The E-domain region of mechano-growth factor inhibits cellular apoptosis and preserves cardiac function during myocardial infarction.

Mavrommatis E, Shioura KM, Los T, Goldspink PH

Molecular and cellular biochemistry28 May 2013Cited by 19 (Europe PMC)

PMID23712705PMCIDPMC3720995DOI10.1007/s11010-013-1689-4PepBankPUB-23712705

Summary

Insulin-like growth factor-1 (IGF-1) isoforms are expressed via alternative splicing. Expression of the minor isoform IGF-1Eb [also known as mechano-growth factor (MGF)] is responsive to cell stress. Since IGF-1 isoforms differ in their E-domain regions, we are interested in determining the biological function of the MGF E-domain. To do so, a synthetic peptide analog was used to gain mechanistic insight into the actions of the E-domain. Treatment of H9c2 cells indicated a rapid cellular uptake mechanism that did not involve IGF-1 receptor activation but resulted in a nuclear localization. Peptide treatment inhibited the intrinsic apoptotic pathway in H9c2 cells subjected to cell stress with sorbitol by preventing the collapse of the mitochondrial membrane potential and inhibition of caspase-3 activation. Therefore, we administered the peptide at the time of myocardial infarction (MI) in mice. At 2 weeks post-MI cardiac function, gene expression and cell death were assayed. A significant decline in both systolic and diastolic function was evident in untreated mice based on PV loop analysis. Delivery of the E-peptide ameliorated the decline in function and resulted in significant preservation of cardiac contractility. Associated with these changes were an inhibition of pathologic hypertrophy and significantly fewer apoptotic nuclei in the viable myocardium of E-peptide-treated mice post-MI. We conclude that administration of the MGF E-domain peptide may provide a means of modulating local tissue IGF-1 autocrine/paracrine actions to preserve cardiac function, prevent cell death, and pathologic remodeling in the heart.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone9

In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

01AnimalNot a test of MGF / PEG-MGF aloneAnimal study (in vivo)Efficacy outcome
In mice after myocardial infarction, E-peptide delivery ameliorated the decline in cardiac function seen in untreated mice.
In plain wordsIn mice after a heart attack, the MGF piece reduced the loss of heart function seen in untreated mice.
Peptide
MGF / PEG-MGF
Outcome
IncreaseCardiac function decline 2 weeks after MI
Study
mousen: not reported in source
Myocardial infarction
Comparator
Untreated mice
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
Delivery of the E-peptide ameliorated the decline in function and resulted in significant preservation of cardiac contractility.
3 context sentences(design, population, supporting numbers)
Summary · context
A significant decline in both systolic and diastolic function was evident in untreated mice based on PV loop analysis.
Summary · context
Therefore, we administered the peptide at the time of myocardial infarction (MI) in mice.
Summary · context
At 2 weeks post-MI cardiac function, gene expression and cell death were assayed.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270506
02AnimalNot a test of MGF / PEG-MGF aloneAnimal study (in vivo)Efficacy outcome
In mice after myocardial infarction, E-peptide delivery resulted in significant preservation of cardiac contractility.
In plain wordsIn mice after a heart attack, the MGF piece helped keep the heart pumping strength.
Peptide
MGF / PEG-MGF
Outcome
IncreaseCardiac contractility
Study
mousen: not reported in source
Myocardial infarction
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
Delivery of the E-peptide ameliorated the decline in function and resulted in significant preservation of cardiac contractility.
2 context sentences(design, population, supporting numbers)
Summary · context
Therefore, we administered the peptide at the time of myocardial infarction (MI) in mice.
Summary · context
At 2 weeks post-MI cardiac function, gene expression and cell death were assayed.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270507
03AnimalNot a test of MGF / PEG-MGF aloneAnimal study (in vivo)Efficacy outcome
In mice after myocardial infarction, E-peptide treatment was associated with inhibition of pathologic hypertrophy.
In plain wordsIn mice after a heart attack, the MGF piece was linked to less harmful heart enlargement.
Peptide
MGF / PEG-MGF
Outcome
DecreasePathologic hypertrophy
Study
mousen: not reported in source
Myocardial infarction
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
Associated with these changes were an inhibition of pathologic hypertrophy
2 context sentences(design, population, supporting numbers)
Summary · context
Therefore, we administered the peptide at the time of myocardial infarction (MI) in mice.
Summary · context
At 2 weeks post-MI cardiac function, gene expression and cell death were assayed.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270508
04AnimalNot a test of MGF / PEG-MGF aloneAnimal study (in vivo)Efficacy outcome
In mice after myocardial infarction, E-peptide-treated mice had significantly fewer apoptotic nuclei in the viable myocardium.
In plain wordsIn mice after a heart attack, treated mice had fewer dying cells in healthy heart tissue.
Peptide
MGF / PEG-MGF
Outcome
DecreaseApoptotic nuclei in viable myocardium
Study
mousen: not reported in source
Myocardial infarction
Outcome group
Cell viability and death · Cardiovascular
Source sentences
Summary
significantly fewer apoptotic nuclei in the viable myocardium of E-peptide-treated mice post-MI.
2 context sentences(design, population, supporting numbers)
Summary · context
Therefore, we administered the peptide at the time of myocardial infarction (MI) in mice.
Summary · context
At 2 weeks post-MI cardiac function, gene expression and cell death were assayed.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270509
05LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In H9c2 cells, an MGF E-domain peptide analog entered the cells quickly and localized to the nucleus.
In plain wordsIn cells, a piece of MGF entered heart cells quickly and moved into the nucleus.
Peptide
MGF / PEG-MGF
Outcome
Not applicableCellular uptake and nuclear localization
Study
ratn: not reported in source
H9c2 cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Treatment of H9c2 cells indicated a rapid cellular uptake mechanism that did not involve IGF-1 receptor activation but resulted in a nuclear localization.
1 context sentence(design, population, supporting numbers)
Summary · context
To do so, a synthetic peptide analog was used to gain mechanistic insight into the actions of the E-domain.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270501
06LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In H9c2 cells, uptake of an MGF E-domain peptide analog did not involve IGF-1 receptor activation.
In plain wordsIn cells, a piece of MGF entered heart cells without switching on the IGF-1 receptor.
Peptide
MGF / PEG-MGF
Outcome
No significant changeIGF-1 receptor activation
Study
ratn: not reported in source
H9c2 cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Treatment of H9c2 cells indicated a rapid cellular uptake mechanism that did not involve IGF-1 receptor activation
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270502
07LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In H9c2 cells stressed with sorbitol, an MGF E-domain peptide analog inhibited the intrinsic apoptotic pathway.
In plain wordsIn cells, a piece of MGF slowed a cell-death pathway in stressed heart cells.
Peptide
MGF / PEG-MGF
Outcome
DecreaseIntrinsic apoptotic pathway under sorbitol stress
Study
ratn: not reported in source
H9c2 cells
Outcome group
Cell viability and death · Cardiovascular
Source sentences
Summary
Peptide treatment inhibited the intrinsic apoptotic pathway in H9c2 cells subjected to cell stress with sorbitol by preventing the collapse of the mitochondrial membrane potential and inhibition of caspase-3 activation.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270503
08LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In H9c2 cells stressed with sorbitol, an MGF E-domain peptide analog prevented the collapse of the mitochondrial membrane potential.
In plain wordsIn cells, a piece of MGF kept the energy membrane of mitochondria from collapsing under stress.
Peptide
MGF / PEG-MGF
Outcome
DecreaseMitochondrial membrane potential collapse
Study
ratn: not reported in source
H9c2 cells
Outcome group
Mitochondrial function · Cardiovascular
Source sentences
Summary
Peptide treatment inhibited the intrinsic apoptotic pathway in H9c2 cells subjected to cell stress with sorbitol by preventing the collapse of the mitochondrial membrane potential and inhibition of caspase-3 activation.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270504
09LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In H9c2 cells stressed with sorbitol, an MGF E-domain peptide analog inhibited caspase-3 activation.
In plain wordsIn cells, a piece of MGF reduced a key cell-death enzyme step in stressed heart cells.
Peptide
MGF / PEG-MGF
Outcome
DecreaseCaspase-3 activation
Study
ratn: not reported in source
H9c2 cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Peptide treatment inhibited the intrinsic apoptotic pathway in H9c2 cells subjected to cell stress with sorbitol by preventing the collapse of the mitochondrial membrane potential and inhibition of caspase-3 activation.
In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.
Show in the study text Report a problemFND-2371270505

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.

Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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