ArticleMolecular and cellular biochemistry2014
Increased DNase I activity in diabetes might be associated with injury of pancreas.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- Synthesis, Biological Evaluation, and Molecular Docking of Pyridine-Containing Squaramides as DNase I Inhibitors.Molecules (Basel, Switzerland) · 2026Article
- 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
- Renoprotective Effect of the Shen-Yan-Fang-Shuai Formula by Inhibiting TNF-Journal of diabetes research · 2017Article
- DNase I aggravates islet β-cell apoptosis in type 2 diabetes.Molecular medicine reports · 2016Article
- Article
- NETs and traps delay wound healing in diabetes.Trends in endocrinology and metabolism: TEM · 2015Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNase I is an endonuclease responsible to destruction of chromatin during apoptosis. However, its role in diabetes is still unclear. With blood samples from our previous study related to type 2 diabetes, we examined the DNase I activity in the serum of these patients and the role of DNase I in the injury of pancreas was further investigated in rats and INS-1 cells. Serum and pancreatic tissues from human and rats were used for the study. Insulin resistance and diabetes were induced by high fat diet and STZ injection, respectively. DNase I activity was determined by radial enzyme-diffusion method. Expressions of DNase I and caspase-3 in pancreas were determined in rat pancreatic tissues and INS-1 cells. Apoptosis of INS-1 cells was determined by both TUNEL assay and Flow Cytometry. There was a significant elevation of DNase I activity in serum of patients with type 2 diabetes and rats with STZ injection. Moreover, increase in DNase I expression was observed in the pancreas of diabetic person and rats. Furthermore, high glucose induced both DNase I and caspase-3 expression and at the same time increased apoptosis rate of INS-1 cells. In conclusion, elevated DNase I in diabetes may be related to pancreatic injury and could be one of the causes that induce diabetes.
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