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Nat Commun:硫酸软骨素让受伤的脊髓更好恢复

  1. 受伤
  2. 恢复
  3. 硫酸软骨素
  4. 脊髓

来源:Nature中文网 2013-11-22 11:31

硫酸软骨素(神经系统瘢痕的一个成分)的生物合成所需的一种酶的去除,使得小鼠在脊髓受伤后运动功能得到更好恢复。

硫酸软骨素(神经系统瘢痕的一个成分)的生物合成所需的一种酶的去除,使得小鼠在脊髓受伤后运动功能得到更好恢复。本期Nature Communications上发表的一篇论文所报告的这项研究加强了我们对脊髓受伤后恢复的认识,同时也可能为这种受伤后的治疗指出了一个新目标。

蛋白多糖是胶质瘢痕的成分,这种瘢痕是脊髓受伤后形成的,其作用是帮助中枢神系统愈合,但也阻止神经元的再生长。用软骨素酶(降解蛋白多糖“硫酸软骨素”的一种酶)处理小鼠,已知会改善脊髓损伤的恢复。现在,Michihiro Igarashi及其同事发现,与用软骨素酶处理过的小鼠相比,若将小鼠用于硫酸软骨素合成的一种酶剔除,小鼠在脊髓受伤后所产生的胶质瘢痕较小,神经元再生长的水平较高,且四肢的运动功能恢复较好。他们发现,这不仅是由于硫酸软骨素的水平降低,而且是由于另一种蛋白多糖“硫酸肝素”水平提高,后者已知促进轴突生长。(生物谷Bioon.com)

生物谷推荐的英文摘要

Nature Communications        doi:10.1038/ncomms3740

Chondroitin sulphate N-acetylgalactosaminyl-transferase-1 inhibits recovery from neural injury

Kosei Takeuchi,Nozomu Yoshioka,Susumu Higa Onaga,Yumi Watanabe,Shinji Miyata,Yoshino Wada,Chika Kudo,Masayasu Okada,Kentaro Ohko,Kanako Oda,Toshiya Sato,Minesuke Yokoyama,Natsuki Matsushita,Masaya Nakamura,Hideyuki Okano,Kenji Sakimura,Hitoshi Kawano,Hiroshi Kitagawa& Michihiro Igarashi

Extracellular factors that inhibit axon growth and intrinsic factors that promote it affect neural regeneration. Therapies targeting any single gene have not yet simultaneously optimized both types of factors. Chondroitin sulphate (CS), a glycosaminoglycan, is the most abundant extracellular inhibitor of axon growth. Here we show that mice carrying a gene knockout for CS N-acetylgalactosaminyltransferase-1 (T1), a key enzyme in CS biosynthesis, recover more completely from spinal cord injury than wild-type mice and even chondroitinase ABC-treated mice. Notably, synthesis of heparan sulphate (HS), a glycosaminoglycan promoting axonal growth, is also upregulated in TI knockout mice because HS-synthesis enzymes are induced in the mutant neurons. Moreover, chondroitinase ABC treatment never induces HS upregulation. Taken together, our results indicate that regulation of a single gene, T1, mediates excellent recovery from spinal cord injury by optimizing counteracting effectors of axon regeneration—an extracellular inhibitor of CS and intrinsic promoters, namely, HS-synthesis enzymes.

 

 

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