Evidence map›Paper›PMID 21330660›Full record

ArticleInvestigative ophthalmology & visual science2011

Impaired epithelial wound healing and EGFR signaling pathways in the corneas of diabetic rats.

Keping Xu, Fu-Shin X Yu

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.

  1. Pooled it
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  7. A c-Cbl/Cbl-b antagonist inhibits EGFR ubiquitylation and sustains EGFR phosphorylation to enhance corneal re-epithelialization.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  14. IFITM1/OVOL1 Axis Is a Novel Regulator of the Expansion of the Limbal Epithelial Stem/Early Transient Amplifying Cell Population.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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29 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Keping XuDepartments of Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan.
Fu-Shin X Yu
Wayne State University · US

Funding

MOLECULAR REGULATION OF CORNEAL WOUND HEALINGR01EY010869 · NEI · WAYNE STATE UNIVERSITY · PI YU, FU-SHIN X · 1995 to 2023
$7.7M
Mechanisms of flagellin-induced protection against microbial keratitisR01EY017960 · NEI · WAYNE STATE UNIVERSITY · PI YU, FU-SHIN X · 2008 to 2020
$4.8M
NEI NIH HHS EY17960NEI NIH HHS R01 EY010869NEI NIH HHS R01 EY017960NEI NIH HHS R01EY10869
6 · The paper itself

Abstract

PURPOSE. The purpose of the study was to investigate the effects of hyperglycemia on EGFR (epidermal growth factor receptor)-mediated wound response and signal transduction in the corneal epithelium of rats with type I diabetes mellitus (DM). METHODS. Corneal epithelia were removed from streptozotocin (STZ)- and weight-matched normal rats. Wound healing was monitored by fluorescein staining at 24 or 48 hours after epithelial debridement. Phosphorylation of EGFR, AKT, ERK, and BAD was determined by Western blot analysis. The distribution of phospho-AKT and proliferating cell nuclear antigen (PCNA) in rat corneas was examined by immunohistochemistry. Cell death was evaluated by TUNEL staining. RESULTS. A significant delay in corneal epithelial wound healing was observed 48 hours after wounding in the diabetic rats compared with the weight-matched control rats. In the DM rat corneas, epithelial cells demonstrated diminished responses to wounding, as assessed by the phosphorylation of EGFR and its downstream signaling molecules, AKT and ERK. Furthermore, although the distribution pattern of phospho-AKT suggested a role for AKT in epithelial migration and proliferation in the normoglycemic rat corneas, it was abrogated in the healing epithelia of the DM rats. Consistent with impaired AKT activity, the number of PCNA-stained cells was also greatly reduced in the healing corneas of the diabetic rats. Finally, decreases in pBAD (Ser(136) and Ser(112)) and increases in TUNEL-positive cells were observed in both the uninjured and healing corneal epithelia of the DM rats, but not of the control rats. CONCLUSIONS. In the corneas of SZT rats, EGFR-PI3K-AKT and ERK, as well as their downstream BAD signaling pathways in migratory epithelium, were altered, resulting in increased apoptosis, decreased cell proliferation, and delayed wound closure.

Indexed as

Animalsbcl-Associated Death ProteinBlotting, WesternCorneal DiseasesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Epithelium, CornealErbB ReceptorsExtracellular Signal-Regulated MAP KinasesImmunohistochemistryIn Situ Nick-End LabelingMalePhosphorylationProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-aktRatsBad protein, ratbcl-Associated Death ProteinEgfr protein, ratErbB ReceptorsExtracellular Signal-Regulated MAP KinasesProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-akt

Identifiers

PMID21330660
PMCPMC3109029
OpenAlexW2049270721

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.