Altering beta-cell number through stable alteration of miR-21 and miR-34a expression

摘要

Aim: An insufficient functional beta-cell mass is a prerequisite to develop diabetes. Thus, means to protect or restore beta-cell mass are important goals in diabetes research. Inflammation and proinflammatory cytokines play important roles in beta-cell dysfunction and death, and recent data show that 2 miRNAs, miR-21 and miR-34a, may be involved in mediating cytokine-induced beta-cell dysfunction. Therefore, manipulation of miR-21 and miR-34a levels may potentially be beneficial to b cells. To study the effect of long-term alterations of miR-21 or miR-34a levels upon net beta-cell number, we stably over-expressed miR-21 and knocked down miR-34a, and investigated essential cellular processes.