Peroxisome proliferator-activated receptor β/δ induces myogenesis by modulating myostatin activity.

Abstract

This article has been withdrawn by the authors. In this article, we reported that PPAR␤/␦ positively regulates myogenesis. After a thorough investigation by the Nanyang Technological University in Singapore, data falsifications have been found in some of the in vitro laboratory studies, which invalidate the results reported. Hence, the co-authors wish to withdraw this publication and offer our sincere apologies to all those investigators who may have been affected and misled by this.

Myostatin Induces Insulin Resistance via Casitas B-Lineage Lymphoma b (Cblb)-mediated Degradation of Insulin Receptor Substrate 1 (IRS1) Protein in Response to High Calorie Diet Intake

“…Transfection and Luciferase Reporter Assays-Co-transfection of plasmids into myoblasts using LF2000 has been previously described (38). After transfection, myoblasts were subsequently differentiated into myotubes for further analysis.…”

“…The Cblb (hCblb)-specific overexpressing lentiviral particles (catalog #OHS5899-202619951) were purchased from Open Biosystems. Generation of ChREBP and SREBP1c shRNA lentiviral particles and lentiviral-mediated transduction of myoblasts/myotubes was performed as previously described (38).…”

Inactivation of PPARβ/δ adversely affects satellite cells and reduces postnatal myogenesis

“…A recent report suggests that activation of PPAR␤/␦, through addition of specific agonist, enhances myogenesis in C2C12 myoblasts by increasing both myoblast proliferation and differentiation (2). Consistent with this, loss of PPAR␤/␦ resulted in reduced proliferation of primary myoblasts and defective differentiation.…”

“…Overexpression of constitutively active PPAR␤/␦ in mouse skeletal muscle promotes muscle development and enhances myogenesis by increasing both myoblast proliferation and differentiation in C2C12 myoblasts (2,13,42). In this study, we used notexin-induced muscle injury to analyze the regeneration capacity of PPAR␤/␦-null muscle and, therefore, understand the role of PPAR␤/␦ in postnatal myogenesis.…”

“…In addition, a recent study reported that skeletal muscle-specific knock out of PPAR␦ in mice [PPAR␦-conditional knockout (cKO)] leads to reduced satellite cell (SC) number and impaired skeletal muscle regeneration upon cardiotoxin-mediated injury (1). Recent results have revealed that PPAR␤/␦ positively regulates postnatal myogenesis through transcriptional activation of Gasp-1, leading to reduced activity of its downstream target myostatin (2).…”