Insulin-like growth factor 1 regulation of proliferation and differentiation of Xenopus laevis myogenic cells in vitro

Abstract

To understand the mechanism of muscle remodeling during Xenopus laevis metamorphosis, we examined the in vitro effect of insulin-like growth factor 1 (IGF-1) on growth and differentiation of three different-fate myogenic cell populations: tadpole tail, tadpole dorsal, and young adult leg muscle. IGF-1 promoted growth and differentiation of both tail and leg myogenic cells only under conditions where these cells could proliferate. Inhibition of cell proliferation by DNA synthesis inhibitor cytosine arabinoside completely canceled the IGF-1's cell differentiation promotion, suggesting the possibility that IGF-1's differentiation-promotion effect is an indirect effect via IGF-1's cell proliferation promotion. IGF-1 promoted differentiation dose dependently with maximum effect at 100-500 ng/ml. RT-PCR analysis revealed the upregulation (11-fold) of ifg1 mRNA expression in developing limbs, suggesting that IGF-1 plays a role in promoting muscle differentiation during limb development. The combined effect of triiodo-L-thyronine (T) and IGF-1 was also examined. In adult leg cells, IGF-1 promoted growth and differentiation irrespective of the presence of T. In larval tail cells, cell count was 76% lower in the presence of T, and IGF-1 did not promote proliferation and differentiation in T-containing medium. In larval dorsal cells, cell count was also lower in the presence of T, but IGF-1 enhanced proliferation and differentiation in T-containing medium. This result is likely due to the presence among dorsal cells of both adult and larval types (1:1). Thus, IGF-1 affects only adult-type myogenic cells in the presence of T and helps accelerate dorsal muscle remodeling during metamorphosis.

MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling

“…It has been well documented that PI3K/AKT is a crucial signaling pathway to promote myogenesis and induce muscle hypertrophy [ 33 , 34 ]. IGF1 is a stimulator of PI3K/AKT signaling during muscle differentiation [ 35 ]. In our study, administration of 75 nM IGF1 recombinant protein totally reversed the inhibitory effects of miR-106a-5p.…”

Omics Approaches in Adipose Tissue and Skeletal Muscle Addressing the Role of Extracellular Matrix in Obesity and Metabolic Dysfunction

“…Thus, integrin striated muscle-specific integrin β1-deficient C57Bl6/J mice exhibit decreased in AKT Ser-473 phosphorylation, glucose uptake, and glycogen synthesis, supporting the role between integrin and insulin signaling in SM [44,45]. Other ECM components such as proteoglycans [46,47], fibronectin [48,49], hepatocyte growth factor (HGF) [50,51], epidermal growth factor (EGF) [52,53], insulin-like growth factor(IGF)-1 [54,55], IGF-2 [56,57], and MMPs [58,59], among others, play crucial roles in myogenesis and adipogenesis. Hence, understanding the inter-tissue connection between WAT and SM in some common genes implicated in ECM remodeling could help to develop strategies against the metabolic disturbances in obesity.…”

Novel Perspective on Mechanism in Muscle Growth Inhibited by Ochratoxin A Associated with Ferroptosis: Model of Juvenile Grass Carp (Ctenopharyngodon idella) In Vivo and In Vitro Trials

“…Our study showed that the addition of SC79 alleviated the differentiation of GCPMt and the protein expressions of MyoG and MyHC in grass carp with OTA inhibition. This was consistent with research on C2C12: the addition of SC79 increased high glucose-inhibited myotube formation and protein expressions of MyoD and MyoG, while the addition of AKT inhibitors was the opposite, indicating that AKT promotes myogenic differentiation in C2C12 cells . The addition of AKT inhibitors blocked taurine deoxycholic acid from improving glucocorticoid-induced inhibition of myotube differentiation index, MyoG, and MHC expressions .…”

“…This was consistent with research on C2C12: the addition of SC79 increased high glucose-inhibited myotube formation and protein expressions of MyoD and MyoG, while the addition of AKT inhibitors was the opposite, indicating that AKT promotes myogenic differentiation in C2C12 cells. 68 The addition of AKT inhibitors blocked taurine deoxycholic acid from improving glucocorticoid-induced inhibition of myotube differentiation index, MyoG, and MHC expressions. 69 The above results indicate that OTA inhibited GCPMs differentiation and fusion mainly by inhibiting the AKT signaling pathway.…”