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http://purl.uniprot.org/citations/28185128http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28185128http://www.w3.org/2000/01/rdf-schema#comment"This study aimed to explore the effects of transient receptor potential melastatin 7 (TRPM7)/microRNA-34a (miR-34a) gene silencing on spatial cognitive function and hippocampal neurogenesis in mice with type 1 diabetes mellitus (T1DM). BALB/c mice were chosen to establish T1DM models and divided into five groups respectively: the negative control (NC), T1DM, T1DM + si-TRPM7, T1DM + si-miR-34a, and T1DM + si-TRPM7 + si-miR-34a groups. Morris water maze (MWM) test was adopted to observe behavioral alterations in mice. In all groups, changes in weight, fasting insulin, blood glucose, and insulin-related antibodies: insulin autoantibody (IAA), islet cell antibody (ICA), and glutamic acid decarboxylase antibody (GAD-Ab) were monitored. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to test TRPM7 and miR-34a expressions. Nissl staining was performed to detect neuron numbers in hippocampal tissues. Ultrastructure of hippocampal neurons was observed by transmission electron microscopy. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to assess cell apoptosis, and Western blotting was applied to examine expressions of apoptosis-related proteins. Compared to the NC group, the mice in the T1DM group had increased expressions of TRPM7 and miR-34a; decreased weight and fasting insulin; increased blood glucose and levels of ICA, IAA, and GAD-Ab; prolonged escape latency; less time spent in the target quadrant; incomplete neuronal structure; reduced neuron numbers; increased cell apoptosis and expressions of activated Bax, Cyt-c, and cleaved caspase-3; but reduced Bcl-2 expression. In comparison to the T1DM group, the T1DM + si-TRPM7, T1DM + si-miR-34a, and T1DM + si-TRPM7 + si-miR-34a groups showed increased weight and fasting insulin; reduced blood glucose and levels of ICA, IAA, and GAD-Ab; shortened escape latency; prolonged time spent in the target quadrant platform; intact neuronal structure; increased neuron numbers; repaired neurons; reduced cell apoptosis and expressions of activated Bax, Cyt-c, and cleaved caspase-3; but increased Bcl-2 expression. The T1DM + si-TRPM7 + si-miR-34a group underwent more obvious changes than the T1DM + si-TRPM7 and T1DM + si-miR-34a groups. Our results demonstrated that TRPM7/miR-34a gene silencing could improve spatial cognitive function and protect hippocampal neurogenesis in mice with T1DM."xsd:string
http://purl.uniprot.org/citations/28185128http://purl.org/dc/terms/identifier"doi:10.1007/s12035-017-0398-5"xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/author"Zhang S.Y."xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/author"Zhang Q.J."xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/name"Mol Neurobiol"xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/pages"1568-1579"xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/title"Effects of TRPM7/miR-34a Gene Silencing on Spatial Cognitive Function and Hippocampal Neurogenesis in Mice with Type 1 Diabetes Mellitus."xsd:string
http://purl.uniprot.org/citations/28185128http://purl.uniprot.org/core/volume"55"xsd:string
http://purl.uniprot.org/citations/28185128http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28185128
http://purl.uniprot.org/citations/28185128http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28185128
http://purl.uniprot.org/uniprot/#_A2AI57-mappedCitation-28185128http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28185128
http://purl.uniprot.org/uniprot/#_B9EK83-mappedCitation-28185128http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28185128
http://purl.uniprot.org/uniprot/#_Q923J1-mappedCitation-28185128http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28185128
http://purl.uniprot.org/uniprot/Q923J1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28185128
http://purl.uniprot.org/uniprot/B9EK83http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28185128
http://purl.uniprot.org/uniprot/A2AI57http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28185128