Evidence map›Paper›PMID 31921409›Full record

ArticleCell & bioscience2020

SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis.

Haiyan Shan, Dawei Guo, Siyang Zhang, Huimeng Qi, Shen Liu, Yanmei Du, Yini He, Bofu Wang, Ming Xu, Xiaosong Yu

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell & bioscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Haiyan ShanDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Dawei GuoDepartment of the Fourth General Surgery, The Fourth Affiliated Hospital of China Medical University, No. 4 Chongshan East Road, Huanggu District, 110032, Shenyang, China.
Siyang ZhangDepartment of the Science and Experiment Center, The China Medical University, No. 77 Puhe Road, Shenbei New Area, 110122, Shenyang, China.
Huimeng QiDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Shen LiuDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Yanmei DuDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Yini HeDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Bofu WangDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Ming XuDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China.
Xiaosong YuDepartment of General Practice, The First Affiliated Hospital of China Medical University, No. 155 Nanjing North Street, Heping District, Shenyang, 110001, China. utmqra@163.com.
China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlenty of long non-coding RNAs (lncRNAs) play vital roles in the progression of atherosclerosis. Small nucleolar RNA host gene 6 (SNHG6) is a well known lncRNA that is aberrantly high expressed in atherosclerosis patients. However, its function and basic mechanism in atherosclerosis events have not been well clarified.

methodsThe expression patterns of SNHG6, miR-135a-5p, ROCK1 and ROCK2 in clinical samples and cells were detected by RT-qPCR assays. Cell Counting Kit-8 (CCK-8), flow cytometry assays, ELISA and reactive oxygen species (ROS) and malondialdehyde (MDA) detection, were performed to assess cell viability, apoptosis, inflammation and oxidative stress, respectively. Western blot analysis was carried out to examine the protein levels of Bax, Bcl-2, and SNHG6. Luciferase reporter and RIP assays were used to confirm the true interaction between SNHG6 and miR-135a-5p, or miR-135a-5p and ROCK.

resultsThe levels of SNHG6, ROCK1 and ROCK2 were notably increased and miR-135a-5p was decreased in atherosclerosis patients and oxidized low-density lipoprotein (ox-LDL)-treated HUVECs. Knockdown of SNHG6 alleviated ox-LDL-induced injury of HUVECs, while this effect was partly reversed by miR-135a-5p inhibitor. Moreover, overexpression of ROCKs aggravated miR-135a-5p-alleviated atherosclerosis cell injury. SNHG6 contributed to ROCK expression through sequestering miR-135a-5p as a molecular sponge.

conclusionSNHG6 functions as a promoter in atherosclerosis events by targeting miR-135a-5p/ROCK axis in ox-LDL-stimulated HUVECs. This finding will help to develop a novel therapeutic strategy for atherosclerosis.

Indexed as

AtherosclerosisEndothelial injurymiR-135a-5pROCKSNHG6

Identifiers

PMID31921409
PMCPMC6947907
OpenAlexW3005359543

What OpenQuestion holds

Textmetadata
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.