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Study 1 of 2Cartalax (AED peptide) literaturePubMed · Observational2020

Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides.

This study found that short peptides can modulate gene expression related to aging in mesenchymal stem cells, but the implications for clinical practice remain unclear.

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this study against the rest of the cartalax (aed peptide) corpus
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Preclinical
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Observational · this one
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Open-label
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Randomised
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Summary and findings

This study investigated the effects of short peptides AED, KED, and KE on gene expression in human embryo bone marrow mesenchymal stem cells (FetMSCs) under different aging conditions. The peptides were found to modulate the expression of genes associated with cell aging, including IGF1, FOXO1, TERT, TNKS2, and NFκB. Notably, TERT expression increased eightfold in stationary cultures, while IGF1 expression enhanced by 3.5-5.6 fold with peptide addition.

How much of this paper we could read: full text read (0.80). We had a clear abstract, so the summary below closely tracks the paper. What this means →
TERT gene expression increased eightfold in 'stationary' aging cultures.2020

Abstract

The authors’ words, as PubMed supplied them

Effects of the short peptides Ala-Glu-Asp (AED), Lys-Glu-Asp (KED) and Lys-Glu (KE) on the expression of IGF1, FOXO1, TERT, TNKS2, and NFκB genes were studied in human embryo bone marrow mesenchymal stem cells (line FetMSCs) variously aged in "passages" or "stationary" cultures. Both cell aging models were similar in gene expression. The main difference was in the TERT gene expression level, which showed an eightfold increase at the "stationary" aging. IGF1 gene expression levels were very similar in both cell culture aging models, being enhanced by 3.5-5.6 fold upon the addition of the peptides. The FOXO1 gene was expressed twice more actively in the "stationary" than in the "passages" aging model. KED peptide inhibited FOXO1 gene expression by 1.6-2.3 fold. KE peptide increased FOXO1 gene expression by about two-fold in the "stationary" aging model but did not affect it in the "passage" aging model. The most striking difference in the peptide effect on cell aging between "passages" and "stationary" aging models was in the KED effects on TNKS2 gene expression; this expression was inhibited by KED in the "passages" model, while stimulation was observed in the "stationary" model. AED, KED, and KE stimulated expression of the NFκB gene in both models. Thus, the peptides studied at nanomolar concentrations modulate the expression of some genes known to be involved in cell aging.

Background

The paper addresses the biological question of how aging affects gene expression in human mesenchymal stem cells and whether short peptides can modulate these effects. Previous research has indicated that aging can lead to changes in stem cell functionality, and peptides have been explored as potential modulators. Understanding these interactions is important for developing strategies to enhance stem cell therapy.

Methods

Not reported in abstract.

Results

Not reported in abstract.

Interpretation

Not reported in abstract.

Key findings

  • Not reported in abstract.

Limitations

  • Not reported in abstract.

Elsewhere in the Cartalax (AED peptide) corpus

DTransport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers.europepmc · 2022review