Search Results
You are looking at 1 - 1 of 1 items for
- Author: Liting Wu x
- Refine by access: All content x
Search for other papers by Liting Wu in
Google Scholar
PubMed
Search for other papers by Li Xiong in
Google Scholar
PubMed
Department of Geriatrics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Search for other papers by Jin Li in
Google Scholar
PubMed
Search for other papers by Zishan Peng in
Google Scholar
PubMed
Search for other papers by Luyao Zhang in
Google Scholar
PubMed
Search for other papers by Peijie Shi in
Google Scholar
PubMed
Department of Geriatrics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Search for other papers by Yingying Gong in
Google Scholar
PubMed
Search for other papers by Haipeng Xiao in
Google Scholar
PubMed
This study aimed to identify circular RNAs differentially expressed in the islets of type 2 diabetes (T2DM) models and clarify their roles in the control of β-cell functions. Circular RNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. Then, the expression level of the selected circular RNA circ-Tulp4 was confirmed by real-time PCR in the islets of diabetic models and Min6 cells. MTS, EdU, western blot, flow cytometric analysis, and luciferase assay were performed to investigate the impact of circ-Tulp4 on β-cell functions. This study identified thousands of circular RNAs in mouse pancreatic islets. The circ-Tulp4 level significantly decreased in the diabetic models and altered in the Min6 cells under lipotoxic condition. The modulation of circ-Tulp4 level in Min6 cells regulated cell proliferation. Furthermore, an interaction was demonstrated between circ-Tulp4 and miR-7222-3p, which suppressed the expression of cholesterol esterification-related gene, sterol O-acyltransferase 1 (SOAT1). The accumulation of soat1 activated cyclin D1 expression, thus promoting cell cycle progression. These findings showed that circ-Tulp4 regulated β-cell proliferation via miR-7222-3p/soat1/cyclin D1 signaling. Our research suggested that circ-Tulp4 might be a potential therapeutic intervention for T2DM. Besides, soat1 might be important for β-cell adaptation to lipotoxicity.