铺平了道路。这项研究的结果发表在近期的PNAS上。
哈佛医学院的Richard Sidman和同事通过将一种能够破坏产多巴胺神经元的化学物质注射给猴子，从而使非洲绿猴表现出帕金森症。
然后，他们将从人类胎儿获得的神经干细胞注射进这些猴子的大脑中。获得干细胞的胚胎是在13周大的时候被流产的。一个月后，这些猴子病情明显好转。
大约四个月后，这些猴子的并且开始恶化，着可能是因为注入的干细胞遭受到猴子免疫系统的攻击。但是，他们仍然比没有治疗的猴子要健康。
对死后的猴子的尸检结果显示，被移植的细胞分散在整个大脑中产多巴胺的结构区域。它们的基本功能似乎是保护大脑不会受到进一步的损伤，而不是替代受损的细胞。这个研究组目前正计划研究免疫抑制药物和重复注射是否能够将这种有益作用延长。
原始出处:
Published online before print March 7, 2007, 10.1073/pnas.0611653104
PNAS | March 13, 2007 | vol. 104 | no. 11 | 4588-4593
OPEN ACCESS ARTICLE
BIOLOGICAL SCIENCES / MEDICAL SCIENCES
Impaired angiogenesis in aminopeptidase N-null mice
Roberto Rangel*, Yan Sun*, Liliana Guzman-Rojas*, Michael G. Ozawa*, Jessica Sun*, Ricardo J. Giordano*, Carolyn S. Van Pelt
, Peggy T. Tinkey, Richard R. Behringer
, Richard L. Sidman
,¶, Wadih Arap*,¶,||, and Renata Pasqualini*,¶,||
Departments of *Genitourinary Medical Oncology, ||Cancer Biology, Molecular Genetics, and Veterinary Medicine and Surgery, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030; and Harvard Medical School and Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Boston, MA 02115
Contributed by Richard L. Sidman, December 29, 2006 (received for review December 21, 2006)
Aminopeptidase N (APN, CD13; EC 3.4.11.2 [EC] ) is a transmembrane metalloprotease with several functions, depending on the cell type and tissue environment. In tumor vasculature, APN is overexpressed in the endothelium and promotes angiogenesis. However, there have been no reports of in vivo inactivation of the APN gene to validate these findings. Here we evaluated, by targeted disruption of the APN gene, whether APN participates in blood vessel formation and function under normal conditions. Surprisingly, APN-null mice developed with no gross or histological abnormalities. Standard neurological, cardiovascular, metabolic, locomotor, and hematological studies revealed no alterations. Nonetheless, in oxygen-induced retinopathy experiments, APN-deficient mice had a marked and dose-dependent deficiency of the expected retinal neovascularization. Moreover, gelfoams embedded with growth factors failed to induce functional blood vessel formation in APN-null mice. These findings establish that APN-null mice develop normally without physiological alterations and can undergo physiological angiogenesis but show a severely impaired angiogenic response under pathological conditions. Finally, in addition to vascular biology research, APN-null mice may be useful reagents in other medical fields such as malignant, cardiovascular, immunological, or infectious diseases.
CD13 | knockout mice | retinopathy | vasculogenesis
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