Friday, August 23, 2013

Through their lens: Emerson Pizzinat studies a life threatening kidney disease

This summer we're sponsoring high school interns in stem cell labs throughout California. We asked those students to contribute to our Instagram photos and YouTube videos about life in the lab, and write about their experiences.

Emerson Pizzinat did a stem cell research internship this summer in the laboratory of Thomas Weimbs at the University of California, Santa Barbara.

Emerson Pizzinat carrying out the final step of his experiment. He submitted this photo to our #CIRMStemCellLab Instagram feed.
This summer I had the amazing opportunity of working in a college level research lab provided to me by the generous people at CIRM. I spent six weeks in the Weimbs laboratory studying Autosomal Polycystic Kidney Disease (ADPKD). I was able to work under the direction of my mentor Jacob Torres in the Department of Molecular, Cellular, and Developmental Biology. Under his direction I learned about one of the most common life threatening genetic diseases prevalent in the world today. I learned that ADPKD causes cysts in the kidneys and leads to death. This disease has no cure so patients diagnosed with it have to undergo kidney transplant or life-long dialysis. Dialysis patients cost the government almost 2 billion dollars a year so finding a treatment would save both lives and money. In our experiment we wanted to look at the p30 fragment of PC1, where the mutation that causes the disease is located, but we first had to run some preliminary tests. In the ADPKD field there is a 3 hit hypothesis that describes how people get the disease. First there is a genetic mutation to PC1 or PC2. Then a somatic mutation occurs which could be in the form of UV light or chemical radiation. Finally the patient has to experience an injury to the kidney. There is also an occurrence of kidney stones in ADPKD patients that is of a higher frequency then that of the general public. When we looked at these two ideas we formulated an experiment to see if kidney stones could be the injury in the 3 hit hypothesis. After testing for five weeks we were able to see that mice that we had given a kidney stone forming agent to had increased expression of certain proteins that appear in patients who have ADPKD. To see this we used immunoflouresence to stain the protein expression with florescent antibody. We confirmed which proteins were active and learned that using sodium oxalate (what we treated the mice with) is a viable way to produce kidney stones and elucidate an injury response in the kidneys. This program had given me an invaluable experience that I will take with me for the rest of my life. Working in a research environment and working to help people has turned me onto the idea of maybe pursuing a degree in the medical field. The need for increased research and funding for stem cells was clearly evident after this program as there is so much potential in this field and so much still needs to be understood.

Emerson Pizzinat

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