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February 2011 Issue

Litsa Kranias, MD, PhD (seated), with Jiang Qian, MD, PhD, and Kobra Haghighi, PhD (left to right)
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Protein Tied to Heart Failure Studied

By Katie Pence
Published February 2011

Researchers in the department of pharmacology and cell biophysics have found that higher levels of a certain protein in the body could cause heart failure—a finding that could help researchers create cellular-targeted treatments and prevent cardiac failure from occurring.
The team led by Jiang Qian, MD, PhD, a postdoctoral student under the direction of Litsa Kranias, PhD, chair of the department, wanted to find out exactly how Heat Shock Protein 20 (Hsp20)—a protein whose expression is increased when cells are exposed to elevated temperatures or stress—affects cardiac muscle.

"Levels of Hsp20 and its phosphorylation (added levels of phosphate to the protein) have been found to be elevated in human failing hearts,” Qian says.

"We found that in cultured adult rat heart cells, the overexpression of phosphorylated Hsp20—or Hsp20-S16D, a mutant Hsp20 protein which mimics the phosphorylated Hsp20 in the body, but naturally does not exist—resulted in enhanced contractility.

However, the role of phosphorylated Hsp20 in the body remains to be known. We wanted to find out why this increased phosphorylation occurs and the impact it has on heart failure.”

Researchers first generated animal models to overexpress Hsp20-S16D by 12 times.

"Unexpectedly, we found that the amount of contractility was significantly slower in these models when compared with those who were not modified to overexpress Hsp20-S16D,” Qian says.

"Contractile function was also significantly impaired in these models; in addition, these models developed scarring in the left ventrical at 8 weeks old, and their life span was markedly shorter.”

Qian says this data could eventually lead to quicker interventions and more targeted therapies, which could save lives.

"Our data indicates that long-term augmentation of cardiac Hsp20 phosphorylation results in increased cardiac cell destruction, possibly contributing to depressed cardiac muscle function and pathological remodeling which could lead to premature death,” Qian says.

"Hopefully, we will one day be able to develop a cellular therapy that will control overexpression of this protein in the body, preventing heart failure from ever developing in the first place.”

More about Qian:

Jiang Qian, MD, PhD, graduated from the Medical School of Soochow University in China in 1998 after obtaining both medical and master’s of science degrees. She practiced as a cardiologist for seven years in the First Affiliated Hospital of Soochow University.

"My interests in cardiovascular research led me to Dr. Kranias’ lab at UC in March 2003,” she says.

"I graduated in June 2010 and hope I can find a research position in the cardiac field.”

In her free time, Qian says she likes reading, traveling and cooking.

"But I have little time to do so after having two kids,” she laughs.

Additional Heart Research: Watch a video explaining more UC-led research that found statin risks may outweigh the cardiovascular benefits for patients with history of brain hemorrhage at

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