Blackburn Explains Award-winning Research

March 16, 2005

Elizabeth Blackburn

About 200 people gathered recently at the Gladstone Institutes to hear UCSF microbiologist Elizabeth H. Blackburn give an update on her groundbreaking research on the roles of telomeres and telomerase in health and disease. Blackburn delivered the 2005 Gladstone Distinguished Lecture in Molecular and Cell Biology on March 7. At UCSF Mission Bay, Blackburn leads a laboratory team that is analyzing telomerase and telomeres in yeasts and in human cancer cells to understand their full roles in cell division processes. She continues to explore how tumor growth can be controlled by either inhibiting or activating telomerase in cancer cells. The recipient of numerous honors and awards, Blackburn's achievements continue to hold enormous possibilities for biomedical research on aging and cancer treatment. The Morris Herzstein Professor of Biology and Physiology in the Department of Biochemistry and Biophysics at UCSF, Blackburn, PhD, began her talk by explaining the function of telomeres and telomerase. Telomeres are DNA-protein complexes that cap the ends of chromosomes and promote genetic stability. Each time a cell divides, a portion of telomeric DNA dwindles away, and after many rounds of cell division, so much telomeric DNA has diminished that the aged cell stops dividing. Thus, telomeres play a critical role in determining the number of times a cell divides, its health and its life span. These factors, in turn, affect the health of the tissues that cells form. Telomerase is an enzyme that replenishes a portion of telomeres with each round of cell division, and protects telomeres. Oxidative stress, which causes DNA damage, has been shown to hasten the shortening of telomeres in cell culture. During the Gladstone lecture, Blackburn also explained her recent research with Elissa Epel, PhD, UCSF assistant professor of psychiatry. They reported last November that they found the first direct evidence that severe and chronic emotional stress can age people biologically. Blackburn, Epel and colleagues discovered that chronic stress, and the perception of life stress, each had a significant impact on three biological factors-- the length of telomeres, the activity of telomerase and levels of oxidative stress -- in immune system cells known as peripheral blood mononucleocytes in healthy premenopausal women. See story. The results of the study -- which involved 39 women who were caregivers of a chronically ill child and 19 who were mothers of a healthy child, who served as the "controls" -- were dramatic. As expected, most women who cared for a chronically ill child reported that they were more stressed than women in the control group, though, as a group, their biological markers were not different from those of the controls. However, in one of the study's key findings, the duration of caregiving -- after controlling for the age of the women -- proved critical: The more years of caregiving, the shorter the length of the telomeres, the lower the telomerase activity and the greater the oxidative stress. Moreover, the perception of being stressed correlated in both the caregiver and control groups with the biological markers. In fact, in the most stunning result, the telomeres of women with the highest perceived psychological stress -- across both groups -- had undergone the equivalent of about 10 years of additional aging, compared with the women across both groups who had the lowest perception of being stressed. The highest-stress group also had significantly decreased telomerase activity and higher oxidative stress than the lowest-stress group. "The results were striking," Blackburn said at the time. "This is the first evidence that chronic psychological stress -- and how a person perceives stress -- may damp down telomerase and have a significant impact on the length of telomeres, suggesting that stress may modulate the rate of cellular aging." Source: Lisa Cisneros and Jennifer O'Brien

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