Event Title

The Effects of Sweeteners on the Expression of MiRNAs Involved in ROS

Location

CSU Ballroom

Start Date

18-4-2016 10:00 AM

End Date

18-4-2016 11:30 AM

Student's Major

Chemistry and Geology

Student's College

Science, Engineering and Technology

Mentor's Name

Theresa Salerno

Mentor's Department

Chemistry and Geology

Mentor's College

Science, Engineering and Technology

Description

Hyperglycemia is a crucial factor in the development of diabetic nephropathy. Studies have shown that microRNAs play a critical role in the development of diabetic kidney damage.MicroRNA-25 targets the expression of the NADPH oxidase (NOX) protein, which normally increases reactive oxygen species (ROS).Studies have shown that miR-25 levels were decreased by high glucose in mesangial cells of the kidney. This increased generation of reactive oxygen species (ROS) because of elevated NOX 4 protein synthesis.MicroRNA- 377 has also been shown to have an important role in kidney oxidative stress, and was up regulated with a high fructose diet. This caused a decrease in the levels of superoxide dismutase resulting in increased levels of oxygen free radicals. The general objective of this research project was to analyze the effect of sweeteners on the expression of miRNAs in rat kidneys. Rats (four per experimental group) were given osmolite diets supplemented with stevia, saccharin, and sucrose. Following a six-week treatment, the kidneys were obtained and frozen in liquid nitrogen. Small RNAs were isolated using the mirVana microRNA kit. Following analysis for quality and quantity, the specific miRNAs were converted into cDNAs with the Taqman MicroRNA Reverse Transcription Kit. This was followed by amplification using the quantitative polymerase chain reaction (qPCR) and analyzed using the delta delta Ct method. Efficiency curves have validated the successful development of methods to measure the expressions of MiR-25 and snU6 RNA, the endogenous control. Initial studies have shown that sucrose diets decrease the relative expression of miR-25.

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Apr 18th, 10:00 AM Apr 18th, 11:30 AM

The Effects of Sweeteners on the Expression of MiRNAs Involved in ROS

CSU Ballroom

Hyperglycemia is a crucial factor in the development of diabetic nephropathy. Studies have shown that microRNAs play a critical role in the development of diabetic kidney damage.MicroRNA-25 targets the expression of the NADPH oxidase (NOX) protein, which normally increases reactive oxygen species (ROS).Studies have shown that miR-25 levels were decreased by high glucose in mesangial cells of the kidney. This increased generation of reactive oxygen species (ROS) because of elevated NOX 4 protein synthesis.MicroRNA- 377 has also been shown to have an important role in kidney oxidative stress, and was up regulated with a high fructose diet. This caused a decrease in the levels of superoxide dismutase resulting in increased levels of oxygen free radicals. The general objective of this research project was to analyze the effect of sweeteners on the expression of miRNAs in rat kidneys. Rats (four per experimental group) were given osmolite diets supplemented with stevia, saccharin, and sucrose. Following a six-week treatment, the kidneys were obtained and frozen in liquid nitrogen. Small RNAs were isolated using the mirVana microRNA kit. Following analysis for quality and quantity, the specific miRNAs were converted into cDNAs with the Taqman MicroRNA Reverse Transcription Kit. This was followed by amplification using the quantitative polymerase chain reaction (qPCR) and analyzed using the delta delta Ct method. Efficiency curves have validated the successful development of methods to measure the expressions of MiR-25 and snU6 RNA, the endogenous control. Initial studies have shown that sucrose diets decrease the relative expression of miR-25.

Recommended Citation

Abdukadir, Azhar. "The Effects of Sweeteners on the Expression of MiRNAs Involved in ROS." Undergraduate Research Symposium, Mankato, MN, April 18, 2016.
http://cornerstone.lib.mnsu.edu/urs/2016/poster-session-A/43