Abstract
Olfactory mucosa mesenchymal stem cells (OM-MSCs) have exhibited their effectiveness in central nervous system diseases and provided an appealing candidate for the treatment of ischemic stroke. Previous evidence have shown that Golgi apparatus (GA) secretory pathway Ca2+-ATPase isoform1 (SPCA1) was a potential therapeutic target for ischemic stroke. In this study, we explored the neuroprotective mechanism of OM-MSCs and its effect on the expression and function of SPCA1 during cerebral ischemia/reperfusion. Based on in vitro and in vivo experiments, we discovered that OM-MSCs attenuated apoptosis and oxidative stress in ischemic stroke models, reduced the cerebral infarction volume, and improved the neurologic deficits of rats. OM-MSCs also upregulated SPCA1 expression and alleviated Ca2+ overload and decreased the edema and dissolution of the GA in neurons. Moreover, we discovered that SPCA1 depletion in oxygen and glucose deprivation/reoxygenation (OGD/R)-treated N2a cells mitigated the protective effects of OM-MSCs. Altogether, OM-MSCs exerted neuroprotective effects in ischemic stroke probably via modulating SPCA1 and reducing the edema and dissolution of the GA in neurons.
Highlights
Stroke is a leading cause of death and disability worldwide, in which ischemic stroke accounts for approximately 71% of all stroke types
We explored the neuroprotective mechanism of OM-mesenchymal stem cells (MSCs) during cerebral ischemia/reperfusion and its effect on the expression as well as function of secretory pathway Ca2+ATPase isoform1 (SPCA1) and further investigated the role of SPCA1 knockdown in the neuroprotective effect of Olfactory mucosa mesenchymal stem cells (OM-MSCs) on cerebral ischemia/reperfusion injury (IRI)
The immunophenotype of OM-MSCs identified by flow cytometry exhibited positive expression of MSC markers (CD44, CD73, CD90, CD105, CD133, and CD146) and negative expression of hematopoietic stem cell (HSC) markers (CD34 and CD45; Figure 1B)
Summary
Stroke is a leading cause of death and disability worldwide, in which ischemic stroke accounts for approximately 71% of all stroke types. In 2017, the global incidence of ischemic stroke events was about 7.7 million, with 2.7 million deaths (GBD 2017 Disease and Injury Incidence and Prevalence Collaborators, 2018; Campbell et al, 2019). The available therapy options regarding ischemic stroke have limited effects (Huang et al, 2018). Current treatments for acute ischemic stroke are based on reperfusion through thrombolysis or endovascular therapy, but both therapies are limited by the therapeutic time window: thrombolysis by the recombinant tissue plasminogen activator (rtPA) is required within 4.5 h of onset; endovascular therapy, 6 h. Many researchers are actively looking for other effective treatments for ischemic stroke, such as cell therapy
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