Sandra Hammer, PhD
Michigan State University, USA
Sandra is currently a postdoctoral fellow in the Busik Laboratory at Michigan State University. Prior to being at MSU, she attended Vanderbilt University where she obtained her PhD in Cell and Developmental Biology under the mentorship of John Penn. Prior to this, she got my BS degree from the University of Miami.
Scientifically, Sandra is interested in the role that cholesterol metabolism and inflammation play in progression of microvascular disease. She’s specifically interested in diabetes-induced retinal diseases. Sandra currently works on elucidating the role that the SIRT1/LXR signaling pathway plays in retinopathy progression. She has discovered the novel involvement of this pathway in preventing disease progression and is very interested in strategies that increase SIRT1/LXR signaling. Her long-term goals are to develop an energetic and productive independent research program well suited to investigate lipid dysregulation in microvascular complications.
Learn about Sandra’s research
Title: The role of SIRT1/LXR signaling in diabetic retinopathy
- Understand the role of SIRT1-LXR activation in control of inflammation and subsequent metabolic changes in retinal endothelial cells.
- Demonstrate how serum starvation promotes activation of the SIRT1-LXR pathway metabolism in retinal endothelial cells.
- Explain how therapeutic fasting may serve to activate the SIRT1-LXR pathway providing the dual benefits of decreasing inflammation and promoting cholesterol metabolism in the retina.
Liver x receptors (LXRs) are hypothesized to serve as a link between lipid metabolism and inflammation by promoting cholesterol efflux as well as exhibiting anti-inflammatory properties. NAD-dependent deacetylase SIRT1 is known to promote insulin secretion, reduce glucose tolerance and to play a critical role in regulating inflammation. SIRT1 has also been shown to interact with LXR to promote LXR activation. Additionally, previous literature has shown that starvation increases SIRT1 levels in mice. The purpose of this study was to investigate the role of SIRT1-LXR activation in control of inflammation and subsequent metabolic changes in retinal endothelial cells.
Bovine retinal endothelial cells (BRECs) were treated with diabetic relevant stimulus TNFα (10ng/ml); LXR activator, DMHCA (1uM); or SIRT1 activator, SRT1720 (1 µM). In order to model calorie restriction in vitro BRECs were serum starved (0% FBS) for 24hrs. SIRT1, IL1β, ABCA1 and ABCG1 were analyzed by qRT-PCR. Sirt1 activity was measured via histone deacetylase activity (HDAC) assay. LXR acetylation was measured via western blot analysis. Results: Treatment with pro-inflammatory cytokine, TNFα (10 ng/mL) for 24 hr significantly increased cholesterol levels (p=0.0233, n=6), IL1β expression, IL6 expression and resulted in decreased levels of HDAC activity in BRECs. Activation of LXR or SIRT1 prevented TNFα-induced inflammation. Serum starvation resulted in a significant increase in HDAC activity (p=0.0005, n=6) and SIRT1 expression levels. Lastly, serum starvation caused a decrease in LXR acetylated levels in BRECs.
The results of this study demonstrate that serum starvation promotes activation of the SIRT1-LXR pathway metabolism in retinal endothelial cells. Therefore, this study suggests that therapeutic fasting may serve to activate the SIRT1-LXR pathway providing the dual benefits of decreasing inflammation and promoting cholesterol metabolism in the retina.
Watch the webinar
Get to know Sandra
Why did you choose cancer research?
The best part of being a researcher is the ability to learn and discover new things every day. This makes my job very exciting and inspires me to do the best work I possibly can. I have been conducting research since high school and have engaged in a wide range of projects from working with plants to cell culture models to animal models. This wide range of projects has given me a great appreciation for basic science and research. I love being able to work on an aspect of human disease with the goal of discovering a new technique or therapy that might be helpful to many.
What motivates you to succeed in your field?
For the past 8 years I have been very interested in further understanding the biochemical mechanism that are responsible for progression of age-related disease such as diabetes and its associated complications. Diabetes is global epidemic, posing a serious burned on a patient’s quality of life. This disease is places massive financial burden on individuals and countries as well. The main motivating force behind my work is knowing that the work I am doing at the bench could translate to potential therapeutic strategies for millions of people affected with diabetes. I am particularly interested in early disease progression in hopes of preventing the onset of complications such as vision loss.
Is outreach/STEM important to you? Why?
Yes! Science outreach is very important to me. It is crucial that we show younger kids the beauty and power STEM holds. Knowledge is the most powerful tool we can provide younger generations with to ensure they have fulfilled and meaningful lives.
What are your top 3 favorite things to do outside of the lab?
- Spend time with my husband and my daughter.
- Go for long walks
Describe yourself with 3 words:
Who is the person you are closest with?
What is your favorite day of your life thus far?
- Science related: Defending my PhD.
- Non science: I have two days that are equally amazing. The day I got married and the day my daughter was born.
What role have the mentors you’ve had in your passion for basic research?
A huge role! I am so lucky to have had the best mentors as an undergraduate, graduate and now fellow. They have been excellent models of hard work, dedication and commitment to science and research.
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