An unbiased transcriptional profiling screen reveals the secreted matrix metalloproteinase MMP-1 is a transcriptional target of the ensheathing glial receptor Draper following acute axon injury in adult Drosophila.
Dark exposure lowers the MMP9 activation threshold, and subsequent light stimulation to an amblyopic eye is sufficient to induce proteolysis at thalamo-cortical synapses in deprived mouse visual cortex.
Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.
Postsynaptic MT1-MMP serves as a molecular switch to synaptogenesis by clearing the surrounding ECM environment that allows effective deposition of nerve-derived synaptogenic factors to induce postsynaptic differentiation at developing NMJs.
The membrane type I-matrix metalloproteinase is essential for the release of collagen fibrils from plasma membrane fibripositors, which is required for the transition from embryonic to postnatal tendon development.
Matrix metalloproteinases play a crucial role in adult visual plasticity in the brains of healthy and stroke-affected mice and their activity has to be within a narrow window for experience-induced plasticity to occur.