Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes.

Sundgren NC, Giraud GD, Schultz JM, Lasarev MR, Stork PJ, Thornburg KL

American journal of physiology. Regulatory, integrative and comparative physiology28 Aug 2003Cited by 102 (Europe PMC)

PMID12947030DOI10.1152/ajpregu.00232.2003PepBankPUB-12947030

Publisher page PubMedAsk about this study

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 study6

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

01AnimalAnimal study (in vivo)Efficacy outcome
In fetal sheep, in vivo administration of LR3 IGF-1 did not stimulate cardiomyocyte hypertrophy.
In plain wordsIn fetal sheep, LR3 IGF-1 did not make heart muscle cells larger.
Peptide
IGF-1 LR3
Outcome
No significant changeCardiomyocyte hypertrophy in vivo
Study
sheepn: not reported in source
Fetal sheep, in vivo
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
In vivo administration of Long R3 IGF-1 (LR3 IGF-1) did not stimulate cardiomyocyte hypertrophy but led to a decreased percentage of cells that were binucleated in vivo.
Report a problemFND-1294703001
02AnimalAnimal study (in vivo)Efficacy outcome
In fetal sheep, in vivo administration of LR3 IGF-1 decreased the percentage of cardiomyocytes that were binucleated.
In plain wordsIn fetal sheep, LR3 IGF-1 lowered the share of heart muscle cells with two nuclei.
Peptide
IGF-1 LR3
Outcome
DecreaseBinucleated cardiomyocytes in vivo
Study
sheepn: not reported in source
Fetal sheep, in vivo
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
In vivo administration of Long R3 IGF-1 (LR3 IGF-1) did not stimulate cardiomyocyte hypertrophy but led to a decreased percentage of cells that were binucleated in vivo.
Report a problemFND-1294703002
03LabIn vitro (cells)Activity measurement
In cultured fetal sheep cardiomyocytes, LR3 IGF-1 increased BrdU uptake three- to five-fold.
In plain wordsIn lab tests on sheep heart cells, LR3 IGF-1 raised cell division markers three- to five-fold.
Peptide
IGF-1 LR3
Outcome
IncreaseCardiomyocyte BrdU uptake in culture
Study
sheepn: not reported in source
Cultured fetal sheep cardiomyocytes
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Measurements
BrdU uptake increase
3 to 5-fold
cultured myocytes
Source sentences
Summary
In culture, LR3 IGF-1 increased myocyte bromodeoxyuridine (BrdU) uptake by three- to five-fold.
Report a problemFND-1294703003
04LabIn vitro (cells)Activity measurement
In cultured fetal sheep cardiomyocytes, LR3 IGF-1 did not increase footprint area.
In plain wordsIn lab tests on sheep heart cells, LR3 IGF-1 did not make the cells larger.
Peptide
IGF-1 LR3
Outcome
No significant changeCardiomyocyte footprint area in culture
Study
sheepn: not reported in source
Cultured fetal sheep cardiomyocytes
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
LR3 IGF-1 did not increase footprint area
Report a problemFND-1294703006

Studies that did not test the peptide alone2

In this study, IGF-1 LR3 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 IGF-1 LR3.

05LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism
In cultured fetal sheep cardiomyocytes, ERK blockade with UO-126 completely abolished the BrdU uptake that LR3 IGF-1 stimulated.
In plain wordsIn lab tests on sheep heart cells, blocking ERK stopped the cell division that LR3 IGF-1 had triggered.
Peptide
IGF-1 LR3
Outcome
DecreaseERK blockade of LR3 IGF-1 stimulated BrdU uptake
Study
sheepn: not reported in source
Cultured fetal sheep cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
The blockade of either ERK or PI3K signaling (by UO-126 or LY-294002, respectively) completely abolished BrdU uptake stimulated by LR3 IGF-1.
In this study, IGF-1 LR3 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 IGF-1 LR3.
Report a problemFND-1294703004
06LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism
In cultured fetal sheep cardiomyocytes, PI3K blockade with LY-294002 completely abolished the BrdU uptake that LR3 IGF-1 stimulated.
In plain wordsIn lab tests on sheep heart cells, blocking PI3K stopped the cell division that LR3 IGF-1 had triggered.
Peptide
IGF-1 LR3
Outcome
DecreasePI3K blockade of LR3 IGF-1 stimulated BrdU uptake
Study
sheepn: not reported in source
Cultured fetal sheep cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
The blockade of either ERK or PI3K signaling (by UO-126 or LY-294002, respectively) completely abolished BrdU uptake stimulated by LR3 IGF-1.
In this study, IGF-1 LR3 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 IGF-1 LR3.
Report a problemFND-1294703005

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

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