Stanniocalcin-2 inhibits skeletal muscle growth and is upregulated in functional overload-induced hypertrophy

Arimantas Lionikas*, Ana I. Hernandez Cordero, Audrius Kilikevicius, Andrew M. Carroll, Guy S. Bewick, Lutz Bunger, Aivaras Ratkevicius, Lora K. Heisler, Mette Harboe, Claus Oxvig

*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Abstract

Aims: Stanniocalcin-2 (STC2) has recently been implicated in human muscle mass variability by genetic analysis. Biochemically, STC2 inhibits the proteolytic activity of the metalloproteinase PAPP-A, which promotes muscle growth by upregulating the insulin-like growth factor (IGF) axis. The aim was to examine if STC2 affects skeletal muscle mass and to assess how the IGF axis mediates muscle hypertrophy induced by functional overload. Methods: We compared muscle mass and muscle fiber morphology between Stc2−/− (n = 21) and wild-type (n = 15) mice. We then quantified IGF1, IGF2, IGF binding proteins −4 and −5 (IGFBP-4, IGFBP-5), PAPP-A and STC2 in plantaris muscles of wild-type mice subjected to 4-week unilateral overload (n = 14). Results: Stc2−/− mice showed up to 10% larger muscle mass compared with wild-type mice. This increase was mediated by greater cross-sectional area of muscle fibers. Overload increased plantaris mass and components of the IGF axis, including quantities of IGF1 (by 2.41-fold, p = 0.0117), IGF2 (1.70-fold, p = 0.0461), IGFBP-4 (1.48-fold, p = 0.0268), PAPP-A (1.30-fold, p = 0.0154) and STC2 (1.28-fold, p = 0.019). Conclusion: Here we provide evidence that STC2 is an inhibitor of muscle growth upregulated, along with other components of the IGF axis, during overload-induced muscle hypertrophy.

OriginalsprogEngelsk
Artikelnummere15793
TidsskriftPhysiological Reports
Vol/bind11
Nummer15
Antal sider12
ISSN2051-817X
DOI
StatusUdgivet - aug. 2023

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