Hedetoft, Cecilie

Hermann, Florian M.

Jensen, Rasmus

Larsen, Sylvester

Miraloglu, Ibrahim H.

Tawfik, Bassam

MiRNAs are post-transcriptional regulators of protein expression and are believed to play a role in the failure of β-cells to secrete sufficient insulin to maintain glucose homeostasis, thus leading to type 2 diabetes mellitus. Syntaxin1a (STX1A), a t-SNARE protein involved in insulin exocytosis, has been reported down-regulated in response to prolonged exposure to high glucose levels (Dubois et al., 2007). Deregulation of STX1A has been connected with an impaired insulin exocytosis (Ohara-Imaizumi et al., 2007). Unpublished data from a research group at Roskilde University show that miR-29a is glucose induced in the INS-1E β-cell line from rats. Databases predict a miR-29a target site in the 3’ UTR of Stx1a. Dual luciferase assays using INS-1E cells with varying glucose concentrations is performed to test the hypothesis that miR-29a is a mediator of STX1A down-regulation due to high glucose levels. There is an insufficient amount of data to conclude whether there is a significant interaction between miR-29a and the predicted target site from Stx1a. Nevertheless the data indicates a tendency of a slight regulation of STX1A by miR-29a. It could not be confirmed that miR-29a is glucose induced. Furthermore the data suggests that the used dual luciferase assay is unreliable under high glucose levels in INS-1E cells.MiRNAs are post-transcriptional regulators of protein expression and are believed to play a role in the failure of β-cells to secrete sufficient insulin to maintain glucose homeostasis, thus leading to type 2 diabetes mellitus. Syntaxin1a (STX1A), a t-SNARE protein involved in insulin exocytosis, has been reported down-regulated in response to prolonged exposure to high glucose levels (Dubois et al., 2007). Deregulation of STX1A has been connected with an impaired insulin exocytosis (Ohara-Imaizumi et al., 2007). Unpublished data from a research group at Roskilde University show that miR-29a is glucose induced in the INS-1E β-cell line from rats. Databases predict a miR-29a target site in the 3’ UTR of Stx1a. Dual luciferase assays using INS-1E cells with varying glucose concentrations is performed to test the hypothesis that miR-29a is a mediator of STX1A down-regulation due to high glucose levels. There is an insufficient amount of data to conclude whether there is a significant interaction between miR-29a and the predicted target site from Stx1a. Nevertheless the data indicates a tendency of a slight regulation of STX1A by miR-29a. It could not be confirmed that miR-29a is glucose induced. Furthermore the data suggests that the used dual luciferase assay is unreliable under high glucose levels in INS-1E cells

Is Syntaxin1a Regulated by MiRNA-29a in INS-1E β-cells?

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Roskilde Universitet