Evidence map›Paper›PMID 31737170›Full record

ArticleOxidative medicine and cellular longevity2019

LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis.

Xiang Kong, Chong-Xiao Liu, Guo-Dong Wang, Hui Yang, Xin-Ming Yao, Qiang Hua, Xiao-Yong Li, Hong-Mei Zhang, Ming-Zhe Ma, Qing Su and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 53 citations in OpenAlex.

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  15. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Xiang KongKey Laboratory of Noncoding RNA Transformation Research of Anhui Higher Education Institution (Wannan Medical College), Wuhu 241002, China.
Chong-Xiao LiuDepartment of Endocrinology, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200137, China.
Guo-Dong WangAnhui Provincial Engineering Research Center for Polysaccharide Drugs, School of Pharmacy, Wannan Medical College, Wuhu 241002, China.
Hui YangKey Laboratory of Noncoding RNA Transformation Research of Anhui Higher Education Institution (Wannan Medical College), Wuhu 241002, China.
Xin-Ming YaoDepartment of Endocrinology, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, Wuhu 241001, China.
Qiang HuaDepartment of Endocrinology, The First Affiliated Hospital of Wannan Medical College, Yijishan Hospital, Wuhu 241001, China.
Xiao-Yong LiDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.
Hong-Mei ZhangDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.ORCID https://orcid.org/0000-0002-4068-7017
Ming-Zhe MaDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.ORCID https://orcid.org/0000-0001-8858-0983
Qing SuDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.ORCID https://orcid.org/0000-0001-7945-1258
Kun LvKey Laboratory of Noncoding RNA Transformation Research of Anhui Higher Education Institution (Wannan Medical College), Wuhu 241002, China.ORCID https://orcid.org/0000-0002-1895-6700
Wannan Medical College · CNXinHua Hospital · CNFirst Affiliated Hospital of Wannan Medical College · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose and/or high serum free fatty acids. Chronic hyperlipidemia causes the dysfunction of pancreatic beta cells, which is aggravated in the presence of hyperglycemia (glucolipotoxicity). Long noncoding RNAs (lncRNAs) have been suggested to play key roles in type 1 diabetes mellitus development. However, their roles in glucolipotoxicity-induced beta cell dysfunction are not fully understood. In the present study, we identified the differentially expressed lncRNAs in INS-1 cells exposed to high glucose and palmitate (HG/PA). Among the dysregulated lncRNAs, NONRATT003679.2 (low expression in glucolipotoxicity-treated beta cells (LEGLTBC)) was involved in glucolipotoxicity-evoked rat islet beta cell damage. LEGLTBC functioned as a molecular sponge of miR-34a in INS-1 cells. Additionally, SIRT1 was identified as a target of miR-34a and LEGLTBC promoted SIRT1 expression by sponging miR-34a. The upregulation of LEGLTBC attenuated HG/PA-induced INS-1 cell injury through the promotion of SIRT1-mediated suppression of ROS accumulation and apoptosis. This is the first study to comprehensively identify the lncRNA expression profiling of HG/PA-treated INS-1 beta cells and to demonstrate that LEGLTBC functions as a competing endogenous RNA and regulates miR-34a/SIRT1-mediated oxidative stress and apoptosis in INS-1 cells undergoing glucolipotoxicity.

Indexed as

AnimalsApoptosisCell LineDiabetes Mellitus, Type 2Disease Models, AnimalDown-RegulationGlucoseHumansHyperglycemiaInsulin-Secreting CellsMicroRNAsOxidative StressRatsRNA, Long NoncodingSirtuin 1GlucoseMicroRNAsMIRN34 microRNA, ratRNA, Long NoncodingSirt1 protein, ratSirtuin 1

Identifiers

PMID31737170
PMCPMC6815544
OpenAlexW2979950874

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.