Evidence map›Paper›PMID 18421078›Full record

ArticleInvestigative ophthalmology & visual science2008

ERK/p44p42 mitogen-activated protein kinase mediates EGF-stimulated proliferation of conjunctival goblet cells in culture.

Marie A Shatos, Jian Gu, Robin R Hodges, Kameran Lashkari, Darlene A Dartt

Open access · greenAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2008. 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
1.7field-weighted citation impact, top 16% 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, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Lipoxin AMucosal immunology · 2017
    Article
  4. Lipoxin AScientific reports · 2016
    Article
  5. Protein kinases are potential targets to treat inflammatory bowel disease.World journal of gastrointestinal pharmacology and therapeutics · 2014
    Review
  6. Review
  7. Article
  8. Article
  9. Osmoprotective effects of supplemental epidermal growth factor in an ex vivo multilayered human conjunctival model under hyperosmotic stress.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2013
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Role of cPKCalpha and nPKCepsilon in EGF-stimulated goblet cell proliferation.Investigative ophthalmology & visual science · 2009
    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

5 authors at 1 institution in 1 country.

Marie A ShatosDepartment of Ophthalmology, Shepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts 02114, USA.
Jian Gu
Robin R Hodges
Kameran Lashkari
Darlene A Dartt
Massachusetts Eye and Ear Infirmary · US

Funding

Conjunctival Goblet Cell Mucin Secretion in Inflammation and Its ResolutionR01EY019470 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI DARTT, DARLENE A · 2009 to 2023
$7.4M
CONTROL OF CONJUNCTIVAL GOBLET CELL MUCOUS PRODUCTIONR01EY009057 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI DARTT, DARLENE A · 1991 to 2009
$3.2M
NEI NIH HHS EY09577NEI NIH HHS R01 EY009057NEI NIH HHS R01 EY019470
6 · The paper itself

Abstract

purposeTo determine whether activation of the ERK pathway by EGF leads to rat and human goblet cell proliferation.

methodsThe conjunctiva was removed from male Sprague-Dawley rats. Human conjunctiva was removed during ocular surgery. The tissue was minced and goblet cells were grown. The cells were stimulated with EGF (10(-7) M) for 1 and 5 minutes and Western blot analysis was performed with an antibody against phosphorylated EGFR, to measure the activation of the EGF receptor (EGFR). The cells were incubated with EGF (10(-7) M) for 24 hours, and cell proliferation was measured by WST-8. Inhibitors were added either 20 minutes before EGF or 2 hours after. The cells were stimulated with EGF (10(-7) M) for 1 minute to 24 hours. The number of cells expressing phosphorylated ERK (pERK) in the nucleus and Ki-67 was determined by immunofluorescence.

resultsEGF increased the activation of EGFR in rat conjunctival goblet cells. EGF-stimulated proliferation was inhibited by the EGFR inhibitor AG1478 and the MEK inhibitor U0126 in rat and human cultured goblet cells. EGF caused the translocation of pERK to the nucleus in a biphasic manner. Inhibition of the second peak with U0126 prevented proliferation. EGF-stimulated goblet cells progressed through the cell cycle expressing pERK in the nucleus.

conclusionsEGF stimulated human and rat conjunctival goblet cell proliferation by activating the EGFR. EGFR stimulated ERK causing its biphasic translocation to the nucleus. The second peak response is responsible for cell proliferation, but the role of the first peak is not known.

Indexed as

AdultAgedAged, 80 and overAnimalsBlotting, WesternCell ProliferationCells, CulturedConjunctivaEpidermal Growth FactorErbB ReceptorsFemaleFluorescent Antibody Technique, IndirectGoblet CellsHumansKi-67 AntigenMaleEGFR protein, humanEgfr protein, ratEpidermal Growth FactorErbB ReceptorsKi-67 AntigenMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3

Identifiers

PMID18421078
PMCPMC2556860
OpenAlexW2007148542

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.