Glia · 2013
Spinal muscular atrophy astrocytes exhibit abnormal calcium regulation and reduced growth factor production.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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McGivern Jered V, Patitucci Teresa N, Nord Joshua A, Barabas Marie-Elizabeth A, Stucky Cheryl L, Ebert Allison D
Аннотация
Spinal muscular atrophy (SMA) is a genetic disorder caused by the deletion of the survival motor neuron 1 (SMN1) gene that leads to loss of motor neurons in the spinal cord. Although motor neurons are selectively lost during SMA pathology, selective replacement of SMN in motor neurons does not lead to full rescue in mouse models. Due to the ubiquitous expression of SMN, it is likely that other cell types besides motor neurons are affected by its disruption and therefore may contribute to disease pathology. Here we show that astrocytes in SMAΔ7 mouse spinal cord and from SMA-induced pluripotent stem cells exhibit morphological and cellular changes indicative of activation before overt motor neuron loss. Furthermore, our in vitro studies show mis-regulation of basal calcium and decreased response to adenosine triphosphate stimulation indicating abnormal astrocyte function. Together, for the first time, these data show early disruptions in astrocytes that may contribute to SMA disease pathology.
Предметные рубрики MeSH
Adenosine TriphosphateAge FactorsAldehyde DehydrogenaseAnalysis of VarianceAnimalsAnimals, NewbornAstrocytesCalciumCell Line, TransformedCholine O-AcetyltransferaseDisease Models, AnimalGene Expression Regulation, DevelopmentalGlial Cell Line-Derived Neurotrophic FactorGlial Fibrillary Acidic ProteinHumansMiceMice, TransgenicMuscular Atrophy, SpinalMutationNestinOxidoreductases Acting on CH-NH Group DonorsPluripotent Stem CellsReceptors, Purinergic P2Y2S100 ProteinsSpinal CordSurvival of Motor Neuron 1 ProteinSurvival of Motor Neuron 2 ProteinFormyltetrahydrofolate Dehydrogenase