Evidence map›Paper›PMID 31792649›Full record

ArticleMolecular and cellular biochemistry2020

LncRNA SNHG1 alleviates hypoxia-reoxygenation-induced vascular endothelial cell injury as a competing endogenous RNA through the HIF-1α/VEGF signal pathway.

Shuangchao Liang, Kai Ren, Buying Li, Fangkuan Li, Zhuowen Liang, Jiqiong Hu, Bei Xu, Andong Zhang

Abstract read
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Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed.

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  18. [Research advances on the role of competing endogenous RNAs in wound healing].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2022
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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

8 authors.

Shuangchao LiangDepartment of Vascular Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, 241100, Anhui, China.
Kai RenDepartment of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, No. 169, West of Changle Road, Xincheng District, Xi'an, 710032, Shannxi, China. renkaisx@163.com.
Buying LiDepartment of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, No. 169, West of Changle Road, Xincheng District, Xi'an, 710032, Shannxi, China.
Fangkuan LiDepartment of Vascular Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, 241100, Anhui, China.
Zhuowen LiangDepartment of Orthopedic, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710032, Shannxi, China.
Jiqiong HuDepartment of Vascular Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, 241100, Anhui, China.
Bei XuDepartment of Vascular Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, 241100, Anhui, China.
Andong ZhangDepartment of Vascular Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, 241100, Anhui, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding ribonucleic acids (lncRNAs) are critical regulators in various biological processes. In the present study, we aimed to explore whether miR140-3p was involved in the underlying molecular mechanisms of small nucleolar RNA host gene 1 (SNHG1) in myocardial ischemia/reperfusion (I/R) injury. A mouse model of I/R injury and hypoxia-reoxygenation (H/R)-stimulated human umbilical vein endothelial cells (HUVECs) was used in this study. Cell proliferation was detected by MTT. The mRNA and protein levels of vascular endothelial growth factor (VEGF), VE-cadherin, and MMP2 were detected by RT-PCR and western blot, respectively. The angiogenesis was assessed by tube formation assay. Cell migration was assessed using wound-healing assay. Results showed that SNHG1 expression was increased in the cardiac microvasculature of a mouse model of I/R injury and in H/R-stimulated HUVECs. H/R stimulation significantly reduced cell proliferation, tube formation, and cell migration, but increased expression of VEGF, VE-cadherin, and MMP2. SNHG1 upregulation under H/R increased HUVECs proliferation, tube formation, and cell migration, and upregulated expression of VEGF, VE-cadherin, and MMP2, compared with the H/R group. SNHG1 knockdown exhibited the opposite effect. SNHG1 functioned as a competing endogenous RNA (ceRNA) of miR-140-3p. HIF-1α was identified as a target of miR-140-3p. SNHG1 upregulation enhanced cell proliferation, tube formation, and expression of VEGF, VE-cadherin, and MMP2 through HIF-1α/VEGF signaling. This process could be offset by miR-140-3p mimic or VEGF inhibitor. Our results reveal a novel protective function of SNHG1 that furthers understanding of cardiac I/R injury and provides experimental evidence for future therapy.

Indexed as

Signal TransductionAnimalsDisease Models, AnimalFemaleHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitMiceMyocardial Reperfusion InjuryNeovascularization, PhysiologicRNA, Long NoncodingVascular Endothelial Growth Factor AHIF1A protein, humanHif1a protein, mouseHypoxia-Inducible Factor 1, alpha Subunitlong non-coding RNA SNHG1, humanRNA, Long NoncodingVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVEGFA protein, humanHIF-1α/VEGFHypoxiaLncRNA SNHG1Vascular endothelial cell

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Read underepoch 390

Registered trials

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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.