ArticleMolecular medicine reports2016
DNase I aggravates islet β-cell apoptosis in type 2 diabetes.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Synergistic effect of schizandrin A and DNase I knockdown on high glucose induced beta cell apoptosis by decreasing intracellular calcium concentration.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Hypoxia-induced human deoxyribonuclease I is a cellular restriction factor of hepatitis B virus.Nature microbiology · 2019Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxyribonuclease I (DNase I) is an endonuclease responsible for the destruction of chromatin during apoptosis. However, its role in diabetes remains unclear. The aim of the current study was to investigate the role of DNase I combined with high glucose levels in β‑cell apoptosis. Human samples were collected and the DNase I activity was examined. High glucose‑cultured INS‑1 cells were transfected with DNase I small interfering RNA (siRNA) and the cell apoptosis was examined by western blotting and flow cytometry. Cell viability was analyzed by the Cell Counting Kit‑8 assay. Cell apoptosis resulting from 50 mU/µl DNase I was also observed by flow cytometry, terminal deoxynucleotidyl transferase dUTP nick‑end labeling stain and western blotting. Compared with healthy controls, the serum DNase I activity of patients with diabetes was significantly increased (P<0.05). In addition, DNase I expression was observed to be significantly increased in human pancreatic tissues. The addition of high glucose upregulated the cell apoptotic rate, whereas DNase I knockdown significantly reduced apoptosis in cells treated with high glucose. In addition, the western blotting results indicated that caspase‑3 was increased subsequent to treatment of cells with 30 mM high glucose, however, this increase can be reversed by transfection with DNase I siRNA (P<0.05). Compared with cells cultured in normal conditions and high glucose, 50 mU/µl DNase I was able to significantly increase the cell apoptotic rate and level of caspase-3. DNase I activity was observed to be increased in type 2 diabetes, and high glucose combined with increased DNase I is suggested to aggravate β-cell apoptosis.
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