Evidence map›Paper›PMID 27957415›Full record

ArticleKidney research and clinical practice2016

The role of local IL6/JAK2/STAT3 signaling in high glucose-induced podocyte hypertrophy.

Hyung Ah Jo, Joo-Young Kim, Seung Hee Yang, Seung Seok Han, Kwon Wook Joo, Yon Su Kim, Dong Ki Kim

Open access · diamondAbstract read
In one paragraph

Article in Kidney research and clinical practice, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

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  11. Targeting inerleukin-6 for renoprotection.Frontiers in immunology · 2024
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  15. JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023
    Review
  16. The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy.International journal of nephrology and renovascular disease · 2023
    Review
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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

7 authors at 2 institutions in 1 country.

Hyung Ah JoDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
Joo-Young KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
Seung Hee YangKidney Research Institute, Seoul National University, Seoul, Korea.
Seung Seok HanDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
Kwon Wook JooDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea; Kidney Research Institute, Seoul National University, Seoul, Korea.
Yon Su KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea; Kidney Research Institute, Seoul National University, Seoul, Korea.
Dong Ki KimDepartment of Internal Medicine, Seoul National University Hospital, Seoul, Korea; Kidney Research Institute, Seoul National University, Seoul, Korea.
Seoul National University Hospital · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterleukin-6 (IL6) is an important regulator of cellular hypertrophy through the gp130/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. We tested the hypothesis that IL6 and its downstream gp130/JAK2/STAT3 pathway participated in high glucose (HG)-induced podocyte hypertrophy.

methodsIL6 levels in the media and lysates of podocytes were measured by enzyme-linked immunosorbent assay. Western blots were performed to determine the protein expression levels of gp130/JAK2/STAT3 among podocytes cultured with normal glucose (NG), NG + mannitol, NG + recombinant IL6, HG, and HG + IL6-neutralizing antibodies (IL6NAb). Immunoprecipitation was examined to determine whether gp130 interacted with JAK2 in response to HG or IL6. Podocyte hypertrophy was verified using protein/cell counts and flow cytometry.

resultsIL6 levels were significantly increased in the media and lysates of podocytes cultured in HG compared with the NG groups. The nuclear phospho-STAT3/STAT3 ratio was increased by HG and NG + IL6 and was attenuated in the HG + IL6NAb groups, indicating that nuclear STAT3 was activated following JAK2 and cytosolic STAT3 activation in response to IL6 secreted by HG-stimulated podocytes. Immunoprecipitation showed increased phospho-JAK2 recruitment to gp130 in the HG and NG + IL6 groups, and the addition of IL6NAb in the HG group significantly abrogated these increases. Podocyte hypertrophy was significantly increased in the HG and NG + IL6 compared with the NG condition and was diminished by the addition of IL6NAbs to the HG group.

conclusionIL6 might play a prominent role in the local activation of JAK2/STAT3 in podocyte hypertrophy under HG conditions.

Indexed as

Diabetic nephropathyHypertrophyInterleukin-6JAK2/STAT3Podocytes

Identifiers

PMID27957415
PMCPMC5143438
OpenAlexW2520012370

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.