Chronic alcohol exposure induces muscle atrophy (myopathy) in zebrafish and alters the expression of microRNAs targeting the Notch pathway in skeletal muscle

Khayrullin, Andrew; Smith, Lauren; Mistry, Dhwani; Dukes, Amy; Pan, Yue; Hamrick, Mark W.

doi:10.1016/j.bbrc.2016.09.117

Cited by 25 publications

(16 citation statements)

References 30 publications

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“…Notch signaling has been identified to be critical in modulating satellite cell function, and it can be used as a therapeutic application to overcome skeletal muscle atrophy [ 39 , 44 ]. However, all previous research used only methods of transient transfection of NICD, which usually has the problems of low transfection efficiency and short duration.…”

Section: Discussionmentioning

confidence: 99%

“…In 2016, Shan et al reviewed that activation of Notch1 signaling promotes the muscle satellite cells’ quiescence and proliferation [ 45 ]. To date, several studies have confirmed several specific genes and miRNAs regulating the proliferation of satellite cells through the Notch signaling pathway [ 39 , 40 , 46 ]. However, the regulated network of the Notch signaling pathway has still not been explored in proliferating satellite cells.…”

Section: Discussionmentioning

confidence: 99%

“…Besides the myomiRs, there are also many miRNAs regulating satellite cell myogenesis, for example miR-31 [ 24 ]; miR-27a [ 25 , 26 ], miR128 [ 27 ], miR-221/miR-222 [ 28 ], miR-682 [ 29 ] and miR-181 [ 30 ]; miR-186 [ 31 ], miR-24 [ 32 ], miR-214 [ 33 , 34 ], miR-26a [ 35 ], miR-29b/c [ 36 ], miR-322/424 [ 37 ] and miR-503 [ 37 ] have been identified to regulate the quiescence, proliferation and differentiation stage of satellite cells respectively. Both Notch signaling and miRNA have been identified to play critical roles in regulating myogenesis, and four miRNAs, miR-1, miR-206, miR-146a and 146b, have been reported to regulate skeletal muscle myogenesis via Notch signaling [ 38 , 39 , 40 , 41 ]. However, none of these four miRNAs were studied in porcine skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

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Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Jiao

Huang

Chen

et al. 2018

IJMS

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Notch signaling as a conserved cell fate regulator is involved in the regulation of cell quiescence, proliferation, differentiation and postnatal tissue regeneration. However, how Notch signaling regulates porcine satellite cells (PSCs) has not been elucidated. We stably transfected Notch1 intracellular domain (N1ICD) into PSCs to analyze the gene expression profile and miRNA-seq. The analysis of the gene expression profile identified 295 differentially-expressed genes (DEGs) in proliferating-N1ICD PSCs (P-N1ICD) and nine DEGs on differentiating-N1ICD PSCs (D-N1ICD), compared with that in control groups (P-Control and D-Control, respectively). Analyzing the underlying function of DEGs showed that most of the upregulated DEGs enriched in P-N1ICD PSCs are related to the cell cycle. Forty-four and 12 known differentially-expressed miRNAs (DEMs) were identified in the P-N1ICD PSCs and D-N1ICD PSCs group, respectively. Furthermore, we constructed the gene-miRNA network of the DEGs and DEMs. In P-N1ICD PSCs, miR-125a, miR-125b, miR-10a-5p, ssc-miR-214, miR-423 and miR-149 are downregulated hub miRNAs, whose corresponding hub genes are marker of proliferation Ki-67 (MKI67) and nuclear receptor binding SET domain protein 2 (WHSC1). By contrast, miR-27a, miR-146a-5p and miR-221-3p are upregulated hub miRNAs, whose hub genes are RUNX1 translocation partner 1 (RUNX1T1) and fibroblast growth factor 2 (FGF2). All the hub miRNAs and genes are associated with cell proliferation. Quantitative RT-PCR results are consistent with the gene expression profile and miRNA-seq results. The results of our study provide valuable information for understanding the molecular mechanisms underlying Notch signaling in PSCs and skeletal muscle development.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Jiao

Huang

Chen

et al. 2018

IJMS

View full text Add to dashboard Cite

show abstract

“…Notch signaling plays a role in SC fate as activation of Notch1 strongly promotes the lineage switch from myogenic towards brown adipogenic fate [ 16 ] . Khayrullin et al reported that upregulation of Notch signaling suppresses myogenesis and maintains muscle SC quiescence and miRNAs targeting Notch are likely to play important roles in alcohol-related myopathy in zebrafish model [ 17 ] . SC self-renewal is an essential process to maintaining the robustness of skeletal muscle regenerative capacity.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of differentially expressed genes in rotator cuff tear patients using microarray data

et al. 2018

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BackgroundRotator cuff tear (RCT) is a common shoulder disorder in the elderly. Muscle atrophy, denervation and fatty infiltration exert secondary injuries on torn rotator cuff muscles. It has been reported that satellite cells (SCs) play roles in pathogenic process and regenerative capacity of human RCT via regulating of target genes. This study aims to complement the differentially expressed genes (DEGs) of SCs that regulated between the torn supraspinatus (SSP) samples and intact subscapularis (SSC) samples, identify their functions and molecular pathways.MethodsThe gene expression profile GSE93661 was downloaded and bioinformatics analysis was made.ResultsFive hundred fifty one DEGs totally were identified. Among them, 272 DEGs were overexpressed, and the remaining 279 DEGs were underexpressed. Gene ontology (GO) and pathway enrichment analysis of target genes were performed. We furthermore identified some relevant core genes using gene–gene interaction network analysis such as GNG13, GCG, NOTCH1, BCL2, NMUR2, PMCH, FFAR1, AVPR2, GNA14, and KALRN, that may contribute to the understanding of the molecular mechanisms of secondary injuries in RCT. We also discovered that GNG13/calcium signaling pathway is highly correlated with the denervation atrophy pathological process of RCT.ConclusionThese genes and pathways provide a new perspective for revealing the underlying pathological mechanisms and therapy strategy of RCT.

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“…Early life stage exposure to EtOH causes skeletal muscle necrosis in chick embryos [ 6 ], decreases both fiber number and fiber size in rat pups born to EtOH-treated mothers [ 7 ], and decreases fiber size in zebrafish embryos exposed to EtOH during primary muscle development [ 8 ]. Adult zebrafish exposed to EtOH have decreased muscle fiber size and exhibit abnormal behavior that varies between strains [ 9 , 10 ]. The effects of EtOH exposure between primary muscle development and adulthood are not understood.…”

Section: Introductionmentioning

confidence: 99%

Ethanol Exposure Causes Muscle Degeneration in Zebrafish

Coffey

Pasquarella

Goody

et al. 2018

JDB

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Alcoholic myopathies are characterized by neuromusculoskeletal symptoms such as compromised movement and weakness. Although these symptoms have been attributed to neurological damage, EtOH may also target skeletal muscle. EtOH exposure during zebrafish primary muscle development or adulthood results in smaller muscle fibers. However, the effects of EtOH exposure on skeletal muscle during the growth period that follows primary muscle development are not well understood. We determined the effects of EtOH exposure on muscle during this phase of development. Strikingly, muscle fibers at this stage are acutely sensitive to EtOH treatment: EtOH induces muscle degeneration. The severity of EtOH-induced muscle damage varies but muscle becomes more refractory to EtOH as muscle develops. NF-kB induction in muscle indicates that EtOH triggers a pro-inflammatory response. EtOH-induced muscle damage is p53-independent. Uptake of Evans blue dye shows that EtOH treatment causes sarcolemmal instability before muscle fiber detachment. Dystrophin-null sapje mutant zebrafish also exhibit sarcolemmal instability. We tested whether Trichostatin A (TSA), which reduces muscle degeneration in sapje mutants, would affect EtOH-treated zebrafish. We found that TSA and EtOH are a lethal combination. EtOH does, however, exacerbate muscle degeneration in sapje mutants. EtOH also disrupts adhesion of muscle fibers to their extracellular matrix at the myotendinous junction: some detached muscle fibers retain beta-Dystroglycan indicating failure of muscle end attachments. Overexpression of Paxillin, which reduces muscle degeneration in zebrafish deficient for beta-Dystroglycan, is not sufficient to rescue degeneration. Taken together, our results suggest that EtOH exposure has pleiotropic deleterious effects on skeletal muscle.

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Chronic alcohol exposure induces muscle atrophy (myopathy) in zebrafish and alters the expression of microRNAs targeting the Notch pathway in skeletal muscle

Cited by 25 publications

References 30 publications

Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells’ Proliferation through Regulating the Cell Cycle

Bioinformatics analysis of differentially expressed genes in rotator cuff tear patients using microarray data

Ethanol Exposure Causes Muscle Degeneration in Zebrafish

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