Opioid receptors and opioid peptides in the cardiomyogenesis of mouse embryonic stem cells
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30536562
DOI
10.1002/jcp.27992
Knihovny.cz E-resources
- Keywords
- dynorphins, enkephalins, heart regeneration, mouse embryonic stem cells, opioid receptors,
- MeSH
- Cell Differentiation physiology MeSH
- Myocytes, Cardiac cytology physiology MeSH
- Myocardium cytology MeSH
- Mouse Embryonic Stem Cells cytology metabolism MeSH
- Mice MeSH
- Opioid Peptides metabolism MeSH
- Receptors, Opioid metabolism MeSH
- Regeneration physiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Opioid Peptides MeSH
- Receptors, Opioid MeSH
The stimulation of myocardium repair is restricted due to the limited understanding of heart regeneration. Interestingly, endogenous opioid peptides such as dynorphins and enkephalins are suggested to support this process. However, the mechanism-whether through the stimulation of the regenerative capacity of cardiac stem cells or through effects on other cell types in the heart-is still not completely understood. Thus, a model of the spontaneous cardiomyogenic differentiation of mouse embryonic stem (mES) cells via the formation of embryoid bodies was used to describe changes in the expression and localization of opioid receptors within cells during the differentiation process and the potential of the selected opioid peptides, dynorphin A and B, and methionin-enkephalins and leucin-enkephalins, to modulate cardiomyogenic differentiation in vitro. The expressions of both κ- and δ-opioid receptors significantly increased during mES cell differentiation. Moreover, their primary colocalization with the nucleus was followed by their growing presence on the cytoplasmic membrane with increasing mES cell differentiation status. Interestingly, dynorphin B enhanced the downregulation gene expression of Oct4 characteristic of the pluripotent phenotype. Further, dynorphin B also increased cardiomyocyte-specific Nkx2.5 gene expression. However, neither dynorphin A nor methionin-enkephalins and leucin-enkephalins exhibited any significant effects on the course of mES cell differentiation. In conclusion, despite the increased expression of opioid receptors and some enhancement of mES cell differentiation by dynorphin B, the overall data do not support the notion that opioid peptides have a significant potential to promote the spontaneous cardiomyogenesis of mES cells in vitro.
Contipro a s Dolni Dobrouc Czech Republic
Institute of Experimental Biology Faculty of Science Masaryk University Brno Czech Republic
International Clinical Research Center St Anne' University Hospital Brno Czech Republic
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