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Long intergenic noncoding RNA p21 suppresses the apoptosis of hippocampus neurons in streptozotocin-diabetic mice by sponging microRNA-221 through upregulation of FOS |
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| Authors: | Qin Sun Qing-Cui Zeng Yan-Qiu Chen Min Zhang Ling-Ling Wei Ping Chen |
| Affiliation: | 1. Department of Geriatrics, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China Qin Sun, Qing-Cui Zeng, and Yan-Qiu Chen contributed equally to the study.;2. Department of Geriatrics, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China;3. Department of Neurology, People's Hospital of Chongqing Yubei District, Chongqing, China Qin Sun, Qing-Cui Zeng, and Yan-Qiu Chen contributed equally to the study.;4. Center of Diabetes Mellitus, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China School of Medicine, University of Electronic Science and Technology of China, Chengdu, China |
| Abstract: | Diabetes is associated with neurological complications, and accumulated evidence shows that biological pathways in diabetes are targeted by noncoding RNA transcripts. In this study, the role of long intergenic noncoding RNA (lincRNA) p21/microRNA-221 (miR-221)/fructooligosaccharide (FOS) axis was investigated in the mice with diabetes treatment. The streptozotocin-induced diabetic mouse model was established. The learning ability and the pathological changes in mice were analyzed. After that, the interaction among miR-221, lincRNA p21, and FOS was explored and verified. The subcellular location of lincRNA p21 was identified. Finally, the cell cycle and apoptosis of the hippocampus neurons were measured. In the diabetic mice, the levels of blood glucose were higher and the leaning abilities were inhibited. miR-221 was highly expressed in the diabetic mice whereas lincRNA p21 and FOS were poorly expressed. miR-221 could bind with both lincRNA p21 and FOS. miR-221 silencing or lincRNA p21 overexpression in the diabetes mice reduced the cell apoptosis rate, and the expression of Bax and cleaved Caspase-3, whereas increase the Bcl-2 expression. Overexpression of lincRNA p21 promotes FOS expression by binding to miR-221, thereby, inhibiting hippocampal neuron apoptosis in diabetic mice. This may offer potential targets for diabetes. |
| Keywords: | diabetes FOS gene hippocampal neuron long intergenic noncoding RNA p21 microRNA-221 |