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Long non-coding RNA LncCplx2 regulates glucose homeostasis and pancreatic β cell function
Linlin Wang1, Liqiao Hu2, Xingyue Wang3
1Guangzhou National Laboratory, Guangzhou, China; National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Molecular Metabolism
|January 13, 2024
Summary
This study identifies LncCplx2, a long non-coding RNA, as crucial for regulating pancreatic beta cell function and glucose homeostasis. Its deficiency disrupts circadian rhythms and exacerbates diabetes in mice.
Area of Science:
- * Endocrinology and chronobiology research.
- * Molecular mechanisms of diabetes.
- * Long non-coding RNA (lncRNA) function.
Background:
- * Clock genes are known regulators of diabetes and pancreatic beta cell function.
- * The role of rhythmic long non-coding RNAs in these processes remains largely unexplored.
- * Understanding these regulators is key to novel therapeutic strategies for metabolic disorders.
Purpose of the Study:
- * To identify and characterize novel long non-coding RNAs involved in pancreatic beta cell function and circadian regulation.
- * To investigate the role of LncCplx2 in glucose homeostasis and its potential link to diabetes.
- * To elucidate the molecular mechanisms by which LncCplx2 influences circadian rhythms and metabolic processes.
Main Methods:
- * RNA sequencing (RNA-seq) and 3' rapid amplification of cDNA ends (RACE)-PCR for LncCplx2 identification.
- * Quantitative real-time PCR (qRT-PCR) and RNA-Scope for subcellular localization.
- * In vitro and in vivo studies involving LncCplx2 overexpression and knockout (KO) models.
- * Molecular assays including immunoblotting (IB), Immunoprecipitation (IP), RNA pull-down, and chromatin immunoprecipitation (ChIP)-PCR.
- * Metabolism cage analysis for circadian behavior assessment.
Main Results:
- * LncCplx2 is a conserved nuclear lncRNA in pancreatic islets, regulated by BMAL1, and downregulated by high glucose.
- * LncCplx2 deficiency in mice leads to diabetic phenotypes (hyperglycemia, impaired glucose tolerance) and altered circadian behavior.
- * Mechanistically, LncCplx2 recruits EZH2 to silence circadian and cell cycle genes, impacting insulin secretion and beta cell function.
Conclusions:
- * LncCplx2 is identified as a novel transcriptional regulator within the circadian system.
- * This finding reveals an integral mechanism coordinating circadian rhythms and glucose homeostasis.
- * LncCplx2 presents a potential therapeutic target for managing diabetes and circadian rhythm disorders.
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