Human erythropoietin-modified human amniotic mesenchymal stem cellsvia subarachnoid transplantation promote neurologic recovery from brain injury / 中国组织工程研究

ABSTRACT

BACKGROUND:Studies have shown that as a regulator of bone marrow functionerythropoietinis a glycoprotein that controls the development of the central nervous system and has neurotrophic and neuroprotective potential. Therefore, transplantation of human amniotic mesenchymal stem cels geneticaly modified by human erythropoietin is a new choice for brain injury treatment. OBJECTIVE:To observe the effect of transplantation of human amniotic mesenchymal stem cels geneticaly modified byhuman erythropoietin on the functional recovery from brain injury in rats. METHODS:Eukaryotic expression plasmid pcDNA3.1 carrying erythropoietin was successfuly constructed and transferred into amniotic mesenchymal stem cels culturedin vitro. Expression of erythropoietin was detected using western blot assay before and after transfection. Rat models of middle cerebral arterial occlusion was made and given transplantation of transfected amniotic mesenchymal stem celsviathe tail vein (transfection group). Additionaly, model and simple cel transplantation groups were set in a comparative study. RESULTS AND CONCLUSION:Findings from western blot detection showed that transfected cels could express human erythropoietin. Compared with the other groups, modified neurologic severity scores, growth-associated protein 43 and aquaporin 9 at mRNA and protein levels were al decreased significantly in the transfection group. Furthermore, the number of cels positive for CM-Dil was highest in the transfectiongroup, folowed by simple cel transplantation group, and lowest in the model group (alP<0.05). Overal findings from this study show that human erythropoietin-modified human amniotic mesenchymal stem cel transplantation promotes neurologic recoveryfrom brain injury through eliciting a reduction in growth-associated protein 43 and aquaporin 9 at mRNA and protein levels as wel as inhibiting cel apoptosis.