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Study · Animal study (in vivo) · mouse · 2024

15 results

Mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to membrane.

Jia H, Zhou LC, Chen YF, Zhang W, Qi W, Wang P, Huang X, Guo JW, Hou WF, Zhang RR, Zhou JJ, Zhang DW

Theranostics19 Aug 2024Cited by 5 (Europe PMC)

PMID39267782 (opens in a new tab)PMCIDPMC11388074 (opens in a new tab)DOI10.7150/thno.100321 (opens in a new tab)PepBankPUB-39267782
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Summary

Rationale: An impairment of plasma membrane repair has been implicated in various diseases such as muscular dystrophy and ischemia/reperfusion injury. MOTS-c, a short peptide encoded by mitochondria, has been shown to pass through the plasma membrane into the bloodstream. This study determined whether this biological behavior was involved in membrane repair and its underlying mechanism. Methods and Results: In human participants, the level of MOTS-c was positively correlated with the abundance of mitochondria, and the membrane repair molecule TRIM72. In contrast to high-intensity eccentric exercise, moderate-intensity exercise improved sarcolemma integrity and physical performance, accompanied by an increase of mitochondria beneath the damaged sarcolemma and secretion of MOTS-c. Furthermore, moderate-intensity exercise increased the interaction between MOTS-c and TRIM72, and MOTS-c facilitated the trafficking of TRIM72 to the sarcolemma. In vitro studies demonstrated that MOTS-c attenuated membrane damage induced by hypotonic solution, which could be blocked by siRNA-TRIM72, but not AMPK inhibitor. Co-immunoprecipitation study showed that MOTS-c interacted with TRIM72 C-terminus, but not N-terminus. The dynamic membrane repair assay revealed that MOTS-c boosted the trafficking of TRIM72 to the injured membrane. However, MOTS-c itself had negligible effects on membrane repair, which was recapitulated in TRIM72-/- mice. Unexpectedly, MOTS-c still increased the fusion of vesicles with the membrane in TRIM72-/- mice, and dot blot analysis revealed an interaction between MOTS-c and phosphatidylinositol (4,5) bisphosphate [PtdIns (4,5) P2]. Finally, MOTS-c blunted ischemia/reperfusion-induced membrane disruption, and preserved heart function. Conclusions: MOTS-c/TRIM72-mediated membrane integrity improvement participates in mitochondria-triggered membrane repair. An interaction between MOTS-c and plasma lipid contributes to the fusion of vesicles with membrane. Our data provide a novel therapeutic strategy for rescuing organ function by facilitating membrane repair with MOTS-c.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study15

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In TRIM72-/- mice, MOTS‑c itself had negligible effects on membrane repair.

    In plain wordsIn mice lacking TRIM72, MOTS‑c on its own had almost no effect on membrane repair.

    Peptide
    MOTS-c
    Outcome
    No significant changeMembrane repair by MOTS-c alone in TRIM72-/- mice
    Study

    mousen: not reported in source

    TRIM72 knockout mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, MOTS-c itself had negligible effects on membrane repair, which was recapitulated in TRIM72-/- mice.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In TRIM72-/- mice, MOTS‑c still increased the fusion of vesicles with the membrane.

    In plain wordsIn mice lacking TRIM72, MOTS‑c still increased the joining of small vesicles to the cell membrane.

    Peptide
    MOTS-c
    Outcome
    IncreaseVesicle fusion with the membrane in TRIM72-/- mice
    Study

    mousen: not reported in source

    TRIM72 knockout mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Unexpectedly, MOTS-c still increased the fusion of vesicles with the membrane in TRIM72-/- mice
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    MOTS‑c blunted ischemia/reperfusion-induced membrane disruption.

    In plain wordsIn ischemia/reperfusion injury tests, MOTS‑c reduced damage to cell membranes.

    Peptide
    MOTS-c
    Outcome
    DecreaseIschemia/reperfusion-induced membrane disruption
    Study

    n: not reported in source

    Ischemia/reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Finally, MOTS-c blunted ischemia/reperfusion-induced membrane disruption
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    MOTS‑c preserved heart function after ischemia/reperfusion.

    In plain wordsIn ischemia/reperfusion injury tests, MOTS‑c preserved heart function.

    Peptide
    MOTS-c
    Outcome
    IncreaseHeart function after ischemia/reperfusion
    Study

    n: not reported in source

    Ischemia/reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Finally, MOTS-c blunted ischemia/reperfusion-induced membrane disruption, and preserved heart function.
  5. 05LabIn vitro (cells)Efficacy outcome

    In vitro, MOTS‑c attenuated membrane damage induced by hypotonic solution.

    In plain wordsIn lab tests, MOTS‑c reduced membrane damage caused by a salt-poor solution.

    Peptide
    MOTS-c
    Outcome
    DecreaseHypotonic membrane damage
    Study

    n: not reported in source

    In vitro membrane damage by hypotonic solution
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies demonstrated that MOTS-c attenuated membrane damage induced by hypotonic solution, which could be blocked by siRNA-TRIM72, but not AMPK inhibitor.
  6. 06LabIn vitro (cells)Mechanism

    In vitro, the protection by MOTS‑c against hypotonic membrane damage was blocked by siRNA-TRIM72.

    In plain wordsIn lab tests, switching off TRIM72 stopped the membrane protection by MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    Not applicableTRIM72 dependence of MOTS-c membrane protection
    Study

    n: not reported in source

    In vitro membrane damage by hypotonic solution
    Comparator
    siRNA-TRIM72
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies demonstrated that MOTS-c attenuated membrane damage induced by hypotonic solution, which could be blocked by siRNA-TRIM72, but not AMPK inhibitor.
  7. 07LabIn vitro (cells)Mechanism

    In vitro, the protection by MOTS‑c against hypotonic membrane damage was not blocked by an AMPK inhibitor.

    In plain wordsIn lab tests, blocking AMPK did not stop the membrane protection by MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    No significant changeAMPK dependence of MOTS-c membrane protection
    Study

    n: not reported in source

    In vitro membrane damage by hypotonic solution
    Comparator
    AMPK inhibitor
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies demonstrated that MOTS-c attenuated membrane damage induced by hypotonic solution, which could be blocked by siRNA-TRIM72, but not AMPK inhibitor.
  8. 08LabIn vitro (cells)Mechanism

    In a dynamic membrane repair assay, MOTS‑c boosted the trafficking of TRIM72 to the injured membrane.

    In plain wordsIn lab tests, MOTS‑c helped the TRIM72 repair protein move to damaged cell membranes.

    Peptide
    MOTS-c
    Outcome
    IncreaseTRIM72 trafficking to injured membrane
    Study

    n: not reported in source

    Dynamic membrane repair assay
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The dynamic membrane repair assay revealed that MOTS-c boosted the trafficking of TRIM72 to the injured membrane.
  9. 09LabIn vitro (cells)Efficacy outcome

    MOTS‑c itself had negligible effects on membrane repair.

    In plain wordsIn lab tests, MOTS‑c on its own had almost no effect on membrane repair.

    Peptide
    MOTS-c
    Outcome
    No significant changeMembrane repair by MOTS-c alone
    Study

    n: not reported in source

    Membrane repair assay
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, MOTS-c itself had negligible effects on membrane repair
  10. 10LabIn vitro (cell-free)Activity measurement

    Dot blot analysis revealed an interaction between MOTS‑c and phosphatidylinositol (4,5) bisphosphate.

    In plain wordsIn lab tests, MOTS‑c bound to a membrane fat molecule called PtdIns(4,5)P2.

    Peptide
    MOTS-c
    Outcome
    Not applicableInteraction of MOTS-c with PtdIns(4,5)P2
    Study

    n: not reported in source

    Dot blot analysis
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    dot blot analysis revealed an interaction between MOTS-c and phosphatidylinositol (4,5) bisphosphate [PtdIns (4,5) P2].

Natural levels measured4

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 11HumanEndogenous levelObservational studyOther

    In human participants, the level of MOTS‑c correlated positively with the abundance of mitochondria.

    In plain wordsIn people, higher levels of the body's own MOTS‑c were linked to more mitochondria.

    Peptide
    MOTS-c
    Outcome
    Not applicableCorrelation of MOTS-c level with mitochondrial abundance
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    In human participants, the level of MOTS-c was positively correlated with the abundance of mitochondria

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  2. 12HumanEndogenous levelObservational studyOther

    In human participants, the level of MOTS‑c correlated positively with the abundance of the membrane repair molecule TRIM72.

    In plain wordsIn people, higher levels of the body's own MOTS‑c were linked to more of the membrane repair protein TRIM72.

    Peptide
    MOTS-c
    Outcome
    Not applicableCorrelation of MOTS-c level with TRIM72
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    In human participants, the level of MOTS-c was positively correlated with the abundance of mitochondria, and the membrane repair molecule TRIM72.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  3. 13HumanEndogenous levelOther designMechanism

    Moderate-intensity exercise improved sarcolemma integrity and physical performance, accompanied by increased secretion of the body's own MOTS‑c.

    In plain wordsModerate exercise was accompanied by more of the body's own MOTS‑c being released, along with better muscle membrane integrity.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c secretion after moderate-intensity exercise
    Study

    n: not reported in source

    Outcome group
    Exercise and physical function · Musculoskeletal

    Source sentences

    Summary
    In contrast to high-intensity eccentric exercise, moderate-intensity exercise improved sarcolemma integrity and physical performance, accompanied by an increase of mitochondria beneath the damaged sarcolemma and secretion of MOTS-c.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  4. 14HumanEndogenous levelOther designMechanism

    Moderate-intensity exercise increased the interaction between the body's own MOTS‑c and TRIM72.

    In plain wordsModerate exercise increased the contact between the body's own MOTS‑c and the repair protein TRIM72.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c and TRIM72 interaction after moderate-intensity exercise
    Study

    n: not reported in source

    Outcome group
    Exercise and physical function · Musculoskeletal

    Source sentences

    Summary
    moderate-intensity exercise increased the interaction between MOTS-c and TRIM72, and MOTS-c facilitated the trafficking of TRIM72 to the sarcolemma.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone1

In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking MOTS-c.

  1. 15LabNot a test of MOTS-c aloneOther designActivity measurement

    Co-immunoprecipitation showed that MOTS‑c interacted with the TRIM72 C-terminus but not the N-terminus.

    In plain wordsIn lab tests, MOTS‑c bound to one end of the TRIM72 protein but not the other.

    Peptide
    MOTS-c
    Outcome
    Not applicableInteraction of MOTS-c with the TRIM72 C-terminus
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Co-immunoprecipitation study showed that MOTS-c interacted with TRIM72 C-terminus, but not N-terminus.

    In this study, MOTS-c was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking MOTS-c.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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