Korean Biological research group in Michigan

KBM은 미시간에서 의학, 약학, 생물학 관련 연구를 수행하는 연구자들간의 시너지를 도모하는 모임 입니다.

매달 학술 세미나 및 네트워킹 세션을 진행 하고 있으며, 미시간에 계시는 모든 연구자들의 참여를 환영합니다.

KBM is first organized by a group of researchers from the University of Michigan working in various bio-related fields. Since 2020, we have been having regular seminars and network sessions through an online platform. We believe now is the right timing for expanding our group beyond the Michigan area. So if you are interested in joining the seminars and meetings, please contact us!

Contact: kbm.president@gmail.com

Intestinal epithelial SLC39A8 regulates manganese homeostasis and inhibits experimental colitis


To determine the contribution of intestinal epithelial-specific SLC39A8, we generated a novel genetic model of an intestinal epithelial cell-specific Slc39a8 knockout mouse (Slc39a8-IEC KO). SLC39A8 IEC-KO mice have significantly reduced Mn levels in the intestine coupled with marked reduced Mn concentrations in blood and other organs. Despite the known ability of SLC39A8 to transport zinc and iron, tissue zinc and iron levels were not different in Slc39a8-IEC KO mice compared with levels in controls.

In experimental colitis models induced by dextran sulfate sodium, Slc39a8-IEC KO mice were highly susceptible to colitis, as manifested by markedly increased morbidity, weight loss, and colon injury, and colonic inflammation compared with controls. Without DSS treatment, Slc39a8-IEC KO mice displayed elevated intestinal permeability by impairing intestinal tight junctions.

Our unbiased transcriptomic analysis reveals that alkaline ceramidase 1 (ACER1), a lipid-generating enzyme that affects intestinal permeability, is significantly up-regulated in the intestines of Slc39a8-IEC KO mice. Based on the observations, we are currently testing whether ACER inhibitor can reduce intestinal permeability and alter the susceptibility of experimental colitis.

Together, this work suggests that intestinal epithelial Slc39a8 is required for intestinal absorption of dietary Mn, and that loss of Slc39a8 exacerbates experimental colitis likely by impairing intestinal barrier functions