Human umbilical cord blood cell (HUCBC) transplants are used to treat patients with stroke as it has restorative effect on the brain function but how the cells help in the treatment was unknown.
A research team from the University of Florida has found that the HUCBCs secretion activates Akt signaling pathway which prevents neuron loss and impacts a specific gene responsible for reduced inflammation in stroke induced animal models. The reduced inflammation helps in the survival of the stroke affected neural cells. Stroke is a serious medical condition that occurs when the blood supply to the brain is cut off. As a result, the brain cells die due to lack of oxygen and nutrients within few minutes. The umbilical cord stem cells prevent the loss of neural cells and restore the activities of the brain.
During the study, four groups of laboratory rats were modeled with stroke by oxygen or glucose deprivation. They were treated with and without HUCBCs to understand the effects of stem cell transplant in the treatment of stroke. The HUCBC treated group confirmed the activation of Akt pathway and found to have 44-68% of reduction in neuron loss compared to other groups. Dr. Allison E. Willing, the lead author of the study said, “Our observations show that HUCB (Human Umbilical Cord Blood) neuroprotection is dependent on the activation of Akt signaling pathway that increases the transcription of the Peroxiredoxin-5 gene (Prdx5).”
The Akt signaling pathway is involved in cell signaling that leads to cell survival or blocking of cell death (apoptosis). When compared to other pathways involved in cell survival, Akt pathway is more important as it activates Prdx5 gene, an antioxidant enzyme gene that reduces inflammation. It also plays a key role in regulating the transportation of some molecules in apoptosis. Generally, patients with severe stroke exhibits lower Prdx5 and higher inflammation rate. This shows that the gene is either degraded or the enzyme production is impaired in severe stroke. Thus, Prdx5 can be considered as a good candidate for therapeutic targeting in stroke and HUCBC transplant can be a good therapy option for patients suffering from stroke.
According to the research findings, HUCBC prevented neuronal loss by increasing the transcription of survival associated genes that inhibit inflammation and rescued the neuronal cells. The HUCBC activated Akt signaling pathway not only ramped up the transcription of genes but also inhibited the genes that cause damaging effect in stroke injury. This study helped the researchers to understand the effect of HUCBC in stroke affected animal models and provide hope for the treatment of stroke in humans using HUCBCs.