Leucine Promotes Proliferation and Differentiation of Primary Preterm Rat Satellite Cells in Part through mTORC1 Signaling Pathway.

Jie-Min Dai,Zhen-Yu Shen,Xiao-Shan Qiu,Mu-Xue Yu,Chu-Yi Guo,Si-Qi Zhuang

doi:10.3390/nu7053387

Abstract

Signaling through the mammalian target of rapamycin (mTOR) in response to leucine modulates many cellular and developmental processes. However, in the context of satellite cell proliferation and differentiation, the role of leucine and mTORC1 is less known. This study investigates the role of leucine in the process of proliferation and differentiation of primary preterm rat satellite cells, and the relationship with mammalian target of rapamycin complex 1 (mTORC1) activation. Dissociation of primary satellite cells occurred with type I collagenase and trypsin, and purification, via different speed adherence methods. Satellite cells with positive expression of Desmin were treated with leucine and rapamycin. We observed that leucine promoted proliferation and differentiation of primary satellite cells and increased the phosphorylation of mTOR. Rapamycin inhibited proliferation and differentiation, as well as decreased the phosphorylation level of mTOR. Furthermore, leucine increased the expression of MyoD and myogenin while the protein level of MyoD decreased due to rapamycin. However, myogenin expressed no affect by rapamycin. In conclusion, leucine may up-regulate the activation of mTORC1 to promote proliferation and differentiation of primary preterm rat satellite cells. We have shown that leucine promoted the differentiation of myotubes in part through the mTORC1-MyoD signal pathway.

Highlights

Limited energy reserves are common in preterm infants at birth
This study investigates the role of leucine in the process of the proliferation and differentiation of primary preterm rat satellite cells, and their relationship with mammalian target of rapamycin complex 1 (mTORC1) signal pathways
In the early differentiation stage of primary preterm rat satellite cells, both the phosphorylation level of mammalian target of rapamycin (mTOR) and the expression of MyoD induced by leucine and rapamycin treatment caused a decline of MyoD protein levels

Summary

Introduction

In order to prevent a catabolic state, adequate provision of calories and protein is needed to match intrauterine accretion rate soon after birth. The use of aggressive amino acids intake is associated with increased protein accretion and decreased extrauterine growth restriction (EUGR). EUGR can have an impact on an infant’s later neurodevelopment, growth outcomes and metabolic disorders [1,2,3]. Higher protein intake (≥3.0 g/kg/day but

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