Microarray profiling of gene expression in C2C12 myotubes trained by electric pulse stimulation

2021 ◽  
Author(s):  
Hideaki Fujita ◽  
Masanobu Horie ◽  
Kazunori Shimizu ◽  
Eiji Nagamori
Keyword(s):  
Gene Expression ◽  
Electric Pulse ◽  
C2c12 Myotubes ◽  
Microarray Profiling ◽  
Pulse Stimulation

scholarly journals Regulation Of Myokine Expression In Exosome-like Vesicles By Electric Pulse Stimulation Of C2C12 Myotubes

2020 ◽  
Vol 52 (7S) ◽  
pp. 927-927
Author(s):  
Ju-Hee Kang ◽  
Sujin Kim ◽  
Sohee Moon ◽  
Hyo-Bum Kwak ◽  
Dong-Ho Park
Keyword(s):  
Electric Pulse ◽  
C2c12 Myotubes ◽  
Pulse Stimulation ◽  
Stimulation Of

scholarly journals Electric Pulse Stimulation of Cultured Murine Muscle Cells Reproduces Gene Expression Changes of Trained Mouse Muscle

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e10970 ◽  
Author(s):  
Nathalie Burch ◽  
Anne-Sophie Arnold ◽  
Flurin Item ◽  
Serge Summermatter ◽  
Gesa Brochmann Santana Santos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Electric Pulse ◽  
Muscle Cells ◽  
Mouse Muscle ◽  
Pulse Stimulation ◽  
Stimulation Of

Accelerated de novo sarcomere assembly by electric pulse stimulation in C2C12 myotubes

2007 ◽  
Vol 313 (9) ◽  
pp. 1853-1865 ◽  
Author(s):  
Hideaki Fujita ◽  
Taku Nedachi ◽  
Makoto Kanzaki
Keyword(s):  
De Novo ◽  
Electric Pulse ◽  
C2c12 Myotubes ◽  
Sarcomere Assembly ◽  
Pulse Stimulation

scholarly journals Regulation of Multiple Core Spliceosomal Proteins by Alternative Splicing-Coupled Nonsense-Mediated mRNA Decay

2008 ◽  
Vol 28 (13) ◽  
pp. 4320-4330 ◽  
Author(s):  
Arneet L. Saltzman ◽  
Yoon Ki Kim ◽  
Qun Pan ◽  
Matthew M. Fagnani ◽  
Lynne E. Maquat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alternative Splicing ◽  
Mrna Decay ◽  
Splice Variants ◽  
Cellular Functions ◽  
Regulate Gene Expression ◽  
Premature Termination Codons ◽  
Microarray Profiling ◽  
Nonsense Mediated Mrna Decay ◽  
Regulate Gene

ABSTRACT Alternative splicing (AS) can regulate gene expression by introducing premature termination codons (PTCs) into spliced mRNA that subsequently elicit transcript degradation by the nonsense-mediated mRNA decay (NMD) pathway. However, the range of cellular functions controlled by this process and the factors required are poorly understood. By quantitative AS microarray profiling, we find that there are significant overlaps among the sets of PTC-introducing AS events affected by individual knockdown of the three core human NMD factors, Up-Frameshift 1 (UPF1), UPF2, and UPF3X/B. However, the levels of some PTC-containing splice variants are less or not detectably affected by the knockdown of UPF2 and/or UPF3X, compared with the knockdown of UPF1. The intron sequences flanking the affected alternative exons are often highly conserved, suggesting important regulatory roles for these AS events. The corresponding genes represent diverse cellular functions, and surprisingly, many encode core spliceosomal proteins and assembly factors. We further show that conserved, PTC-introducing AS events are enriched in genes that encode core spliceosomal proteins. Where tested, altering the expression levels of these core spliceosomal components affects the regulation of PTC-containing splice variants from the corresponding genes. Together, our results show that AS-coupled NMD can have different UPF factor requirements and is likely to regulate many general components of the spliceosome. The results further implicate general spliceosomal components in AS regulation.

Abstract 117: MicroRNA-138 regulates S100A1 in Endothelial Cells

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Anagha Sen ◽  
Shumei Ren ◽  
Jianxin Sun ◽  
Patrick Most ◽  
Karsten Peppel
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Reporter Gene ◽  
Recombinant Adenovirus ◽  
Limb Ischemia ◽  
Bioinformatic Analysis ◽  
Reporter Gene Expression ◽  
Luciferase Reporter ◽  
C2c12 Myotubes ◽  
Luciferase Reporter Construct

Rationale: The EF-hand Ca2+ sensor S100A1 is essential for proper endothelial nitric oxide (NO) synthase (eNOS) activation. S100A1 levels are greatly reduced in endothelial cells (ECs) subjected to hypoxia, rendering them dysfunctional. Objective: To determine if the 3’UTR mediates the rapid hypoxia-induced downregulation of S100A1 in ECs. Methods and Results: ECs transfected with a S100A1 - 3’ untranslated region (UTR) luciferase reporter construct displayed significantly reduced gene expression when subjected to gas or chemical hypoxia. Bioinformatic analysis suggested that microRNA -138 (miR-138) could target the 3’UTR of S100A1. Hypoxia greatly increased miR-138 levels in ECs, but not in skeletal muscle C2C12 myotubes. Consistent with this finding, patients with critical limb ischemia (CLI) or mice subjected to femoral artery resection (FAR) displayed increased miR-138 levels. Transfection of a miR-138 mimic into ECs reduced S100A1 - 3 ‘UTR reporter gene expression, while transfection of an anti miR-138 (antagomir) prevented the hypoxia-induced downregulation of the reporter gene. The increased levels of miR-138 are dependent on Hif1-α activation as treatment with siRNA against Hif1-α prevented S100A1 reporter gene downregulation after hypoxia. Conversely, specific activation of Hif1-α by a selective prolyl-hydroxylase inhibitor (IOX2) reduced reporter gene expression. Finally, ECs transfected with miR-138 mimic displayed reduced tube formation when plated onto Matrigel matrix and expressed less NO when stimulated with VEGF. These effects were reversed by gene transfer of S100A1 using recombinant adenovirus. Conclusions: Our study shows that miR-138 is an essential mediator of EC dysfunction via its ability to target the 3’UTR of S100A1 in a hypoxia-induced manner. MiR-138 might thus be an attractive target for the treatment of pathologies that are linked to endothelial dysfunction.

scholarly journals Distinct effects of oleic acid and itstrans-isomer elaidic acid on the expression of myokines and adipokines in cell models

2011 ◽  
Vol 105 (8) ◽  
pp. 1226-1234 ◽  
Author(s):  
Nuria Granados ◽  
Jaume Amengual ◽  
Joan Ribot ◽  
Andreu Palou ◽  
M. Luisa Bonet
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Oleic Acid ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Elaidic Acid ◽  
C2c12 Myotubes ◽  
Cell Models ◽  
Monounsaturated Fat ◽  
Expression Levels

Trans-fatty acids (TFA) andcis-monounsaturated fat appear to exert detrimental and beneficial effects, respectively, on glucose metabolism and insulin sensitivity. Adipose tissue and skeletal muscle are a source of signalling proteins (adipokines and myokines), some of which have been related to the control of insulin sensitivity. Here, we investigated the possible differential effects of elaidic acid (EA;trans-9-18 : 1) – the major component in industrially produced TFA – and oleic acid (OA;cis-9-18 : 1) – itscis-isomer naturally present in food – on cellular glucose uptake and the expression of selected myokines and adipokines using cell models. Differentiated C2C12 myotubes and 3T3-L1 adipocytes were pretreated with the vehicle (control cells) or fatty acids for 24 h, after which basal and insulin-stimulated 2-deoxyglucose uptake and the expression of selected signalling proteins were measured. In C2C12 myotubes, pretreatment with OA, but not with EA, led to increased insulin-stimulated 2-deoxyglucose uptake and IL-6 expression levels, while pretreatment with EA, but not with OA, led to reduced IL-15 mRNA levels and increased TNF-α expression levels. In 3T3-L1 adipocytes, exposure to OA, but not to EA, resulted in reduced resistin gene expression and increased adiponectin gene expression. The results show evidence of distinct, direct effects of OA and EA on muscle glucose uptake and the expression of target myokines and adipokines, thus suggesting novel mechanisms by whichcis- andtrans-monounsaturated fat may differentially affect systemic functions.

scholarly journals Transcriptome Analyses of In Vitro Exercise Models by Clenbuterol Supplementation or Electrical Pulse Stimulation

2021 ◽  
Vol 11 (21) ◽  
pp. 10436
Author(s):  
Taku Fukushima ◽  
Miho Takata ◽  
Ayano Kato ◽  
Takayuki Uchida ◽  
Takeshi Nikawa ◽  
...  
Keyword(s):  
Gene Ontology ◽  
Electrical Pulse ◽  
C2c12 Myotubes ◽  
Rna Seq ◽  
Gene Expressions ◽  
Beneficial Effects ◽  
Electrical Pulse Stimulation ◽  
Transcriptional Changes ◽  
Pulse Stimulation

Exercise has beneficial effects on human health and is affected by two different pathways; motoneuron and endocrine. For the advancement of exercise research, in vitro exercise models are essential. We established two in vitro exercise models using C2C12 myotubes; EPS (electrical pulse stimulation) for a motoneuron model and clenbuterol, a specific β2 adrenergic receptor agonist, treatment for an endocrine model. For clenbuterol treatment, we found that Ppargc1a was induced only in low glucose media (1 mg/mL) using a 1-h treatment of 30 ng/mL clenbuterol. Global transcriptional changes of clenbuterol treatment were analyzed by RNA-seq and gene ontology analyses and indicated that mitogenesis and the PI3K-Akt pathway were enhanced, which is consistent with the effects of exercise. Cxcl1 and Cxcl5 were identified as candidate myokines induced by adrenaline. As for the EPS model, we compared 1 Hz of 1-pulse EPS and 1 Hz of 10-pulse EPS for 24 h and determined Myh gene expressions. Ten-pulse EPS induced higher Myh2 and Myh7 expression. Global transcriptional changes of 10-pulse EPS were also analyzed using RNA-seq, and gene ontology analyses indicated that CaMK signaling and hypertrophy pathways were enhanced, which is also consistent with the effects of exercise. In this paper, we provided two transcriptome results of in vitro exercise models and these databases will contribute to advances in exercise research.

scholarly journals LOW-INTENSITY EXERCISE ENHANCES MUSCULAR ANDROGEN/ANDROGEN RECEPTOR TO INHIBIT MYOSTATIN PATHWAY

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S85-S86
Author(s):  
Bo-Kyung Son ◽  
Masato Eto ◽  
Miya Oura ◽  
Masahiro Akishita
Keyword(s):  
Skeletal Muscle ◽  
Androgen Receptor ◽  
Electric Pulse ◽  
Negative Regulator ◽  
Muscle Size ◽  
C2c12 Myotubes ◽  
Protein Levels ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Response To Exercise

Abstract Background: Physical exercise is well documented to induce muscle size, strength, and energy metabolism. Although the contribution of systemic or local androgen in exercise-adapted muscle hypertrophy has been suggested, less is known about the molecular pathway of androgen in response to exercise. In the present study, we examined roles of androgen/androgen receptor (AR) after exercise, especially for the suppression of myostatin, a potent negative regulator of muscle mass. Methods and Results: To examine the effects of exercise, we employed low-intensity exercise in mice and electric pulse stimulation (EPS) in C2C12 myotubes. Both mRNA and protein levels of AR significantly increased in skeletal muscle of low-intensity exercised mice and C2C12 myotubes exposed to EPS. Production of testosterone and DHT from EPS-treated C2C12 myotubes was markedly increased. Of interest, we found that myostatin was clearly inhibited by EPS, and its inhibition was significantly abrogated by flutamide, a specific antagonist of AR. Furthermore, IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide. Similar downregulation of myostatin and IL-6 was seen in skeletal muscle of low-intensity exercised mice. Conclusion: Muscle AR expression and androgen production were increased by exercise and EPS treatment. As a mechanistical insight, it is suggested that AR inhibited myostatin expression transcriptionally, which downregulates IL-6/pSTAT3 pathway and thus contributes to the prevention of muscle degradation.

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