The NF-κB-modulated microRNAs miR-195 and miR-497 inhibit myoblast proliferation by targetingIgf1r,Insrand cyclin genes

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.

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Effect of ionizing radiation on human skeletal muscle precursor cells

Radiology and Oncology ◽

10.2478/raon-2013-0058 ◽

2013 ◽

Vol 47 (4) ◽

pp. 376-381 ◽

Cited By ~ 9

Author(s):

Mihaela Jurdana ◽

Maja Cemazar ◽

Katarina Pegan ◽

Tomaz Mars

Keyword(s):

Skeletal Muscle ◽

Stress Response ◽

Ionizing Radiation ◽

Human Skeletal Muscle ◽

Long Term Effects ◽

Post Irradiation ◽

Acute Response ◽

Proliferation Capacity ◽

Myoblast Proliferation

Abstract Background. Long term effects of different doses of ionizing radiation on human skeletal muscle myoblast proliferation, cytokine signalling and stress response capacity were studied in primary cell cultures. Materials and methods. Human skeletal muscle myoblasts obtained from muscle biopsies were cultured and irradiated with a Darpac 2000 X-ray unit at doses of 4, 6 and 8 Gy. Acute effects of radiation were studied by interleukin - 6 (IL-6) release and stress response detected by the heat shock protein (HSP) level, while long term effects were followed by proliferation capacity and cell death. Results. Compared with non-irradiated control and cells treated with inhibitor of cell proliferation Ara C, myoblast proliferation decreased 72 h post-irradiation, this effect was more pronounced with increasing doses. Post-irradiation myoblast survival determined by measurement of released LDH enzyme activity revealed increased activity after exposure to irradiation. The acute response of myoblasts to lower doses of irradiation (4 and 6 Gy) was decreased secretion of constitutive IL-6. Higher doses of irradiation triggered a stress response in myoblasts, determined by increased levels of stress markers (HSPs 27 and 70). Conclusions. Our results show that myoblasts are sensitive to irradiation in terms of their proliferation capacity and capacity to secret IL-6. Since myoblast proliferation and differentiation are a key stage in muscle regeneration, this effect of irradiation needs to be taken in account, particularly in certain clinical conditions.

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

Cell Death and Disease ◽

10.1038/s41419-021-03419-y ◽

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.

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Expression and Regulation of Cyclin Genes in Breast Cancer

Acta Oncologica ◽

10.3109/02841869509094043 ◽

1995 ◽

Vol 34 (5) ◽

pp. 651-656 ◽

Cited By ~ 21

Author(s):

Robert L. Sutherland ◽

Jenny A. Hamilton ◽

Kimberley J. E. Sweeney ◽

Colin K. W. Watts ◽

Elizabeth A. Musgrove

Keyword(s):

Breast Cancer ◽

Cyclin Genes

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Effects of inhibitors of ornithine and S-adenosylmethionine decarboxylases on L6 myoblast proliferation

Journal of Cellular Physiology ◽

10.1002/jcp.1041100209 ◽

1982 ◽

Vol 110 (2) ◽

pp. 161-168 ◽

Cited By ~ 21

Author(s):

Christa M. Stoscheck ◽

Bradley G. Erwin ◽

James R. Florini ◽

Robert A. Richman ◽

Anthony E. Pegg

Keyword(s):

Myoblast Proliferation ◽

L6 Myoblast

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Retinoid acid-induced microRNA-27b-3p impairs C2C12 myoblast proliferation and differentiation by suppressing α-dystrobrevin

Experimental Cell Research ◽

10.1016/j.yexcr.2016.11.009 ◽

2017 ◽

Vol 350 (2) ◽

pp. 301-311 ◽

Cited By ~ 8

Author(s):

Nan Li ◽

Yi Tang ◽

Bo Liu ◽

Wei Cong ◽

Chao Liu ◽

...

Keyword(s):

C2c12 Myoblast ◽

Proliferation And Differentiation ◽

Myoblast Proliferation ◽

Retinoid Acid

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Anemic Hypoxemia Reduces Myoblast Proliferation and Muscle Growth in Late Gestation Fetal Sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00342.2020 ◽

2021 ◽

Author(s):

Paul J. Rozance ◽

Stephanie R Wesolowski ◽

Sonnet S. Jonker ◽

Laura D Brown

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Muscle Growth ◽

Late Gestation ◽

Whole Body ◽

Myoblast Differentiation ◽

Fetal Sheep ◽

Body Protein ◽

Skeletal Muscle Growth ◽

Myoblast Proliferation

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.

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Differential effects of Cdc68 on cell cycle-regulated promoters in Saccharomyces cerevisiae

Molecular and Cellular Biology ◽

10.1128/mcb.14.11.7455-7465.1994 ◽

1994 ◽

Vol 14 (11) ◽

pp. 7455-7465 ◽

Cited By ~ 1

Author(s):

D Lycan ◽

G Mikesell ◽

M Bunger ◽

L Breeden

Keyword(s):

Cell Cycle ◽

Chromatin Structure ◽

Gene Activation ◽

High Level Expression ◽

Specific Component ◽

Allele Specific ◽

High Level ◽

Cyclin Genes ◽

Regulated Promoters

Swi4 and Swi6 form a complex which is required for Start-dependent activation of HO and for high-level expression of G1 cyclin genes CLN1 and CLN2. To identify other regulators of this pathway, we screened for dominant, recessive, conditional, and allele-specific suppressors of swi4 mutants. We isolated 16 recessive suppressors that define three genes, SSF1, SSF5, and SSF9 (suppressor of swi four). Mutations in all three genes bypass the requirement for both Swi4 and Swi6 for HO transcription and activate transcription from reporter genes lacking upstream activating sequences (UASs). SSF5 is allelic with SIN4 (TSF3), a gene implicated in global repression of transcription and chromatin structure, and SSF9 is likely to be a new global repressor of transcription. SSF1 is allelic with CDC68 (SPT16). cdc68 mutations have been shown to increase expression from defective promoters, while preventing transcription from other intact promoters, including CLN1 and CLN2. We find that CDC68 is a required activator of both SWI4 and SWI6, suggesting that CDC68's role at the CLN promoters may be indirect. The target of CDC68 within the SWI4 promoter is complex in that known activating elements (MluI cell cycle boxes) in the SWI4 promoter are required for CDC68 dependence but only within the context of the full-length promoter. This result suggests that there may be both a chromatin structure and a UAS-specific component to Cdc68 function at SWI4. We suggest that Cdc68 functions both in the assembly of repressive complexes that form on many intact promoters in vivo and in the relief of this repression during gene activation.

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