TY - JOUR
T1 - MICAL flavoprotein monooxygenases
T2 - Expression during neural development and following spinal cord injuries in the rat
AU - Pasterkamp, R. Jeroen
AU - Dai, Hai Ning
AU - Terman, Jonathan R.
AU - Wahlin, Karl J.
AU - Kim, Byung
AU - Bregman, Barbara S.
AU - Popovich, Phillip G.
AU - Kolodkin, Alex L.
N1 - Funding Information:
We thank members of the Kolodkin, Ginty, and Pasterkamp laboratories for helpful discussions; David Kantor and Rejji Kuruvilla for help with the EGCG experiments; Alain Chedotal, Marc Tessier-Lavigne, Renping Zhou, and Yuling Luo for constructs and cells. This work was supported by grants from The Netherlands Organization for Scientific Research and Human Frontier Science Program (to R.J.P); NIH/NIMH (MH069787 to J.R.T); and The Christopher Reeve Paralysis Foundation and NIH/NINDS (to A.L.K.). A.L.K. is an Investigator of the Howard Hughes Medical Institute.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2006/1
Y1 - 2006/1
N2 - 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.
AB - 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.
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U2 - 10.1016/j.mcn.2005.09.001
DO - 10.1016/j.mcn.2005.09.001
M3 - Article
C2 - 16230022
AN - SCOPUS:30044443383
SN - 1044-7431
VL - 31
SP - 52
EP - 69
JO - Molecular and Cellular Neurosciences
JF - Molecular and Cellular Neurosciences
IS - 1
ER -