Lifespan-extending interventions inhibited consistent expression patterns of IL-11 signaling across mouse livers and adipose tissues – UROP Symposium

Lifespan-extending interventions inhibited consistent expression patterns of IL-11 signaling across mouse livers and adipose tissues

Nicholas Hankins

Research Mentor: Xinna Li
Mentor Department: Pathology, Medicine
Author(s): Not Available
Session: Session 2 (10:00 AM – 10:50 AM)
Presentation Type: Poster 61

Abstract

As people age, they often experience weight gain, changing metabolism, chronic inflammation, and a higher risk of diseases such as diabetes and cancer. Understanding the biological factors that promote healthy aging is important for developing ways to prevent these age-related conditions, which is one of the main focus points within Dr. Xinna’s Lab. PTEN is a gene that helps regulate how cells use energy and grow. Mice with increased PTEN levels (PTEN transgenic) have been shown to burn more energy, store less fat, respond better to insulin, and live longer. However, it is not known whether these mice share other biological traits commonly found in well-known slow-aging mouse models. In this project, we are testing whether PTEN transgenic mice show similar changes across multiple tissues (hippocampus, inguinal/perigonadal fat, liver, adipose tissue, etc) that are seen in other slow-aging mice. The lab dissected tissues from PTEN transgenic and control mice and isolated RNA and protein from these samples. I personally measured gene activity using real-time PCR and measured the protein levels using Western blotting. We have found that PTEN transgenic mice display many of the same biological changes observed in other slow-aging mouse models. These results suggest that increasing PTEN activity may promote healthier aging across the body. This research helps improve our understanding of how metabolism, aging, and disease are connected and may contribute to future strategies aimed at reducing obesity, diabetes, and other age-related conditions.

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