|Dr. Michael Chin|
Following the exposures, the expression of heart genes in the four groups was compared. The scientists identified three candidates genes (Mir133a-2, Ptprf, and Pamr1) that were expressed differently in the group of mice exposed to both diesel exhaust and TAC surgery. The target genes identified in this study are the first genes identified as likely playing an role in adult heart failure.
Further examination found that in those mice exposed to both diesel exhaust and TAC surgery, DNA methylation was altered in the promoter region of the Mir133a-2 candidate gene. DNA methylation, also known as epigenetics, consists of chemical groups that attach to the DNA molecule and work as on/off switches to regulate gene expression.
Mir133a-2 has been identified as a biomarker for patient outcomes after heart valve replacement in humans and is presently being studied as a potential treatment to improve patient outcome after a heart attack. Finding out whether Mir133a-2 can protect against heart failure from exposure to diesel exhaust will help further drug development for patients with heart failure associated with air pollution.
Chin suggests that these findings can inform public policy: "Our study adds to the large body of evidence that air pollution exposure has significant harmful effect on the cardiovascular system, and extends these findings to show the effects of this exposure on the developing heart -- effects that can last for decades. By demonstrating this potential public and global health problem, we hope that our study prompts leaders to develop thoughtful environmental regulatory policies that promote the health and wellbeing of future generations."
Dr. Chin, M.D., Ph.D., is associate professor of medicine at the UW Center for Cardiovascular Biology in the School of Medicine and a member of the UW EDGE Center.