Abstract
Human umbilical cord mesenchymal stem cells (hUC-MSCs) are a pivotal source of therapeutically active cells for regenerative medicine due to their multipotent differentiation potential, immunomodulatory and anti-inflammatory proprieties, as well as logistical collection advantages without ethical concerns. However, it remains poorly understood whether MSCs from different compartments of the human umbilical cord are therapeutically superior than others. In this study, MSCs were isolated from Wharton’s jelly (WJ-MSCs), perivascular region (PV-MSCs) and cord lining (CL-MSCs) of hUC. These cells expressed the mesenchymal markers (CD90, CD73), stemness marker (OCT4), endothelial cell adhesion molecular marker (CD146), and the monocyte/macrophage marker (CD14) found within the MSC population implicated as a key regulator of inflammatory responses to hypoxia, was displayed by WJ-, PV-, and CL-MSCs respectively. A direct consequence of oxygen and glucose deprivation during stroke and reperfusion is impaired mitochondrial function that contributes to cellular death. Emerging findings of mitochondria transfer provide the basis for the replenishment of healthy mitochondria as a strategy for the treatment of stroke. Cell Energy Phenotype and Mito Stress tests were performed the energy metabolic profile of the three MSC populations and their mitochondrial function in both ambient and OGD cell culture conditions. PV-MSCs showed the highest mitochondrial activity. CL-MSCs were the least affected by OGD/R condition, suggesting their robust survival in ischemic environment. In this study, MSC populations in UC possess comparable metabolic capacities and good survival under normal and hypoxic conditions suggesting their potential as transplantable cells for mitochondrial-based stem cell therapy in stroke and other ischemic diseases.
Highlights
Stroke is the second leading cause of death and disability worldwide behind heart diseases [1]
A cell viability test showed that all three hUCMSCs cellular populations showed good survival and maintained their proliferation following oxygen and glucose deprivation (OGD)/R, further suggesting their ability to survive in ischemic/reperfused conditions (Fig. 5, perivascular region (PV)-mesenchymal stem cells (MSCs) p = 0.0005; Wharton’s jelly (WJ)-MSC p = 0.0198). These results demonstrate the adaptive capacity of PV, WJ- and cord lining (CL)-MSCs under OGD/R conditions
Emerging evidence of mitochondria transfer from stem cells to ischemic cells paved the way for mitochondrial-based stem cell therapy of stroke [6, 7, 10]. Human umbilical cord (hUC) received only three blood vessels suggesting that hUC-MSCs are normally adapted to survive in a relatively hypoxic and glucose-poor environment, these cells represent an attractive source for stem cell-based therapy in ischemic pathologies, such as stroke [13]
Summary
Stroke is the second leading cause of death and disability worldwide behind heart diseases [1]. A novel therapeutic mechanism of stem cells has been demonstrated to involve the transfer of healthy mitochondria into damaged cells [6]. Mitochondria can be released through tunneling nanotubes (TNTs), microvesicles, gap junctions, cell fusion and direct uptake of isolated mitochondria [7]. In the last few years, mitochondrial transfer has been shown to occur between several cell types, including mesenchymal stem cells (MSCs), astrocytes and neurons, and endothelial progenitor cells [9, 10]. Taken together, these observations suggest that the transfer of healthy mitochondria into damaged cells may be a novel therapeutic strategy for stroke
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