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Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging
Author(s) -
Jha Mithilesh Kumar,
Lee Youngjin,
Russell Katelyn A.,
Yang Fang,
Dastgheyb Raha M.,
Deme Pragney,
Ament Xanthe H.,
Chen Weiran,
Liu Ying,
Guan Yun,
Polydefkis Michael J.,
Hoke Ahmet,
Haughey Norman J.,
Rothstein Jeffrey D.,
Morrison Brett M.
Publication year - 2020
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23710
Subject(s) - biology , myelin , endocrinology , medicine , schwann cell , knockout mouse , microbiology and biotechnology , sphingomyelin , peripheral nervous system , axon , receptor , central nervous system , biochemistry , cholesterol
Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre +/− , MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory, but not motor, peripheral nerves during maturation and aging. Furthermore, reduced mechanical sensitivity is evident in aged P0‐Cre +/− , MCT1 f/f mice. MCT1 deletion in SCs impairs both their glycolytic and mitochondrial functions, leading to altered lipid metabolism of triacylglycerides, diacylglycerides, and sphingomyelin, decreased expression of myelin‐associated glycoprotein, and increased expression of c‐Jun and p75‐neurotrophin receptor, suggesting a regression of SCs to a less mature developmental state. Taken together, our results define the contribution of SC MCT1 to both SC metabolism and peripheral nerve maturation and aging.