MMP2 Modulates Inflammatory Response during Axonal Regeneration in the Murine Visual System.
Lien AndriesLuca MasinManuel Salinas NavarroSamantha ZaunzMarie ClaesSteven BergmansVéronique BrouwersEvy LefevereCatherine VerfaillieKiavash MovahediLies De GroefLieve MoonsPublished in: Cells (2021)
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.
Keyphrases
- optic nerve
- stem cells
- spinal cord injury
- bone marrow
- anti inflammatory
- induced apoptosis
- poor prognosis
- cell migration
- cell cycle arrest
- inflammatory response
- oxidative stress
- mouse model
- wound healing
- dendritic cells
- acute myeloid leukemia
- immune response
- endoplasmic reticulum stress
- optical coherence tomography
- cell death
- single molecule
- lipopolysaccharide induced
- traumatic brain injury
- mesenchymal stem cells
- dna methylation
- blood brain barrier
- signaling pathway
- cell proliferation
- high glucose
- long non coding rna
- cerebral ischemia
- single cell
- replacement therapy
- diabetic rats
- brain injury
- cognitive impairment
- toll like receptor