期刊
CELLS
卷 10, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/cells10071672
关键词
matrix metalloproteinases; optic nerve injury; myeloid cells; axonal regeneration; inflammatory stimulation; expression profiling
类别
资金
- Research Council of KU Leuven [KU Leuven BOFOT/14/064]
- Research Foundation Flanders (FWO) [G0B2315N, G053217N]
- Research Foundation Flanders
Neuroinflammation can trigger axonal regrowth in the CNS, and MMP2 plays a key role in linking inflammation and axonal regeneration. MMP2 deficiency leads to reduced long-distance axonal regeneration, but this phenotype can be rescued by restoring MMP2 expression in myeloid cells. Additionally, MMP2 deficiency affects the coordinated expression of pro- and anti-inflammatory molecules, showcasing a new mechanism by which MMP2 facilitates axonal regeneration.
Neuroinflammation has been put forward as a mechanism triggering axonal regrowth in the mammalian central nervous system (CNS), yet little is known about the underlying cellular and molecular players connecting these two processes. In this study, we provide evidence that MMP2 is an essential factor linking inflammation to axonal regeneration by using an in vivo mouse model of inflammation-induced axonal regeneration in the optic nerve. We show that infiltrating myeloid cells abundantly express MMP2 and that MMP2 deficiency results in reduced long-distance axonal regeneration. However, this phenotype can be rescued by restoring MMP2 expression in myeloid cells via a heterologous bone marrow transplantation. Furthermore, while MMP2 deficiency does not affect the number of infiltrating myeloid cells, it does determine the coordinated expression of pro- and anti-inflammatory molecules. Altogether, in addition to its role in axonal regeneration via resolution of the glial scar, here, we reveal a new mechanism via which MMP2 facilitates axonal regeneration, namely orchestrating the expression of pro- and anti-inflammatory molecules by infiltrating innate immune cells.
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