ArticleInvestigative ophthalmology & visual science2011
Human corneal endothelial cells employ phosphorylation of p27(Kip1) at both Ser10 and Thr187 sites for FGF-2-mediated cell proliferation via PI 3-kinase.
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 16 papers.
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16 citing papers in PubMed, 27 citations in OpenAlex.
- Human cathelicidin antimicrobial peptide LL-37 promotes lymphangiogenesis in lymphatic endothelial cells through the ERK and Akt signaling pathways.Molecular biology reports · 2020Article
- A fine-tuned β-catenin regulation during proliferation of corneal endothelial cells revealed using proteomics analysis.Scientific reports · 2020Article
- PTEN Inhibition Accelerates Corneal Endothelial Wound Healing through Increased Endothelial Cell Division and Migration.Investigative ophthalmology & visual science · 2020Article
- The myristoylated alanine-rich C kinase substrate differentially regulates kinase interacting with stathmin in vascular smooth muscle and endothelial cells and potentiates intimal hyperplasia formation.Journal of vascular surgery · 2019Article
- Fibroblast growth factor 2 induces proliferation and fibrosis via SNAI1-mediated activation of CDK2 and ZEB1 in corneal endothelium.The Journal of biological chemistry · 2018Article
- Ribonuclease 5 facilitates corneal endothelial wound healing via activation of PI3-kinase/Akt pathway.Scientific reports · 2016Article
- CRM-1 knockdown inhibits extrahepatic cholangiocarcinoma tumor growth by blocking the nuclear export of p27Kip1.International journal of molecular medicine · 2016Article
- WNT10B enhances proliferation through β-catenin and RAC1 GTPase in human corneal endothelial cells.The Journal of biological chemistry · 2015Article
- Substrates for Expansion of Corneal Endothelial Cells towards Bioengineering of Human Corneal Endothelium.Journal of functional biomaterials · 2015Review
- Article
- Interleukin-1β-induced Wnt5a enhances human corneal endothelial cell migration through regulation of Cdc42 and RhoA.Molecular and cellular biology · 2014Article
- Interleukin-1β enhances cell migration through AP-1 and NF-κB pathway-dependent FGF2 expression in human corneal endothelial cells.Biology of the cell · 2013Article
- Corneal endothelial expansion promoted by human bone marrow mesenchymal stem cell-derived conditioned medium.PloS one · 2013Article
- ROCK inhibitor enhances adhesion and wound healing of human corneal endothelial cells.PloS one · 2013Article
- NF-κB is the transcription factor for FGF-2 that causes endothelial mesenchymal transformation in cornea.Investigative ophthalmology & visual science · 2012Article
- Research progress on the negative factors of corneal endothelial cells proliferation.International journal of ophthalmology · 2012Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeFGF-2 stimulates cell proliferation of rabbit corneal endothelial cells (rCECs) by degrading the cyclin-dependent kinase inhibitor p27(Kip1) (p27) through its phosphorylation mechanism. The authors investigated whether the cell proliferation of human CECs (hCECs) is also induced by FGF-2 stimulation through the p27 phosphorylation pathway.
methodsExpression and activation of protein were analyzed by immunoblotting. Cell proliferation was measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Transfection of hCECs with small interference RNA (siRNA) was performed using a transfection reagent.
resultsFGF-2 stimulated cell proliferation in hCECs; the FGF-2 action was completely blocked by pathway-specific inhibitors for PI 3-kinase (LY294002) and MEK1/2 (U0126), respectively. Using immunoblotting, the authors showed that FGF-2 induced phosphorylation of p27 at both serine 10 (Ser10) and threonine 187 (Thr187) sites. These effects were also completely blocked by LY294002 or U0126. The authors then determined cross-talk between PI 3-kinase and extracellular signal-regulated kinase (ERK)1/2; blocking of ERK1/2 activation by LY294002 indicated that in hCECs ERK1/2 works as a downstream effector to PI 3-kinase for cell proliferation induced by FGF-2, whereas the ERK1/2 pathway in rCECs is parallel to the PI 3-kinase pathway. However, the downstream mechanism involved in cell cycle progression in hCECs is identical to that of rCECs: phosphorylation of p27 at Ser10 was mediated by kinase-interacting stathmin (KIS), confirmed with siRNA to KIS, and phosphorylation of p27 at Thr187 was mediated by cell division cycle 25A (Cdc25A), confirmed using Cdc25A inhibitor. CONCLUSIONS; FGF-2 stimulates proliferation of hCECs through PI 3-kinase and its downstream target ERK1/2 pathways. This linear signal transduction significantly downregulates p27 through its phosphorylation at both Ser10 and Thr187 sites mediated by KIS and Cdc25A, respectively.
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