The Role Of Long Noncoding RNA TUG1 In The Function Of Mouse Pancreatic Islets

The incidence of diabetes showed increasing trend. The imbalance of islet cell proliferation and apoptosis can lead to the destruction of islet structure, functional disorders, thereby causing insufficient insulin secretion, causing diabetes. Pancreatic islets of Langerhans are an excellent model of a specialized tissue that is closely linked to human disease. The non-coding RNAs (ncRNAs) comprise small RNAs such as microRNAs and long non-coding RNAs (IncRNAs). The length of lncRNAs is more than 200 nt. Numerous mammalian lncRNAs are expressed in a cell type and tissue specific manner Evidence of regulation showed that numerous lncRNAs have specific biological functions. Generally, lncRNAs have been implicated in gene regulatory roles, including X inactivation, imprinting, transcription, translation, splicing, epigenetic regulatory, pluripotency, cancer, cell cycle control, cell differentiation, and others.Taurine could ptotecct the function of islets by promote cell proliferation.lncRNA TUG1 could be upregulated by taurine.The role of TUG1 in diabetes is largely unknown. In this study, we explore the relationship between TUG1 and the function of beta cells. Surprisingly, we demonstrated that TUG1 is high expressed in pancreas when comparing with other tissues or organs. Knockdown mTUGla in mouse beta cells could promote cell apoptosis. Down-regulation of mTUGla could influence the GSIS function of mouse beta cells in vitro. After downregulating TUG1 in vivo, the fasting blood glucose and the rate of beta cell apoptosis were both increased. Otherwise, TUG1 is glucose dependent regulation. Insulin secretion was decreased in TUG1 RNAi group. Otherwise, the morphology of the insulin-positive cell mass in the TUG1 siRNA group differ form the group of scrambled siRNA-treated ICR mice. Thus, we hypothesized that TUG1 would affect the function of beta cells through promoting the rate of cell apoptosis.