Evidence map›Paper›PMID 27009340›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen stimulation in renal proximal tubular cells.

Ryan O'Leary, Harrison Penrose, Kayoko Miyata, Ryousuke Satou

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Validity of mental and physical stress models.Neuroscience and biobehavioral reviews · 2024
    Review
  3. IL-6 and diabetic kidney disease.Frontiers in immunology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. The Role of Cytokines in Nephrotic Syndrome.Mediators of inflammation · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Ryan O'LearyDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Harrison PenroseDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Kayoko MiyataDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Ryousuke SatouDepartment of Physiology and Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana rsato@tulane.edu.ORCID 0000-0001-6505-9722
Tulane University · US

Funding

Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI HAMM, L LEE · 2012 to 2016
$5.8M
Histone deacetylase 9 is an epigenetic suppressor of intrarenal angiotensinogen, serving as a key mechanism in angiotensinogen augmentation in hypertensionR01DK107694 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI SATO, RYOSUKE · 2016 to 2020
$1.4M
NIDDK NIH HHS R01 DK107694NIGMS NIH HHS P30 GM103337
6 · The paper itself

Abstract

The development of ANG II-dependent hypertension involves increased infiltration of macrophages (MΦ) and T cells into the kidney and the consequent elevation of intrarenal cytokines including IL-6, which facilitates the progression of hypertension and associated kidney injury. Intrarenal renin-angiotensin system (RAS) activation, including proximal tubular angiotensinogen (AGT) stimulation, has also been regarded as a cardinal mechanism contributing to these diseases. However, the interaction between immune cells and intrarenal RAS activation has not been fully delineated. Therefore, the present study investigated whether ANG II-treated MΦ induce AGT upregulation in renal proximal tubular cells (PTCs). MΦ were treated with 0-10(-6) M ANG II for up to 48 h. PTCs were incubated with the collected medium from MΦ. In ANG II-treated MΦ, IL-6 mRNA and protein levels were increased (1.86 ± 0.14, protein level, ratio to control); moreover, IL-6 levels were higher than TNF-α and IL-1β in culture medium isolated from ANG II-treated MΦ. Elevated AGT expression (1.69 ± 0.04, ratio to control) accompanied by phosphorylated STAT3 were observed in PTCs that received culture medium from ANG II-treated MΦ. The addition of a neutralizing IL-6 antibody to the collected medium attenuated phosphorylation of STAT3 and AGT augmentation in PTCs. Furthermore, a JAK2 inhibitor also suppressed STAT3 phosphorylation and AGT augmentation in PTCs. These results demonstrate that ANG II-induced IL-6 elevation in MΦ enhances activation of the JAK-STAT pathway and consequent AGT upregulation in PTCs, suggesting involvement of an immune response in driving intrarenal RAS activity.

Indexed as

AngiotensinogenAnimalsCells, CulturedCulture Media, ConditionedHypertensionInterleukin-1betaInterleukin-6Janus KinasesKidney Tubules, ProximalMacrophagesMaleRatsReceptor, Angiotensin, Type 1STAT3 Transcription FactorTumor Necrosis Factor-alphaAngiotensinogenCulture Media, ConditionedInterleukin-1betaInterleukin-6Janus KinasesReceptor, Angiotensin, Type 1Stat3 protein, ratSTAT3 Transcription FactorTumor Necrosis Factor-alphaangiotensin IIangiotensinogeninterleukin-6macrophagerenin-angiotensin system

Identifiers

PMID27009340
PMCPMC4983453
OpenAlexW2396407599

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.