Abstract：
AIMS:Cerebral atrophy resulting from neurodegeneration is highly prevalent in individuals with diabetes; however, the underlying mechanisms for diabetic neurodegeneration are not fully understood. Here we hypothesized that hyperglycemia induces molecular signaling that favors induction of proliferation in post mitotic, fully differentiated hippocampal neurons. MATERIALS AND METHODS:Streptozotocin (150 mg/kg) was intraperitoneally injected to four months old male mice to induce diabetes. Hippocampal tissue was subjected to molecular analysis of wingless-related integration site, extracellular signal regulated kinase, and brain derived neurotrophic factor signaling, and cell cycle regulation. KEY FINDINGS:Hyperglycemia did not alter wingless-related integration site signaling or cyclin E levels in the hippocampus. There were reductions in extracellular signal regulated kinase activation and brain derived neurotrophic factor levels along with elevated cyclin D1 levels. SIGNIFICANCE:These findings indicate that hyperglycemic conditions can stimulate cell cycle progression in the hippocampus in vivo. These new insights into the disease mechanisms could support the development of novel therapeutics aimed to provide neuroprotection in diabetic patients.
journal_name
Life Scijournal_title
Life sciencesauthors
Yang E,Gavini K,Bhakta A,Dhanasekaran M,Khan I,Parameshwaran Kdoi
10.1016/j.lfs.2018.05.019subject
Has Abstractpub_date
2018-07-15 00:00:00pages
131-135eissn
0024-3205issn
1879-0631pii
S0024-3205(18)30271-6journal_volume
205pub_type
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