Ellinwood N Matthew, Colle Marie-Anne, Weil Margaret A, Casal Margret L, Vite Charles H, Wiemelt Staci, Hasson Christopher W, O'Malley Thomas M, He Xingxuan, Prociuk Ulana, Verot Lucie, Melniczek John R, Lannon Anne, Aguirre Gustavo D, Knox Van W, Evans Sydney M, Vanier Marie T, Schuchman Edward H, Walkley Steven U, Haskins Mark E
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Mol Genet Metab. 2007 Jul;91(3):239-50. doi: 10.1016/j.ymgme.2007.03.001. Epub 2007 May 7.
Severe mucopolysaccharidosis type I (MPS I) is a fatal neuropathic lysosomal storage disorder with significant skeletal involvement. Treatment involves bone marrow transplantation (BMT), and although effective, is suboptimal, due to treatment sequelae and residual disease. Improved approaches will need to be tested in animal models and compared to BMT. Herein we report on bone marrow transplantation to treat feline mucopolysaccharidosis I (MPS I). Five MPS I stably engrafted kittens, transplanted with unfractionated bone marrow (6.3x10(7)-1.1x10(9) nucleated bone marrow cells per kilogram) were monitored for 13-37 months post-engraftment. The tissue total glycosaminoglycan (GAG) content was reduced to normal levels in liver, spleen, kidney, heart muscle, lung, and thyroid. Aorta GAG content was between normal and affected levels. Treated cats had a significant decrease in the brain GAG levels relative to untreated MPS I cats and a paradoxical decrease relative to normal cats. The alpha-l-iduronidase (IDUA) activity in the livers and spleens of transplanted MPS I cats approached heterozygote levels. In kidney cortex, aorta, heart muscle, and cerebrum, there were decreases in GAG without significant increases in detectable IDUA activity. Treated animals had improved mobility and decreased radiographic signs of disease. However, significant pathology remained, especially in the cervical spine. Corneal clouding appeared improved in some animals. Immunohistochemical and biochemical analysis documented decreased central nervous system ganglioside storage. This large animal MPS I study will serve as a benchmark of future therapies designed to improve on BMT.
重度I型黏多糖贮积症(MPS I)是一种致命的神经性溶酶体贮积病,伴有明显的骨骼受累。治疗方法包括骨髓移植(BMT),尽管有效,但由于治疗后遗症和残留疾病,效果并不理想。需要在动物模型中测试改进的方法,并与BMT进行比较。在此,我们报告了骨髓移植治疗猫I型黏多糖贮积症(MPS I)的情况。对5只稳定植入的MPS I小猫进行了移植,每千克体重移植未分级的骨髓(6.3×10⁷ - 1.1×10⁹个有核骨髓细胞),并在植入后监测13 - 37个月。肝脏、脾脏、肾脏、心肌、肺和甲状腺中的组织总糖胺聚糖(GAG)含量降至正常水平。主动脉GAG含量介于正常水平和患病水平之间。与未治疗的MPS I猫相比,治疗后的猫脑GAG水平显著降低,而与正常猫相比则出现了矛盾的降低。移植的MPS I猫肝脏和脾脏中的α-L-艾杜糖醛酸酶(IDUA)活性接近杂合子水平。在肾皮质、主动脉、心肌和大脑中,GAG含量降低,但可检测到的IDUA活性没有显著增加。治疗后的动物活动能力有所改善,疾病的放射学体征减少。然而,仍存在明显的病理变化,尤其是在颈椎。一些动物的角膜混浊似乎有所改善。免疫组织化学和生化分析表明中枢神经系统神经节苷脂贮积减少。这项大型动物MPS I研究将作为未来旨在改进BMT的治疗方法的基准。