Adriamycin nephrotoxicity is reduced by metallothionein over-expression and kidney gene expression is modified by diabetes in the OVE26 diabetic model.

Yang, Lu

doi:10.18297/etd/1618

Cited by 2 publications

(3 citation statements)

References 80 publications

(103 reference statements)

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“…For female mice, plasma insulin levels in OVE26 mice significantly reduced after 4 weeks old. Still a low level of insulin exists in OVE26 mice, the results are similar to previous reports …”

Section: Resultssupporting

confidence: 92%

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Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time

Jiang

Tang

Wang

et al. 2019

J Cellular Molecular Medi

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To detect the changes in the liver function in both male and female OVE26 mice from young to adults for better understanding of type 1 diabetes‐induced hepatic changes, OVE26 mice and wild‐type FVB mice were raised in the same environment without any intervention, and then killed at 4, 12, 24 and 36 weeks for examining liver's general properties, including pathogenic and molecular changes. The influence of diabetes on the bodyweight of male and female mice was different. Both male and female OVE26 mice did not obtain serious liver injury or non‐alcoholic fatty liver disease, manifested by mild elevation of plasma alanine transaminase, and less liver lipid content along with significantly suppressed lipid synthesis. Uncontrolled diabetes also did not cause hepatic glycogen accumulation in OVE26 mice after 4 weeks. Oxidative stress test showed no change in lipid peroxidation, but increased protein oxidation. Changed endoplasmic reticulum stress and apoptosis along with increased antioxidant capacity was observed in OVE26 mice. In conclusion, uncontrolled type 1 diabetes did not cause hepatic lipid deposition most likely because of reduced lipids synthesis in response to insulin deficiency. Enhanced antioxidant capacity might not only prevent the occurrence of severe acute liver injury but also the self‐renewal, leading to liver dysfunction.

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Section: Resultssupporting

confidence: 92%

“…Still a low level of insulin exists in OVE26 mice, the results are similar to previous reports. 5,6,19…”

Section: Type 1 Diabetes Did Not Induce Lipids Deposition In Ove26 Mi...mentioning

confidence: 99%

Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time

Jiang

Tang

Wang

et al. 2019

J Cellular Molecular Medi

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“…Diabetic nephropathy (DN) is the changes in chronic kidney structure and dysfunction caused by diabetes, which has become the leading cause of chronic kidney disease and end-stage renal disease [ 1 ]. According to statistics from the International Diabetes Federation (IDF), the number of diabetes patients worldwide in 2015 was 415 million, and it is expected to increase to 552 million in 2035 [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Renal Tissue-Derived Exosomal miRNA-34a in Diabetic Nephropathy Induces Renal Tubular Cell Fibrosis by Promoting the Polarization of M1 Macrophages

Zheng,

Zeng,

Chu

et al. 2024

IET Nanobiotechnology

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Background. Diabetic nephropathy (DN) is the leading cause of chronic kidney disease, and the activation and infiltration of phagocytes are critical steps of DN. This study aimed to explore the mechanism of exosomes in macrophages and diabetes nephropathy and the role of miRNA-34a, which might provide a new path for treating DN. Materials and Methods. The DN model was established, and the success of the model establishment was confirmed by detecting general indicators, HE staining, and immunohistochemistry. Electron microscopy and NanoSight Tracking Analysis (NTA) were used to see the morphology and size of exosomes. MiRNA-34a inhibitor, miRNA-34a mimics, pc-PPARGC1A, and controls were transfected in macrophages with or without kidney exosomal. A dual-luciferase reporter gene experiment verifies the targeting relationship between miRNA-34a and PPARGC1A. After exosomal culture, macrophages are co-cultured with normal renal tubular cells to detect renal tubular cell fibrosis. Q-PCR and western blot were undertaken to detect related RNA and proteins. Results. An animal model of diabetic nephropathy was successfully constructed. Macrophages could phagocytose exosomes. After ingesting model exosomes, M1 macrophages were activated, while M2 macrophages were weakened, indicating the model mice’s kidney exosomes caused the polarization. MiRNA-34a inhibitor increased PPARGC1A expression. MiRNA-34a expressed higher in diabetic nephropathy Model-Exo. MiRNA-34a negatively regulated PPARGC1A. PPARGC1A rescued macrophage polarization and renal tubular cell fibrosis. Conclusion. Exosomal miRNA-34a of tubular epithelial cells promoted M1 macrophage activation in diabetic nephropathy via negatively regulating PPARGC1A expression, which may provide a new direction for further exploration of DN treatment.

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Adriamycin nephrotoxicity is reduced by metallothionein over-expression and kidney gene expression is modified by diabetes in the OVE26 diabetic model.

Cited by 2 publications

References 80 publications

Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time

Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time

Renal Tissue-Derived Exosomal miRNA-34a in Diabetic Nephropathy Induces Renal Tubular Cell Fibrosis by Promoting the Polarization of M1 Macrophages

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