Low Expression of MDR1 Gene Links Mitochondria Function to Severe Colitis, Mouse Study Shows

Low Expression of MDR1 Gene Links Mitochondria Function to Severe Colitis, Mouse Study Shows
Researchers identified a gene, known as multidrug resistance-1 (MDR1), that may underlie the most severe and incurable forms of inflammatory bowel diseases (IBD). The findings may lead to the development of new therapies for IBD patients. The study “MDR1 deficiency impairs mitochondrial homeostasis and promotes intestinal inflammation” was published in the journal Mucosal Immunology. The MDR1 gene carries vital functions in the gut by preventing the cells’ uptake of damaging substances or by promoting the substances' rapid elimination. Researchers at the University of Edinburgh looked at the expression of MDR1 in IBD patients and compared it to biopsies of the colon from patients with inflamed IBD, to those who showed no signs of inflammation. They found that MDR1 function was decreased in inflamed colons of IBD patients. To understand the significance of a lower expression on MDR1 in the colon, researchers used mice that lack MDR1 altogether. These mice, they learned, had defective mitochondria. Mitochondria are small organelles that exist inside cells and perform vital functions; one of the most important being the production of energy cells needed to function properly and protect against damaging molecules, known as reactive oxygen species (ROS). Defective mitochondria, upon loss of MDR1 function, led to the development of colitis, the inflammatory status in the colon that defines IBD. Researchers performed more in-depth studies and found that “many (∼5%) of IBD susceptibility genes with direct roles in regul
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