A recent study entitled “Hyaluronan Synthase 3 Null Mice Exhibit Decreased Intestinal Inflammation and Tissue Damage in the DSS-Induced Colitis Model” was published in the International Journal of Cell Biology by Sean P. Kessler and colleagues from the Department of Pathobiology, Lerner Research Institute Cleveland Clinic, Cleveland, USA. In the study, researchers suggest that the control of Hyaluronan Synthase 3 (HAS3) expression in the intestinal microvasculature may be a potential novel therapeutic intervention strategy for patients with inflammatory bowel diseases (IBD).
Hyaluronan (HA) is a carbohydrate polymer produced by different types of cells and present in the extracellular matrix of all healthy and inflamed tissues. Higher production of HA has been shown to be a feature of several inflammatory diseases, including IBD. IBD, which includes Crohn's disease and ulcerative colitis, seem to be induced by an intricate interaction of external and genetic factors, epithelial barrier defects and alterations of the gut immune system. The regulation of HA production is done at the cytoplasmic membrane surface by hyaluronan synthase (HAS1, HAS2, or HAS3) enzymes, before delivered into the extracellular matrix to function as a space-filling and supporting anionic molecule.
The research team has been studying the role of HA in intestinal infl