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Study · In vitro (cells) · 2022

4 results

Parathyroid Hormone-Related Peptide and Its Analog, Abaloparatide, Attenuate Lethal Myocardial Ischemia-Reperfusion Injury.

Wider J, Undyala VVR, Lanske B, Datta NS, Przyklenk K

Journal of clinical medicine19 Apr 2022Cited by 1 (Europe PMC)

PMID35566399 (opens in a new tab)PMCIDPMC9105604 (opens in a new tab)DOI10.3390/jcm11092273 (opens in a new tab)PepBankPUB-35566399
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Summary

Parathyroid hormone-related peptide (PTHrP) is well-known to play a role in bone formation, and abaloparatide, an analog of PTHrP(1-34), is approved for the treatment of osteoporosis in post-menopausal women. PTHrP has also been reported to have cardiovascular effects, with recent data demonstrating that exogenously administered PTHrP can limit the death of isolated cardiomyocytes subjected to oxidative stress via upregulation of classic ‘survival kinase’ signaling. Our aim in the current study was to extend this concept and, employing both in vitro and in vivo models, establish whether PTHrP(1-36) and abaloparatide are cardioprotective in the setting of lethal myocardial ischemia-reperfusion injury. We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059. Moreover, using the translationally relevant swine model of acute coronary artery occlusion-reperfusion, we make the novel observation that myocardial infarct size was significantly reduced in pigs pretreated with PTHrP(1-36) when compared with placebo-controls (13.1 ± 3.3% versus 42.0 ± 6.6% of the area of at-risk myocardium, respectively; p < 0.01). Taken together, these data provide the first evidence in support of the concept that pretreatment with PTHrP(1-36) and abaloparatide renders cardiomyocytes resistant to lethal myocardial ischemia-reperfusion injury.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In HL-1 cardiomyocytes under simulated ischemia-reperfusion, preischemic abaloparatide attenuated cell death.

    In plain wordsIn cells under simulated ischemia-reperfusion, abaloparatide pretreatment reduced cell death.

    Peptide
    Abaloparatide (Tymlos)
    Outcome
    DecreaseCardiomyocyte death
    Study

    n: not reported in source

    HL-1 cardiomyocytes under simulated ischemia-reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059.
  2. 02LabIn vitro (cells)Mechanism

    In HL-1 cardiomyocytes under simulated ischemia-reperfusion, abaloparatide pretreatment augmented phospho-ERK expression.

    In plain wordsIn cells under simulated ischemia-reperfusion, abaloparatide pretreatment increased phospho-ERK expression.

    Peptide
    Abaloparatide (Tymlos)
    Outcome
    IncreasePhospho-ERK expression
    Study

    n: not reported in source

    HL-1 cardiomyocytes under simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059.
  3. 03LabIn vitro (cells)Mechanism

    In HL-1 cardiomyocytes under simulated ischemia-reperfusion, abaloparatide pretreatment improved phospho-Akt preservation.

    In plain wordsIn cells under simulated ischemia-reperfusion, abaloparatide pretreatment improved phospho-Akt preservation.

    Peptide
    Abaloparatide (Tymlos)
    Outcome
    IncreasePhospho-Akt preservation
    Study

    n: not reported in source

    HL-1 cardiomyocytes under simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059.

Studies that did not test the peptide alone1

In this study, Abaloparatide (Tymlos) 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 Abaloparatide (Tymlos).

  1. 04LabNot a test of Abaloparatide (Tymlos) aloneIn vitro (cells)Mechanism

    In HL-1 cardiomyocytes, PD98059 blocked the protective effect of preischemic abaloparatide against simulated ischemia-reperfusion.

    In plain wordsIn cells, PD98059 blocked abaloparatide's protective effect against simulated ischemia-reperfusion.

    Peptide
    Abaloparatide (Tymlos)
    Outcome
    Not applicableMEK-ERK inhibitor blockade
    Study

    n: not reported in source

    HL-1 cardiomyocytes under simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    We report that preischemic administration of PTHrP(1-36) and abaloparatide attenuated cell death in HL-1 cardiomyocytes subjected to simulated ischemia-reperfusion, an effect that was accompanied by the augmented expression of phospho-ERK and improved preservation of phospho-Akt, and blocked by co-administration of the MEK-ERK inhibitor PD98059.

    In this study, Abaloparatide (Tymlos) 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 Abaloparatide (Tymlos).

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

    22 Oct 2026, 02:25 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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