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MICAL flavoprotein monooxygenases: expression during neural development and following spinal cord injuries in the rat
R Jeroen Pasterkamp1, Hai-ning Dai, Jonathan R Terman
1Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. j.pasterkamp@med.uu.nl
Abstract:
MICALs comprise of a family of phylogenetically conserved, multidomain cytosolic flavoprotein monooxygenases. Drosophila (D-)MICAL binds the neuronal Sema1a receptor PlexA, and D-MICAL-PlexA interactions are required in vivo for Sema1a-induced axon repulsion. The biological functions of vertebrate MICAL proteins, however, remain unknown. Here, we describe three rodent MICAL genes and analyze their expression in the intact rat nervous system and in two models of spinal cord injury. MICAL-1, -2, and -3 expression patterns in the embryonic, postnatal, and adult nervous system support the idea that MICALs play roles in neural development and plasticity. In addition, MICAL expression is elevated in oligodendrocytes and in meningeal fibroblasts at sites of spinal cord injury but is unchanged in lesioned corticospinal tract neurons. Furthermore, we find that the selective monooxygenase inhibitor EGCG attenuates the repulsive effects of Sema3A and Sema3F in vitro, but not those of several other repulsive cues and substrates. These results implicate MICALs in neuronal regeneration and support the possibility of employing EGCG to attenuate Sema3-mediated axon repulsion in the injured spinal cord.
Insights
Mammalian MICAL proteins are involved in neural development and plasticity. Their expression increases after spinal cord injury, and EGCG may reduce axon repulsion, aiding neuronal regeneration.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- MICALs (Monooxygenase Catalyzed And Light-activated) are conserved cytosolic flavoprotein monooxygenases.
- Drosophila MICAL (D-MICAL) interacts with PlexA, mediating Sema1a-induced axon repulsion.
- Vertebrate MICAL functions remain largely uncharacterized.
Purpose of the Study:
- To investigate the roles of vertebrate MICAL proteins in the nervous system.
- To analyze MICAL gene expression in development and spinal cord injury models.
- To explore the therapeutic potential of MICAL inhibition in neuronal regeneration.
Main Methods:
- Identification and analysis of three rodent MICAL genes.
- Expression profiling in embryonic, postnatal, and adult rat nervous systems.
- Analysis of MICAL expression in two spinal cord injury models.
- In vitro assessment of EGCG effects on semaphorin-mediated axon repulsion.
Main Results:
- MICAL-1, -2, and -3 show expression patterns consistent with roles in neural development and plasticity.
- MICAL expression is upregulated in oligodendrocytes and meningeal fibroblasts post-spinal cord injury.
- EGCG selectively attenuates Sema3A and Sema3F repulsive effects in vitro.
- MICAL expression is not altered in lesioned corticospinal tract neurons.
Conclusions:
- Vertebrate MICALs are implicated in neural development, plasticity, and potentially neuronal regeneration after injury.
- EGCG shows promise as a therapeutic agent to mitigate Sema3-mediated axon repulsion in spinal cord injury.
- Further research into MICAL function could reveal novel strategies for treating neurological damage.
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