Evidence map›Paper›PMID 33875793›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

LncRNA GAS5 activates the HIF1A/VEGF pathway by binding to TAF15 to promote wound healing in diabetic foot ulcers.

Wei-Xia Peng, Pei-Xiang He, Li-Jun Liu, Ting Zhu, Ya-Qin Zhong, Lin Xiang, Ke Peng, Jing-Jin Yang, Guang-Da Xiang

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Targeting Signalling Pathways in Chronic Wound Healing.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Wei-Xia PengThe First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, PR China.
Pei-Xiang HeDepartment of Endocrine, Yiyang Central Hospital, Yiyang, Hunan, PR China.
Li-Jun LiuDepartment of Endocrine, Yiyang Central Hospital, Yiyang, Hunan, PR China.
Ting ZhuDepartment of Endocrine, Yiyang Central Hospital, Yiyang, Hunan, PR China.
Ya-Qin ZhongDepartment of Endocrine, Yiyang Central Hospital, Yiyang, Hunan, PR China.
Lin XiangDepartment of Endocrine, Central Theater General Hospital of PLA, Wuhan, Hubei, PR China.
Ke PengDepartment of Endocrine, Yiyang Central Hospital, Yiyang, Hunan, PR China.
Jing-Jin YangDepartment of Endocrine, Huaihua First People's Hospital, Huaihua, Hunan, PR China.
Guang-Da XiangThe First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, PR China. xianggdd015@163.com.
Central Hospital of Wuhan · CNHuaian First People’s Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A diabetic foot ulcer (DFU) is one of the most devastating complications of diabetes. It has been reported that lncRNA GAS5 plays a vital role in wound healing in DFUs. However, the specific mechanism remains unclear. In this research, we aimed to investigate the role of GAS5 in wound healing in DFUs as well as the underlying mechanism. qPCR or western blotting was performed to measure the expression levels of GAS5, HIF1A, VEGF and TAF15. CCK-8 or EdU assays, flow cytometry, wound healing assays and tube formation assays were carried out to assess the proliferation, apoptosis, wound healing and in vitro angiogenesis of HUVECs, respectively. RNA pull-down and RIP assays were performed to verify the interaction between GAS5 and TAF15. ChIP and luciferase assays were conducted to verify the binding of TAF15 to the HIF1A promoter. In the DFU mouse model, H&E and Masson staining were used to determine epidermal and dermal thickness and collagen formation. GAS5 and HIF1A were downregulated in the skin tissues of DFU patients, and GAS5 overexpression promoted cell proliferation, wound healing and tubule formation in HG-treated HUVECs. In addition, GAS5 facilitated HIF1A expression by interacting with TAF15. Rescue assays demonstrated that the suppression of HIF1A/VEGF pathway activation partially reversed the functional roles of GAS5 in HUVECs. Furthermore, GAS5 accelerated wound healing by activating the HIF1A/VEGF pathway in mice with DFUs. GAS5 activates the HIF1A/VEGF pathway by binding to TAF15, resulting in accelerated wound healing in DFUs. Our findings may provide a theoretical basis for the clinical treatment of DFUs.

Indexed as

RNA, Long NoncodingTATA-Binding Protein Associated FactorsAdultAgedAnimalsCell ProliferationCells, CulturedDiabetic FootDisease Models, AnimalFemaleHumansHuman Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMiddle AgedGAS5 long non-coding RNA, humanHypoxia-Inducible Factor 1, alpha Subunitlong non-coding RNA GAS5, mouseRNA, Long NoncodingTAF15 protein, humanTAF15 protein, mouseTATA-Binding Protein Associated FactorsVascular Endothelial Growth Factor A

Identifiers

PMID33875793
OpenAlexW3154209020

What OpenQuestion holds

Textmetadata
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.