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Sialic Acid Alterations in Mouse Models of Atrophy and Hypertrophy
Author(s) -
Busam Sara,
Goines Bria.,
Weisleder Noah L.,
Crowe Kelly E.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.07240
Subject(s) - atrophy , muscle hypertrophy , sialidase , sialic acid , muscle atrophy , myopathy , biology , medicine , wasting , endocrinology , hindlimb , skeletal muscle , chemistry , microbiology and biotechnology , biochemistry , enzyme , neuraminidase
Sialic acids (SAs) are negatively charged nine‐carbon sugars that are typically found at the ends of glycan chains on glycolipids and glycoproteins. As such, they play important structural and signaling roles for the cell. Skeletal muscle seems to be particularly sensitive to SA perturbations; in GNE myopathy, hypomorphic mutations in a key enzyme of SA biosynthesis leads to muscle weakness and wasting, and SA abundance has been shown to correlate with muscle function in mice. Additionally, enzymatic activity of sialidases, which removes SAs, is altered in both atrophy and hypertrophy. However, linkage‐specific SA changes have not yet been described in atrophy and hypertrophy. Here, we have used a panel of lectins to probe alterations in SA abundance in mouse models of hind‐limb suspension atrophy and hind‐limb overload‐induced hypertrophy.