scholarly journals Corrigendum to: “Different roles of the IGF-I Ec peptide (MGF) and mature IGF-I in myoblast proliferation and differentiation” [FEBS Lett. 522 (2002) 156-160]

FEBS Letters ◽  
2006 ◽  
Vol 580 (10) ◽  
pp. 2530-2530 ◽  
Author(s):  
Shi Yu Yang ◽  
Geoffrey Goldspink
Keyword(s):  
Proliferation And Differentiation ◽  
Igf I ◽  
Myoblast Proliferation

Myogenic differentiation during regrowth of atrophied skeletal muscle is associated with inactivation of GSK-3β

2007 ◽  
Vol 292 (5) ◽  
pp. C1636-C1644 ◽  
Author(s):  
Jos L. J. van der Velden ◽  
Ramon C. J. Langen ◽  
Marco C. J. M. Kelders ◽  
Jodil Willems ◽  
Emiel F. M. Wouters ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Glycogen Synthase ◽  
Myogenic Differentiation ◽  
Hindlimb Suspension ◽  
Akt Phosphorylation ◽  
Proliferation And Differentiation ◽  
Igf I ◽  
Myoblast Proliferation ◽  
Gsk 3Β ◽  
First Time

Muscle atrophy contributes to morbidity and mortality in aging and chronic disease, emphasizing the need to gain understanding of the mechanisms involved in muscle atrophy and (re)growth. We hypothesized that the magnitude of muscle regrowth during recovery from atrophy determines whether myonuclear accretion and myogenic differentiation are required and that insulin-like growth factor (IGF)-I/Akt/glycogen synthase kinase (GSK)-3β signaling differs between regrowth responses. To address this hypothesis we subjected mice to hindlimb suspension (HS) to induce atrophy of soleus (−40%) and plantaris (−27%) muscle. Reloading-induced muscle regrowth was complete after 14 days and involved an increase in IGF-IEa mRNA expression that coincided with Akt phosphorylation in both muscles. In contrast, phosphorylation and inactivation of GSK-3β were observed during soleus regrowth only. Furthermore, soleus but not plantaris regrowth involved muscle regeneration based on a transient increase in expression of histone 3.2 and myosin heavy chain-perinatal, which are markers of myoblast proliferation and differentiation, and a strong induction of muscle regulatory factor (MRF) expression. Experiments in cultured muscle cells showed that IGF-I-induced MRF expression is facilitated by inactivation of GSK-3β and selectively occurs in the myoblast population. This study suggests that induction of IGF-I expression and Akt phosphorylation during recovery from muscle atrophy is independent of the magnitude of muscle regrowth. Moreover, our data demonstrate for the first time that the regenerative response characterized by myoblast proliferation, differentiation, and increased MRF expression in recovering muscle is associated with the magnitude of regrowth and may be regulated by inactivation of GSK-3β.

scholarly journals MicroRNA-27b-3p Targets the Myostatin Gene to Regulate Myoblast Proliferation and Is Involved in Myoblast Differentiation

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 423
Author(s):  
Genxi Zhang ◽  
Mingliang He ◽  
Pengfei Wu ◽  
Xinchao Zhang ◽  
Kaizhi Zhou ◽  
...  
Keyword(s):  
Muscle Growth ◽  
Luciferase Reporter ◽  
Myoblast Differentiation ◽  
Regulation Mechanism ◽  
Rna Seq ◽  
Myostatin Gene ◽  
Primary Myoblasts ◽  
Chicken Muscle ◽  
Proliferation And Differentiation ◽  
Myoblast Proliferation

microRNAs play an important role in the growth and development of chicken embryos, including the regulation of skeletal muscle genesis, myoblast proliferation, differentiation, and apoptosis. Our previous RNA-seq studies showed that microRNA-27b-3p (miR-27b-3p) might play an important role in regulating the proliferation and differentiation of chicken primary myoblasts (CPMs). However, the mechanism of miR-27b-3p regulating the proliferation and differentiation of CPMs is still unclear. In this study, the results showed that miR-27b-3p significantly promoted the proliferation of CPMs and inhibited the differentiation of CPMs. Then, myostatin (MSTN) was confirmed to be the target gene of miR-27b-3p by double luciferase reporter assay, RT-qPCR, and Western blot. By overexpressing and interfering with MSTN expression in CPMs, the results showed that overexpression of MSTN significantly inhibited the proliferation and differentiation of CPMs. In contrast, interference of MSTN expression had the opposite effect. This study showed that miR-27b-3p could promote the proliferation of CPMs by targeting MSTN. Interestingly, both miR-27b-3p and MSTN can inhibit the differentiation of CPMs. These results provide a theoretical basis for further understanding the function of miR-27b-3p in chicken and revealing its regulation mechanism on chicken muscle growth.

scholarly journals CircRILPL1 promotes muscle proliferation and differentiation via binding miR-145 to activate IGF1R/PI3K/AKT pathway

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Xuemei Shen ◽  
Jia Tang ◽  
Rui Jiang ◽  
Xiaogang Wang ◽  
Zhaoxin Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Muscle Development ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Luciferase Assay ◽  
Circular Rnas ◽  
Akt Signaling Pathway ◽  
Sequencing Data ◽  
Proliferation And Differentiation ◽  
Myoblast Proliferation

AbstractMany novel non-coding RNAs, such as microRNAs (miRNAs) and circular RNAs (circRNAs), are involved in various physiological and pathological processes. The PI3K/AKT signaling pathway is important for its role in regulating skeletal muscle development. In this study, molecular and biochemical assays were used to confirm the role of miRNA-145 (miR-145) in myoblast proliferation and apoptosis. Based on sequencing data and bioinformatics analysis, we identified a new circRILPL1, which acts as a sponge for miR-145. The interactions between circRILPL1 and miR-145 were examined by bioinformatics, a luciferase assay, and RNA immunoprecipitation. Mechanistically, knockdown or exogenous expression of circRILPL1 in the primary myoblasts was performed to prove the functional significance of circRILPL1. We investigated the inhibitory effect of miR-145 on myoblast proliferation by targeting IGF1R to regulate the PI3K/AKT signaling pathway. A novel circRILPL1 was identified that could sponge miR-145 and is related to AKT activation. In addition, circRILPL1 was positively correlated with muscle proliferation and differentiation in vitro and could inhibit cell apoptosis. The newly identified circRILPL1 functions as a miR-145 sponge to regulate the IGF1R gene and rescue the inhibitory effect of miR-145 on the PI3K/AKT signaling pathway, thereby promoting myoblast growth.

scholarly journals Insulin-like growth factor-I signaling is modified during chondrocyte differentiation

2004 ◽  
Vol 183 (3) ◽  
pp. 477-486 ◽  
Author(s):  
Chanika Phornphutkul ◽  
Ke-Ying Wu ◽  
Xu Yang ◽  
Qian Chen ◽  
Philip A Gruppuso
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Chondrocyte Differentiation ◽  
Erk Pathway ◽  
Insulin Like Growth Factor ◽  
Erk Activation ◽  
Atdc5 Cell ◽  
Factor I ◽  
Proliferation And Differentiation ◽  
Igf I

Insulin-like growth factor-I (IGF-I) is a critical regulator of skeletal growth. While IGF-I has been shown to be a potent chondrocyte mitogen in vitro, its role in chondrocyte differentiation is less well characterized. We chose to study the action of IGF-I on an accepted model of chondrocyte differentiation, the ATDC5 cell line. Insulin concentrations sufficiently high to interact with the IGF-I receptor are routinely used to induce ATDC5 cells to differentiate. Therefore, we first examined the ability of IGF-I to promote chondrocyte differentiation at physiological concentrations. IGF-I could induce differentiation of these cells at concentrations below 10 nM. However, increasing IGF-I concentrations were less potent at inducing differentiation. We hypothesized that mitogenic effects of IGF-I might inhibit its differentiating effects. Indeed, the extracellular-signal-regulated kinase (ERK)-pathway inhibitor PD98059 inhibited ATDC5 cell DNA synthesis while enhancing differentiation. This suggested that the ability of IGF-I to promote both proliferation and differentiation might require that its signaling be modulated through the differentiation process. We therefore compared IGF-I-mediated ERK activation in proliferating and hypertrophic chondrocytes. IGF-I potently induced ERK activation in proliferating cells, but minimal ERK response was seen in hypertrophic cells. In contrast, IGF-I-mediated Akt activation was unchanged by differentiation, indicating intact upstream IGF-I receptor signaling. Similar findings were observed in the RCJ3.1C5.18 chondrogenic cell line and in primary chick chondrocytes. We conclude that IGF-I promotes both proliferation and differentiation of chondrocytes and that the differentiation effects of IGF-I may require uncoupling of signaling to the ERK pathway.

scholarly journals Gga-miR-205a Affecting Myoblast Proliferation and Differentiation by Targeting CDH11

2018 ◽  
Vol 9 ◽  
Author(s):  
Zhijun Wang ◽  
Hongjia Ouyang ◽  
Xiaolan Chen ◽  
Jiao Yu ◽  
Bahareldin A. Abdalla ◽  
...  
Keyword(s):  
Proliferation And Differentiation ◽  
Myoblast Proliferation

scholarly journals Cooperation between Shh and IGF-I in promoting myogenic proliferation and differentiation via the MAPK/ERK and PI3K/Akt pathways requires smo activity

2012 ◽  
Vol 227 (4) ◽  
pp. 1455-1464 ◽  
Author(s):  
D. Madhala-Levy ◽  
V.C. Williams ◽  
S.M. Hughes ◽  
R. Reshef ◽  
O. Halevy
Keyword(s):  
Proliferation And Differentiation ◽  
Igf I
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