https://www.selleckchem.com/products/cb1954.html
The relationship between miR-18b and KCNQ1OT1 or HMGA2 was determined via dual-luciferase reporter analysis, RNA immunoprecipitation, and pull-down. KCNQ1OT1 expression was increased and miR-18b expression was decreased in DN patients and HG-challenged HMCs. miR-18b was targeted via KCNQ1OT1. Knockdown of KCNQ1OT1 weakened HG-caused proliferation, oxidative stress, and ECM accumulation of HMCs by increasing miR-18b. HMGA2 was targeted via miR-18b. miR-18b alleviated HG-induced cell proliferation, oxidative stress, and ECM accumulation by
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