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Published on: June 25, 2014
LINC-p21 Regulates Pancreatic β-Cell Function in Type 2 Diabetes Mellitus
Zengkun Qian1, Fan Cui2, Zheng Mao2
1Department of Clinical Laboratory, Wuhu Hospital Affiliated to Anhui University of Science and Technology (The First People's Hospital of Wuhu), Wuhu, 241000, Anhui, China. worldqian1978@163.com.
None:
This study aimed to investigate the underlying mechanism and assess the biological role of long intergenic non-coding RNA (LINCRNA)-p21 in type 2 diabetes mellitus (T2DM). LINC-p21 and miR-335-3p expression levels were evaluated in blood from T2DM patients, healthy individuals, and mouse islet β-cell line MIN6 cells grown in a high glucose environment. Apoptosis-related proteins, iNOS, and IGF-1 were detected in vitro and in vivo. Bioinformatics was used to predict that miR-335-3p had complementary binding sites to IGF-1, and a dual-luciferase reporter confirmed the targeting link between LINC-p21 and miR-335-3p. LINC-p21 was highly expressed in the T2DM serum and cells, and LINC-p21 was significantly associated with T2DM prognosis. In vitro and in vivo dysfunction of β-cells was reduced by LINC-p21 knockdown. MiR-335-3p and IGF-1 may be potential targets of LINC-p21 and miR-335-3p, respectively, after the prediction of the target of LINC-p21 was verified by dual-luciferase assay. Anti-miR-335-3p made LINC-p21 knockdown function again; however, interference of IGF-1 mRNA restored the function of LINC-p21. The miR-335-3p/IGF-1 axis may have a role in the functional protection of pancreatic β-cells by LINC-p21 silencing, boosting insulin production, and slowing the course of diabetes.
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