Ciliary neurotrophic factor (CNTF) promotes skeletal muscle progenitor cell (MPC) viability via the phosphatidylinositol 3‐kinase–Akt pathway. (13th November 2012)

• Record Type: Journal Article
• Authors: Hiatt, Kelly; Lewis, Davina; Shew, Mathew; Bijangi‐Vishehsaraei, Khadijeh; Halum, Stacey
• Is Part Of: Journal of tissue engineering and regenerative medicine. Volume 8:Number 12(2014)
• Page Start: 963
• Page End: 968
• Publication Date: 2012-11-13
• Subjects: Tissue engineering -- Periodicals; Regeneration (Biology) -- Periodicals; 610.28
• DOI: 10.1002/term.1598
• Languages: English
• ISSNs: 1932-6254

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>Muscle progenitor cells (MPCs) are currently being investigated as cellular vectors to deliver neurotrophic factor (NF) for the promotion of re‐innervation after axonal injury. Ideally NF delivery in such a model would enhance axonal regeneration while simultaneously promoting MPC viability. To date, insulin‐like growth factor 1 (IGF‐1) is one of the few NFs known to promote both re‐innervation and MPC viability. We herein identify ciliary neurotrophic factor (CNTF) as a factor that promotes MPC viability in culture, and demonstrate CNTF to impart greater viability effects on MPCs than IGF‐1. We demonstrate that pharmacological inhibition via LY294002 results in abrogation of CNTF‐mediated viability, suggesting that the CNTF‐mediated MPC viability benefit occurs via the PI3–Akt pathway. Finally, we employ a genetic model, establishing MPC cultures from mice deficient in class I_A PI‐3 K (<italic>p85</italic>α<italic>^−/−</italic>) mice, and demonstrate that the viability benefit imparted by CNTF is completely abrogated in PI‐3 K‐deficient MPCs compared to wild‐type controls. In summary, our investigations define CNTF as a promoter of MPC viability beyond IGF‐1, and reveal that the CNTF‐mediated MPC viability effects occur via the PI3–Akt pathway. Copyright © 2012 John Wiley &amp; Sons, Ltd.</p> </abstract>