ArticleMolecular medicine reports2016
Shox2 influences mesenchymal stem cell fate in a co-culture model in vitro.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Conversion of Unmodified Stem Cells to Pacemaker Cells by Overexpression of Key Developmental Genes.Cells · 2023Article
- Nkx2.5: a crucial regulator of cardiac development, regeneration and diseases.Frontiers in cardiovascular medicine · 2023Review
- Transcription factor Tbx18 induces the differentiation of c-kitAmerican journal of translational research · 2018Article
- SHOX2 is a Potent Independent Biomarker to Predict Survival of WHO Grade II-III Diffuse Gliomas.EBioMedicine · 2016Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sinoatrial node (SAN) dysfunction is a common cardiovascular problem, and the development of a cell sourced biological pacemaker has been the focus of cardiac electrophysiology research. The aim of biological pacemaker therapy is to produce SAN-like cells, which exhibit spontaneous activity characteristic of the SAN. Short stature homeobox 2 (Shox2) is an early cardiac transcription factor and is crucial in the formation and differentiation of the sinoatrial node (SAN). The present study aimed to improve pacemaker function by overexpression of Shox2 in canine mesenchymal stem cells (cMSCs) to induce a phenotype similar to native pacemaker cells. To achieve this objective, the cMSCs were transfected with lentiviral pLentis‑mShox2‑red fluorescent protein, and then co‑cultured with rat neonatal cardiomyocytes (RNCMs) in vitro for 5-7 days. The feasibility of regulating the differentiation of cMSCs into pacemaker‑like cells by Shox2 overexpression was investigated. Reverse transcription-quantitative polymerase chain reaction and western blotting showed that Shox2‑transfected cMSCs expressed high levels of T box 3, hyperpolarization-activated cyclic nucleotide‑gated cation channel and Connexin 45 genes, which participate in SAN development, and low levels of working myocardium genes, Nkx2.5 and Connexin 43. In addition, Shox2‑transfected cMSCs were able to pace RNCMs with a rate faster than the control cells. In conclusion, these data indicate that overexpression of Shox2 in cMSCs can greatly enhance the pacemaker phenotype in a co-culture model in vitro.
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