A Museum of Stem Cells Points to Muse Cells as Robust Transplantable Cells for Stroke: Review
Stem cell-based therapy stands as a robust experimental treatment for ischemic stroke. Stem cells derived from fetal, embryonic, and adult tissues serve as potential sources for transplantable cells in the setting of ischemic stroke. However, the search c
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A Museum of Stem Cells Points to Muse Cells as Robust Transplantable Cells for Stroke: Review You Jeong Park, Jeffrey Farooq, Justin Cho, Blaise Cozene, Bella Gonzales-Portillo, Nadia Sadanandan, Madeline Saft, Jea Young Lee, and Cesar V. Borlongan Abstract
Stem cell-based therapy stands as a robust experimental treatment for ischemic stroke. Stem cells derived from fetal, embryonic, and adult tissues serve as potential sources for transplantable cells in the setting of ischemic stroke. However, the search continues for finding an optimal cell line for clinical use. Muse cells, a distinct subset of mesenchymal stem cells found sporadically in the connective tissue of nearly every organ, may be a suitable candidate due to its safety and accessibility. These cells have been investigated for therapeutic usage in chronic kidney disease, liver disease, acute myocardial infarction, and stroke. Muse cells display the ability to engraft and differentiate into the host neural network unlike many other cell lines which only display bystander immunomodulating effects. Taking advantage of this unique engraftment and differentiation mechanism behind Muse cells’ therapeutic effects on the central nervous system, as well as other organ systems, will Y. J. Park, J. Farooq, J. Cho, B. Cozene, B. GonzalesPortillo, N. Sadanandan, M. Saft, J. Y. Lee, and C. V. Borlongan (*) Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA e-mail: [email protected]
undoubtedly advance the cells’ utility for cell-based regenerative medicine in stroke. Keywords
Stem cells · Stroke · Transplantation · Regenerative medicine · Brain repair
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Introduction
Stroke is currently the fifth leading cause of death in the United States and can cause disabling neurological deficits including cognitive impairment, hemiparesis, sensory disturbance, and aphasia (Ovbiagele et al. 2013). Ischemic stroke comprises 87% of all stroke cases and is characterized by inadequate perfusion to vital organs like the brain, leading to oxygen and nutrient deprivation and eventually cell death (Benjamin et al. 2019; Sacco et al. 2013). The ischemic cascade following stroke is divided into three phases. The acute phase occurs within the first few hours after the ischemic event. Blood flow, ATP, and energy stores in the affected brain tissue plummet, causing ionic disruption and metabolic failure. The ensuing ionic imbalance and neurotransmitter release (glutamate excitotoxicity) promotes an excess influx of sodium and calcium into the cell. Increased intracellular calcium activates downstream phospholipases and proteases that degrade
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integral membrane components and proteins, while the surplus of sodium leads to cellular swelling (Lo et al. 2003). In addition, the production of oxygen free radicals and other reactive oxygen species during the acute phase causes further damage and cell death (Hao et al. 2014; Lakhan et al. 2009). The subacute phase occurs after the acute phase and lasts for the first f
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