IGF-1 expression in infarcted myocardium and MGF E peptide actions in rat cardiomyocytes in vitro.

Stavropoulou A, Halapas A, Sourla A, Philippou A, Papageorgiou E, Papalois A, Koutsilieris M

Molecular medicine (Cambridge, Mass.)6 Mar 2009Cited by 56 (Europe PMC)

PMID19295919PMCIDPMC2656994DOI10.2119/molmed.2009.00012PepBankPUB-19295919

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

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

Natural levels measured1

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.

01AnimalEndogenous levelAnimal study (in vivo)Other
In rats with myocardial infarction, MGF expression rose at the transcript and protein level in infarcted myocardium at 4 and 8 weeks.
In plain wordsIn rats with a heart attack, the body's own MGF rose in the damaged heart muscle at 4 and 8 weeks.
Peptide
MGF / PEG-MGF
Outcome
IncreaseMGF expression in infarcted myocardium (late phase)
Study
ratn: not reported in source
Rat myocardial infarction (left anterior descending coronary artery ligation)
Outcome group
Growth hormone and IGF-1 · Cardiovascular
Source sentences
Summary
IGF-1Ea and MGF expression were significantly increased, both at transcriptional and translational levels, during the late postinfarction period (4 and 8 wks) in infarcted rat myocardium.
1 context sentence(design, population, supporting numbers)
Summary · context
We investigated the expression pattern of IGF-1 gene transcripts in rat myocardium from 1 h up to 8 wks after myocardial infarction induced by left anterior descending coronary artery ligation.
This result measures the body's own MGF / PEG-MGF. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-1929591901

Studies that did not test the peptide alone3

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.

02LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In rat H9C2 myocardial-like cells, an anti-IGF-1R neutralizing antibody did not block the action of synthetic MGF E peptide, but it completely blocked IGF-1 action on proliferation.
In plain wordsIn rat heart-like cells, blocking the IGF-1 receptor did not stop the effect of the MGF E peptide. It did stop the effect of IGF-1.
Peptide
MGF / PEG-MGF
Outcome
Not applicableEffect of anti-IGF-1R antibody on synthetic MGF E peptide action
Study
ratn: not reported in source
H9C2 myocardial-like cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Furthermore, specific anti-IGF-1R neutralizing antibody failed to block the synthetic MGF E peptide action, whereas it completely blocked IGF-1 action on the proliferation of H9C2 cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial-like cells in vitro.
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.
Report a problemFND-1929591902
03LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In rat H9C2 myocardial-like cells, synthetic MGF E peptide did not activate Akt phosphorylation.
In plain wordsIn rat heart-like cells, the MGF E peptide did not switch on the Akt signal.
Peptide
MGF / PEG-MGF
Outcome
No significant changeAkt phosphorylation by synthetic MGF E peptide
Study
ratn: not reported in source
H9C2 myocardial-like cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Moreover, this synthetic MGF E peptide did not activate Akt phosphorylation, whereas it activated ERK1/2 in H9C2 rat myocardial cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial-like cells in vitro.
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.
Report a problemFND-1929591903
04LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism
In rat H9C2 myocardial-like cells, synthetic MGF E peptide activated ERK1/2.
In plain wordsIn rat heart-like cells, the MGF E peptide switched on the ERK1/2 signal.
Peptide
MGF / PEG-MGF
Outcome
IncreaseERK1/2 activation by synthetic MGF E peptide
Study
ratn: not reported in source
H9C2 myocardial-like cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Moreover, this synthetic MGF E peptide did not activate Akt phosphorylation, whereas it activated ERK1/2 in H9C2 rat myocardial cells.
1 context sentence(design, population, supporting numbers)
Summary · context
In addition, we characterized IGF-1 and MGF E peptide action and their respective signaling in H9C2 myocardial-like cells in vitro.
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.
Report a problemFND-1929591904

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.

Publication types

MeSH terms

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