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Axonal Contact Regulates Expression of α2 and β2 Isoforms of Na + ,K + ‐ATPase in Schwann Cells: Adhesion Molecules and Nerve Regeneration
Author(s) -
Kawai Hiromichi,
Yasuda Hitoshi,
Terada Masahiko,
OmatsuKanbe Mariko,
Kikkawa Ryuichi
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.69010330.x
Subject(s) - sciatic nerve , gene isoform , schwann cell , wallerian degeneration , regeneration (biology) , axon , sciatic nerve injury , ouabain , nerve injury , microbiology and biotechnology , chemistry , biology , anatomy , neuroscience , biochemistry , sodium , organic chemistry , gene
Three isoforms of catalytic α subunits and two isoforms of β subunits of Na + ,K + ‐ATPase were detected in rat sciatic nerves by western blotting. Unlike the enzyme in brain, sciatic nerve Na + ,K + ‐ATPase was highly resistant to ouabain. The ouabain‐resistant α1 isoform was demonstrated to be the predominant form in rat intact sciatic nerve by quantitative densitometric analysis and is mainly responsible for sciatic nerve Na + ,K + ‐ATPase activity. After sciatic nerve injury, the α3 and β1 isoforms completely disappeared from the distal segment owing to Wallerian degeneration. In contrast, α2 and β2 isoform expression and Na + ,K + ‐ATPase activity sensitive to pyrithiamine (a specific inhibitor of the α2 isoform) were markedly increased in Schwann cells in the distal segment of the injured sciatic nerve. These latter levels returned to baseline with nerve regeneration. Our results suggest that α3 and β1 isoforms are exclusive for the axon and α2 and β2 isoforms are exclusive for the Schwann cell, although axonal contact regulates α2 and β2 isoform expressions. Because the β2 isoform of Na + ,K + ‐ATPase is known as an adhesion molecule on glia (AMOG), increased expression of AMOG/β2 on Schwann cells in the segment distal to sciatic nerve injury suggests that AMOG/β2 may act as an adhesion molecule in peripheral nerve regeneration.