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Journal of Histochemistry and Cytochemistry
Volume 51 (12): 1611-1620, 2003
Copyright ©The Histochemical Society, Inc.

Insulin-like Growth Factor-II Delays Early but Enhances Late Regeneration of Skeletal Muscle

Sonnie P. Kirk, Jenny M. Oldham, Ferenc Jeanplong and John J. Bass

Functional Muscle Genomics, AgResearch, Ruakura Agricultural Research Centre, Hamilton, New Zealand

Correspondence to: Dr. Jenny Oldham, Functional Muscle Genomics, AgResearch, Ruakura Agricultural Research Centre, Private Bag 3123, Hamilton, New Zealand. E-mail: jenny.oldham{at}agresearch.co.nz

This study tested whether administration of insulin-like growth factor-II (IGF-II) enhances muscle regeneration. Rat biceps femoris muscle was damaged with notexin and then IGF-II was administered for up to 7 days. Results show that the proportion of nuclei containing or surrounded by immunoreactivity to MyoD, myogenin, and developmental myosin heavy chain (dMHC) is less in the IGF-II treatment group relative to the control group on days 1 (p=0.057), 2 (p=0.034), and 3 (p=0.047), respectively. This indicates a delay in muscle precursor cell (MPC) proliferation and differentiation with IGF-II administration. This effect was not associated with decreased binding capacity of the type 1 IGF receptor, as determined by receptor autoradiography in day 1 muscle sections (NS), but was associated with inhibition of phagocytic processes. The cross-sectional area of regenerating muscle fibers was significantly greater in the IGF-II treatment group than in the control group by day 7 (p=0.0092). The enhancing effect of IGF-II on late muscle regeneration, when the main process taking place is fiber enlargement, coincides with the period in which IGF-II is normally expressed by regenerating muscle, indicating that greater endogenous production of IGF-II would be associated with improved regeneration.

(J Histochem Cytochem 51:1611–1620, 2003)

Key Words: developmental myosin heavy • chain • proliferation • myogenin • differentiation • MyoD • satellite cell • damage • type 1 IGF receptor • rat


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