Opioid receptors and opioid peptides in the cardiomyogenesis of mouse embryonic stem cells.
Romana ŠínováJana KudováKristina NešporováSergej KarelRomana ŠulákováVladimír VelebnýLukáš KubalaPublished in: Journal of cellular physiology (2018)
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.
Keyphrases
- chronic pain
- pain management
- stem cells
- gene expression
- induced apoptosis
- cell cycle arrest
- poor prognosis
- dna methylation
- heart failure
- cell therapy
- endoplasmic reticulum stress
- mesenchymal stem cells
- cell proliferation
- machine learning
- amino acid
- single cell
- cell death
- bone marrow
- climate change
- deep learning
- long non coding rna
- wound healing