Evidence map›Paper›PMID 29053707›Full record

ArticlePloS one2017

High glucose augments angiotensinogen in human renal proximal tubular cells through hepatocyte nuclear factor-5.

Juan Wang, Yuki Shibayama, Hiroyuki Kobori, Ya Liu, Hideki Kobara, Tsutomu Masaki, Zhiyu Wang, Akira Nishiyama

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. SGLT2 inhibition effect on salt-induced hypertension, RAAS, and NaAmerican journal of physiology. Renal physiology · 2022
    Article
  6. Molecular Mechanisms of SGLT2 Inhibitor on Cardiorenal Protection.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
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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 at 2 institutions in 2 countries.

Juan WangDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Yuki ShibayamaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Hiroyuki KoboriDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Ya LiuDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Hideki KobaraDepartment of Gastroenterology and Neurology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Tsutomu MasakiDepartment of Gastroenterology and Neurology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Zhiyu WangDepartment of Immuno-oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
Akira NishiyamaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, Kagawa, Japan.ORCID http://orcid.org/0000-0001-5971-820X
Kagawa University · JPHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High glucose has been demonstrated to induce angiotensinogen (AGT) synthesis in the renal proximal tubular cells (RPTCs) of rats, which may further activate the intrarenal renin-angiotensin system (RAS) and contribute to diabetic nephropathy. This study aimed to investigate the effects of high glucose on AGT in the RPTCs of human origin and identify the glucose-responsive transcriptional factor(s) that bind(s) to the DNA sequences of AGT promoter in human RPTCs. Human kidney (HK)-2 cells were treated with normal glucose (5.5 mM) and high glucose (15.0 mM), respectively. Levels of AGT mRNA and AGT secretion of HK-2 cells were measured by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Consecutive 5'-end deletion mutant constructs and different site-directed mutagenesis products of human AGT promoter sequences were respectively transfected into HK-2 cells, followed by AGT promoter activity measurement through dual luciferase assay. High glucose significantly augmented the levels of AGT mRNA and AGT secretion of HK-2 cells, compared with normal glucose treatment. High glucose also significantly augmented AGT promoter activity in HK-2 cells transfected with the constructs of human AGT promoter sequences, compared with normal glucose treatment. Hepatocyte nuclear factor (HNF)-5 was found to be one of the glucose-responsive transcriptional factors of AGT in human RPTCs, since the mutation of its binding sites within AGT promoter sequences abolished the above effects of high glucose on AGT promoter activity as well as levels of AGT mRNA and its secretion. The present study has demonstrated, for the first time, that high glucose augments AGT in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy.

Indexed as

AngiotensinogenAnimalsCell LineEnzyme-Linked Immunosorbent AssayForkhead Box Protein M1GlucoseHumansKidney Tubules, ProximalPromoter Regions, GeneticRatsRNA, MessengerTranscription FactorsAngiotensinogenForkhead Box Protein M1FOXM1 protein, humanGlucoseRNA, MessengerTranscription Factors

Identifiers

PMID29053707
PMCPMC5650141
OpenAlexW2767124076

What OpenQuestion holds

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LicenceCC BY
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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.