GSNOR Deficiency Enhances In Situ Skeletal Muscle Strength, Fatigue Resistance, and RyR1 S-Nitrosylation Without Impacting Mitochondrial Content and Activity.

ABSTRACT:

Aim

Nitric oxide (NO) plays important, but incompletely defined roles in skeletal muscle. NO exerts its regulatory effects partly though S-nitrosylation, which is balanced by denitrosylation by enzymes such as S-nitrosoglutathione reductase (GSNOR), whose functions in skeletal muscle remain to be fully deciphered.

Results

GSNOR null (GSNOR^-/-) tibialis anterior (TA) muscles showed normal growth and were stronger and more fatigue resistant than controls in situ. However, GSNOR^-/- lumbrical muscles showed normal contractility and Ca²⁺ handling in vitro, suggesting important differences in GSNOR function between muscles or between in vitro and in situ environments. GSNOR^-/- TA muscles exhibited normal mitochondrial content, and capill

SUBMITTER: Moon Y 

PROVIDER: S-EPMC5278832 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature