Development and Molecular Characterization of Human Placental Mesenchymal Stem Cells from Human Aborted Fetal Tissue as a Model to Study Mechanism of Spontaneous Abortion

Abstract

Mesenchymal stem cells (MSCs) have become an important component in stem cell therapies and can be isolated from various adult tissues. The human placenta is a fetomaternal organ having a high population of multipotent stem cells with better plasticity and differential potential. It is interesting to see the molecular phenotypes of these stem cells in placenta obtained from aborted fetus to understand the mechanism of spontaneous abortion. In the present study, we have proposed to isolate multipotent stem cells from human aborted placental tissue and characterized them by using molecular and morphological analysis. Our study has shown that the placenta derived Mesenchymal stem cells (hPMSCs) have elongated epithelioid like morphology and showed high pluripotency potential by expressing Oct4, Nanog and Sox2 along with expression of Mesenchymal, hematopoietic, cytokine and chemokine markers. We have further shown that hPMSCs cells have the capacity for spontaneous differentiation into cardiomyocytes and osteocytes which have confirmed the expression of specific cardiac and osteogenic markers. Interestingly, this study has clearly shown that there is an abnormal expression of CD 73, CD 100, CD 45, Ki67 and Vimentin in aborted fetal tissue thus indicates some role of these genes in the maintenance of pregnancies. Thus, this study concludes that hPMSCs cells can be used as an in vitro model system for the evaluation of the mechanism of spontaneous abortion. Similarly, due to their multipotent characteristic they can be used for future regenerative therapies for various disorders.

Spontaneous Unexplained Preterm Labor with Intact Membrane: Finding Protein Biomarkers through Placenta Proteome

“…Vimentin was presumed to play a vital role in anchoring and positioning organelles in the cytosol, maintenance of cell integrity, and stabilization of cytoskeletal interactions [22,23]. Downregulation of vimentin was observed in the obese placenta as well as in human-aborted placenta tissues [24,25]. A deficiency of this protein could result in the dramatic reorganization of vimentin filaments in the cytoplasm, leading to morphological changes and cellular fragmentation and ultimately destabilizes the overall cytoplasm architecture which might lead to PTL [23].…”