Evidence map›Paper›PMID 21780115›Full record

ArticleJournal of cellular physiology2012

Src family kinases regulate renal epithelial dedifferentiation through activation of EGFR/PI3K signaling.

Shougang Zhuang, Meili Duan, Yan Yan

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. International journal of nanomedicine · 2026
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  5. Review
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  9. Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.International journal of biological sciences · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. A look at transactivation of the EGF receptor by angiotensin II.Journal of the American Society of Nephrology : JASN · 2012
    Article
  14. Article
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

3 authors at 3 institutions in 2 countries.

Shougang ZhuangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China. szhuang@lifespan.org
Meili Duan
Yan Yan
Beijing Friendship Hospital · CNMedical University of South Carolina · USShanghai East Hospital · CN

Funding

Histone deacetylases as novel therapeutic targets for kidney fibrosisR01DK085065 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2010 to 2017
$2.8M
Dedifferentiation Following Renal Cell InjuryR01DK071997 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2006 to 2009
$1.1M
NIDDK NIH HHS DK-071997NIDDK NIH HHS DK-085065NIDDK NIH HHS R01 DK071997NIDDK NIH HHS R01 DK085065
6 · The paper itself

Abstract

Dedifferentiation, a process by which differentiated cells become mesenchymal-like proliferating cells, is the first step in renal epithelium repair and occurs in vivo after acute kidney injury and in vitro in primary culture. However, the underlying mechanism remains poorly understood. In this report, we studied the signaling events that mediate dedifferentiation of proximal renal tubular cells (RPTC) in primary culture. RPTC dedifferentiation characterized by increased expression of vimentin concurrent with decreased expression of cytokeratin-18 was observed at 24 h after the initial plating of freshly isolated proximal tubules and persisted for 72 h. At 96 h, RPTC started to redifferentiate as revealed by reciprocal expression of cytokeratin-18 and vimentin and completed at 120 h. Phosphorylation levels of Src, epidermal growth factor receptor (EGFR), AKT (a target of phosphoinositide-3-kinase (PI3K)), and ERK1/2 were increased in the early time course of culture (<72 h). Inhibition of Src family kinases (SFKs) with PP1 blocked EGFR, AKT, and ERK1/2 phosphorylation, as well as RPTC dedifferentiation. Inhibition of EGFR with AG1478 also blocked AKT and ERK1/2 phosphorylation and RPTC dedifferentiation. Although inactivation of the PI3K/AKT pathway with LY294002 inhibited RPTC dedifferentiation, blocking the ERK1/2 pathway with U0126 did not show such an effect. Moreover, inhibition of SFKs, EGFR, PI3K/AKT, but not ERK1/2 pathways abrogated RPTC outgrowth and SFK inhibition decreased RPTC proliferation and migration. These findings demonstrate a critical role of SFKs in mediating RPTC dedifferentiation through activation of the EGFR/PI3K signaling pathway.

Indexed as

AnimalsCell DedifferentiationCell MovementCell ProliferationCells, CulturedEpithelial CellsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesKidney Tubules, ProximalMiceProto-Oncogene Proteins c-aktSignal Transductionsrc-Family KinasesErbB ReceptorsExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktsrc-Family Kinases

Identifiers

PMID21780115
PMCPMC4559864
OpenAlexW2070389970

What OpenQuestion holds

Textmetadata
LicenceTDM
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.