When a person has a heart attack, heart muscle cells die and are never replaced. This makes them unusual amongst the cells of major mammalian organs—liver, bone, and skin cells, for example, can restore themselves after injury—and is a main reason why recovery can be difficult, prolonged, or impossible. Improvements could be made with the discovery of a drug that could stimulate heart muscle regeneration, but in order to develop such a drug, cardiovascular researchers need to understand how and why those cells do or don't proliferate. A new paper by researchers at Thomas Jefferson University in the journal Development announced an exciting step towards such an understanding. And among that paper's five authors was Haverford senior biology major Sabrina Emms.

For the paper, the Jefferson team used genetically modified mice who had the mechanical linkages between cells (known as alpha-catenin) removed, and discovered that the heart muscle cells then proliferated by allowing a protein called Yap to accumulate in a cell's nucleus to induce cell-cycle regulators.

"If you think of the nucleus of the cell as a big recipe book, with all the things a cell could possibly need to grow and behave, then Yap acts like a trendy food blogger," said Emms. "Once it is activated, it moves into the nucleus and starts the process of 'copying' and 'making' some of the recipes for stuff the cell would need to proliferate. It isn't doing the cooking, but it's what brings the 'recipes' to the attention of the cell so it can make them. If you take away catenins, which is what we did, you see that the cells don't make the same strong zippers, and when that happens, you get more active Yap and proliferation."

Emms joined the lab of the paper's lead author, Glenn Radice, at Jefferson's Center for Translational Medicine two years ago. Her specific role in its research included preparing and quantifying the tissue samples, doing the "western blotting" (an analytical technique for looking at and separating the proteins in the samples), and taking care of the mice. 

"Working with Dr. Radice has been one of the best experiences of my Haverford career, and it definitely pushed me from being more pre-med to where I am now, going to graduate school," said Emms, who is conducting her senior thesis research on a different aspect of heart-muscle-cell proliferation in his lab. "I've really enjoyed having one a foot in a research lab and one in the classroom because they really play off each other."

Emms, who is also minoring in creative writing at Bryn Mawr College, learned about the opportunity in Radice's lab through the Center for Career and Professional Advising's job board. Radice selected her for his team because of her strong molecular biology background, her experience working with animals—she was a former member of the 4H Club—and her enthusiasm for her work, which has only grown over the past two years.

"Sabrina has been exposed to many techniques during her time in the lab," said Radice. "If a technique did not work at first, Sabrina showed incredible perseverance. She would troubleshoot the problem until it was solved and the experiment was completed."

Her Haverford advisor, Professor Phil Meneely, is similarly impressed with her dedication. In fact, the course on human genetics and eugenics that he is teaching this semester owes its existence to her persistent urging that he teach it. (She is now its teaching assistant.)

"Sabrina is a good example of a Haverford student because she hard-working, sincere, mature, and intellectually engaged in the broader issues in life," said Meneely. "She is wonderful to work with. She's not shy about sharing her ideas, but she is eager to learn, and my conversations with her usually go longer than either of us had planned." 

Up next for the budding researcher is graduate school. She starts a Ph.D. program in molecular biology in the fall.