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基质金属蛋白酶-28作为髓鞘形成的调节因子。

MMP-28 as a regulator of myelination.

作者信息

Werner Sean R, Dotzlaf Joseph E, Smith Rosamund C

机构信息

Biotechnology Discovery Research, Lilly Corporate Center, Indianapolis, IN 46225, USA.

出版信息

BMC Neurosci. 2008 Sep 9;9:83. doi: 10.1186/1471-2202-9-83.

DOI:10.1186/1471-2202-9-83
PMID:18778487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2551619/
Abstract

BACKGROUND

Matrix metalloproteinase-28 (MMP-28) is a poorly understood member of the matrix metalloproteinase family. Metalloproteinases are important mediators in the development of the nervous system and can contribute to the maturation of the neural micro-environment.

RESULTS

MMP-28 added to myelinating rat dorsal root ganglion (DRG) co-cultures reduces myelination and two antibodies targeted to MMP-28 (pAb180 and pAb183) are capable of binding MMP-28 and inhibiting its activity in a dose-dependent manner. Addition of 30 nM pAb180 or pAb183 to rat DRG cultures resulted in the 2.6 and 4.8 fold enhancement of myelination respectively while addition of MMP-28 to DRG co-cultures resulted in enhanced MAPK, ErbB2 and ErbB3 phosphorylation. MMP-28 protein expression was increased within demyelinated lesions of mouse experimental autoimmune encephalitis (EAE) and human multiple sclerosis lesions compared to surrounding normal tissue.

CONCLUSION

MMP-28 is upregulated in conditions of demyelination in vivo, induces signaling in vitro consistent with myelination inhibition and, neutralization of MMP-28 activity can enhance myelination in vitro. These results suggest inhibition of MMP-28 may be beneficial under conditions of dysmyelination.

摘要

背景

基质金属蛋白酶-28（MMP-28）是基质金属蛋白酶家族中了解较少的成员。金属蛋白酶是神经系统发育中的重要介质，可促进神经微环境的成熟。

结果

添加到大鼠背根神经节（DRG）髓鞘形成共培养物中的MMP-28会减少髓鞘形成，两种靶向MMP-28的抗体（pAb180和pAb183）能够结合MMP-28并以剂量依赖性方式抑制其活性。向大鼠DRG培养物中添加30 nM pAb180或pAb183分别导致髓鞘形成增强2.6倍和4.8倍，而向DRG共培养物中添加MMP-28导致MAPK、ErbB2和ErbB3磷酸化增强。与周围正常组织相比，小鼠实验性自身免疫性脑脊髓炎（EAE）脱髓鞘病变和人类多发性硬化症病变中的MMP-28蛋白表达增加。

结论

MMP-28在体内脱髓鞘条件下上调，在体外诱导与髓鞘形成抑制一致的信号传导，并且中和MMP-28活性可在体外增强髓鞘形成。这些结果表明，在髓鞘形成异常的情况下抑制MMP-28可能有益。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/17e5721b3b7c/1471-2202-9-83-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/1a15d6c3e9a5/1471-2202-9-83-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/ee2a718cd446/1471-2202-9-83-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/6b8ce3ccccc7/1471-2202-9-83-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/ee99922f3ccc/1471-2202-9-83-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/6be592fd6667/1471-2202-9-83-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/adc82e0b9817/1471-2202-9-83-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/17e5721b3b7c/1471-2202-9-83-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/1a15d6c3e9a5/1471-2202-9-83-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/ee2a718cd446/1471-2202-9-83-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/6b8ce3ccccc7/1471-2202-9-83-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/ee99922f3ccc/1471-2202-9-83-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/6be592fd6667/1471-2202-9-83-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/adc82e0b9817/1471-2202-9-83-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2294/2551619/17e5721b3b7c/1471-2202-9-83-7.jpg

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