ArticleInvestigative ophthalmology & visual science2009
Role of cPKCalpha and nPKCepsilon in EGF-stimulated goblet cell proliferation.
Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
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- Signaling Pathways Used by the Specialized Pro-Resolving Mediator Maresin 2 Regulate Goblet Cell Function: Comparison with Maresin 1.International journal of molecular sciences · 2022Article
- Conjunctival epithelial and goblet cell function in chronic inflammation and ocular allergic inflammation.Current opinion in allergy and clinical immunology · 2014Review
- Tear film mucins: front line defenders of the ocular surface; comparison with airway and gastrointestinal tract mucins.Experimental eye research · 2013Article
- Role of PKCα activation of Src, PI-3K/AKT, and ERK in EGF-stimulated proliferation of rat and human conjunctival goblet cells.Investigative ophthalmology & visual science · 2013Article
- Effect of VIP on intracellular [Ca2+], extracellular regulated kinase 1/2, and secretion in cultured rat conjunctival goblet cells.Investigative ophthalmology & visual science · 2013Article
- Signaling pathways used by EGF to stimulate conjunctival goblet cell secretion.Experimental eye research · 2012Article
- Cholinergic agonists activate P2X7 receptors to stimulate protein secretion by the rat lacrimal gland.Investigative ophthalmology & visual science · 2011Article
- Significance of lipid mediators in corneal injury and repair.Journal of lipid research · 2010Review
- Protein kinase C{gamma} mediates regulation of proliferation by the serotonin 5-hydroxytryptamine receptor 2B.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
purposeThe authors determined the role of the protein kinase C (PKC) isoforms cPKCalpha and nPKCepsilon in EGF-stimulated proliferation of cultured rat and human conjunctival goblet cells.
methodsRat and human conjunctivas were minced, and goblet cells were allowed to grow. Passage 1 cells were serum starved for 24 to 48 hours and were incubated with the PKC inhibitors calphostin C and Gö 6983 (10(-10)-10(-7) M) for 20 minutes before stimulation with EGF (10(-7) M) for 24 hours. The presence and localization of PKC isoforms in cultured rat goblet cells were determined by Western blot analysis and immunofluorescence microscopy, respectively. Cultured rat goblet cells were serum starved and incubated with adenoviruses containing genes for dominant-negative cPKCalpha (Ad DNPKCalpha, 10(4) pfu), dominant-negative nPKCepsilon (Ad DNPKCepsilon, 10(4) pfu), and wild-type cPKCalpha (Ad WTPKCalpha, 10(7) pfu), and proliferation was measured.
resultsIn rat goblet cells, EGF-stimulated proliferation was completely inhibited by calphostin C, whereas Gö 6983 inhibited proliferation by 53%+/-15%. In human goblet cells, EGF-stimulated proliferation was completely inhibited by calphostin C. PKCalpha, -betaI, -betaII, -delta, -epsilon, -iota/lambda, -theta, -gamma, and -zeta were found in cultured rat goblet cells. Ad DNPKCalpha and Ad DNPKCepsilon inhibited EGF-stimulated proliferation in rat goblet cells by 78%+/-6% and 92%+/-8%, respectively. Incubation with Ad WTPKCalpha alone significantly increased proliferation.
conclusionscPKCalpha and nPKCepsilon play key roles in conjunctival goblet cell proliferation.
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