Skip to content

Study · Animal study (in vivo) · mouse · 2014

3 results

Effect of exercise intensity on isoform-specific expressions of NT-PGC-1 α mRNA in mouse skeletal muscle.

Wen X, Wu J, Chang JS, Zhang P, Wang J, Zhang Y, Gettys TW, Zhang Y

BioMed research international2 Jul 2014Cited by 50 (Europe PMC)

PMID25136584 (opens in a new tab)PMCIDPMC4106048 (opens in a new tab)DOI10.1155/2014/402175 (opens in a new tab)PepBankPUB-25136584
Download PDFPubMedAsk about this study
Jump to 3 results

Summary

PGC-1α is an inducible transcriptional coactivator that regulates mitochondrial biogenesis and cellular energy metabolism in skeletal muscle. Recent studies have identified two additional PGC-1α transcripts that are derived from an alternative exon 1 (exon 1b) and induced by exercise. Given that the PGC-1α gene also produces NT-PGC-1α transcript by alternative 3(') splicing between exon 6 and exon 7, we have investigated isoform-specific expression of NT-PGC-1α mRNA in mouse skeletal muscle during physical exercise with different intensities. We report here that NT-PGC-1α-a mRNA expression derived from a canonical exon 1 (exon 1a) is increased by high-intensity exercise and AMPK activator AICAR in mouse skeletal muscle but not altered by low- and medium-intensity exercise and β 2-adrenergic receptor agonist clenbuterol. In contrast, the alternative exon 1b-driven NT-PGC-1α-b (PGC-1α4) and NT-PGC-1α-c are highly induced by low-, medium-, and high-intensity exercise, AICAR, and clenbuterol. Ectopic expression of NT-PGC-1α-a in C2C12 myotube cells upregulates myosin heavy chain (MHC I, MHC II a) and Glut4, which represent oxidative fibers, and promotes the expression of mitochondrial genes (Cyc1, COX5B, and ATP5B). In line with gene expression data, citrate synthase activity was significantly increased by NT-PGC-1α-a in C2C12 myotube cells. Our results indicate the regulatory role for NT-PGC-1α-a in mitochondrial biogenesis and adaptation of skeletal muscle to endurance exercise.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mouse skeletal muscle, AICAR increased canonical exon-derived NT-PGC-1α-a mRNA expression.

    In plain wordsIn mice, AICAR increased NT-PGC-1α-a gene expression in muscle.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseNT-PGC-1α-a mRNA expression
    Study

    mousen: not reported in source

    skeletal muscle
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We report here that NT-PGC-1α-a mRNA expression derived from a canonical exon 1 (exon 1a) is increased by high-intensity exercise and AMPK activator AICAR in mouse skeletal muscle but not altered by low- and medium-intensity exercise and β 2-adrenergic receptor agonist clenbuterol.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mouse skeletal muscle, AICAR strongly induced alternative exon-derived NT-PGC-1α-b expression.

    In plain wordsIn mice, AICAR increased NT-PGC-1α-b gene expression in muscle.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseNT-PGC-1α-b mRNA expression
    Study

    mousen: not reported in source

    skeletal muscle
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In contrast, the alternative exon 1b-driven NT-PGC-1α-b (PGC-1α4) and NT-PGC-1α-c are highly induced by low-, medium-, and high-intensity exercise, AICAR, and clenbuterol.
    1 context sentence
    Summary · context
    We report here that NT-PGC-1α-a mRNA expression derived from a canonical exon 1 (exon 1a) is increased by high-intensity exercise and AMPK activator AICAR in mouse skeletal muscle but not altered by low- and medium-intensity exercise and β 2-adrenergic receptor agonist clenbuterol.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mouse skeletal muscle, AICAR strongly induced alternative exon-derived NT-PGC-1α-c expression.

    In plain wordsIn mice, AICAR increased NT-PGC-1α-c gene expression in muscle.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseNT-PGC-1α-c mRNA expression
    Study

    mousen: not reported in source

    skeletal muscle
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In contrast, the alternative exon 1b-driven NT-PGC-1α-b (PGC-1α4) and NT-PGC-1α-c are highly induced by low-, medium-, and high-intensity exercise, AICAR, and clenbuterol.
    1 context sentence
    Summary · context
    We report here that NT-PGC-1α-a mRNA expression derived from a canonical exon 1 (exon 1a) is increased by high-intensity exercise and AMPK activator AICAR in mouse skeletal muscle but not altered by low- and medium-intensity exercise and β 2-adrenergic receptor agonist clenbuterol.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.