For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
5
views
37
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      635
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Bradykinin potentially stimulates cell proliferation in rabbit corneal endothelial cells through the ZO-1/ZONAB pathway

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Bradykinin (BK) has been demonstrated to induce proliferation in several types of cell in ex vivo corneas. However, the mechanisms underlying the action of BK on corneal endothelial cells (CECs) remain largely unknown. The present study aimed to investigate the effect of BK on rabbit corneal endothelial cell (RCEC) proliferation, and assess the involvement of the zonula occludens-1(ZO-1)/ZO-1associated nucleic acid binding protein (ZONAB) pathway. Cell proliferation and cell cycle distribution was analyzed following treatment with BK (0.01, 0.1,1.0 or 10.0 µM) for the indicated time intervals (24, 48, 72 and 96 h), or following BK treatment combined with transfection of ZONAB-small interfering (si)RNA for 72 h. In addition, the expression of tight junction ZO-1, nuclear ZONAB, proliferating cell nuclear antigen(PCNA) and cyclin D1 were evaluated using western blotting or immunofluorescence. BK treatment was demonstrated to induce time- and concentration-dependent cell proliferation and cell cycle progression, along with the upregulation of tight junction ZO-1 and nuclear ZONAB, as well as PCNA and cyclin D1 protein expression. Furthermore, knockdown with ZONAB-siRNA inhibited cell proliferation, induced cell cycle arrest and downregulated PCNA and cyclin D1 protein expression. ZONAB knockdown therefore successfully reversed the increase in proliferation induced by BK treatment. Taken together, these results suggested that BK stimulated RCEC proliferation, potentially via the ZO-1/ZONAB pathway. The signaling paradigm disclosed in the present study potentially serves as an important therapeutic target for cornea regeneration and transplantation.

          Related collections

          Most cited references37

          • Record: found
          • Abstract: found
          • Article: not found

          Cyclin D1, cancer progression, and opportunities in cancer treatment.

          Shuo Qie, J. Diehl (2016)
          Mammalian cells encode three D cyclins (D1, D2, and D3) that coordinately function as allosteric regulators of cyclin-dependent kinase 4 (CDK4) and CDK6 to regulate cell cycle transition from G1 to S phase. Cyclin expression, accumulation, and degradation, as well as assembly and activation of CDK4/CDK6 are governed by growth factor stimulation. Cyclin D1 is more frequently dysregulated than cyclin D2 or D3 in human cancers, and as such, it has been more extensively characterized. Overexpression of cyclin D1 results in dysregulated CDK activity, rapid cell growth under conditions of restricted mitogenic signaling, bypass of key cellular checkpoints, and ultimately, neoplastic growth. This review discusses cyclin D1 transcriptional, translational, and post-translational regulations and its biological function with a particular focus on the mechanisms that result in its dysregulation in human cancers.
          Article 0 comments Cited 258 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Central corneal endothelial cell changes over a ten-year period.

            Michael W. Bourne, D Hodge, Randall L. Nelson (1997)
            To obtain longitudinal data to estimate long-term morphometric changes in normal human corneal endothelia. Ten years after an initial study, the authors rephotographed the central corneal endothelium of 52 normal subjects with the same contact specular microscope. The findings for the 10 subjects younger than 18 years of age at the initial examination were considered separately. For the remaining 42 adult subjects, the time between examinations averaged 10.6 +/- 0.2 years (range, 10.1 to 11 years). At the recent examination, these subjects' ages averaged 59.5 +/- 16.8 years (range, 30 to 84 years). Outlines of 100 cells for each cornea were digitized. For the 42 adult subjects, the mean endothelial cell density decreased during the 10.6-year interval from 2715 +/- 301 cells/mm2 to 2539 +/- 284 cells/mm2 (P < 0.001). The calculated exponential cell loss rate over this interval was 0.6% +/- 0.5% per year. There was no statistically significant correlation between cell loss rate and age. During the 10.6-year interval, the coefficient of variation of cell area increased from 0.26 +/- 0.05 to 0.29 +/- 0.06 (P < 0.001), and the percentage of hexagonal cells decreased from 67% +/- 8% to 64% +/- 6% (P = 0.003). For the 10 subjects 5 to 15 years of age at the initial examination, the exponential cell loss rate was 1.1% +/- 0.8% per year. Human central endothelial cell density decreases at an average rate of approximately 0.6% per year in normal corneas throughout adult life, with gradual increases in polymegethism and pleomorphism.
            Article 0 comments Cited 130 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The ZO-1–associated Y-box factor ZONAB regulates epithelial cell proliferation and cell density

              Maria Balda, Michelle Garrett, Karl Matter (2003)
              Epithelial tight junctions regulate paracellular permeability, restrict apical/basolateral intramembrane diffusion of lipids, and have been proposed to participate in the control of epithelial cell proliferation and differentiation. Previously, we have identified ZO-1–associated nucleic acid binding proteins (ZONAB), a Y-box transcription factor whose nuclear localization and transcriptional activity is regulated by the tight junction–associated candidate tumor suppressor ZO-1. Now, we found that reduction of ZONAB expression using an antisense approach or by RNA interference strongly reduced proliferation of MDCK cells. Transfection of wild-type or ZONAB-binding fragments of ZO-1 reduced proliferation as well as nuclear ZONAB pools, indicating that promotion of proliferation by ZONAB requires its nuclear accumulation. Overexpression of ZONAB resulted in increased cell density in mature monolayers, and depletion of ZONAB or overexpression of ZO-1 reduced cell density. ZONAB was found to associate with cell division kinase (CDK) 4, and reduction of nuclear ZONAB levels resulted in reduced nuclear CDK4. Thus, our data indicate that tight junctions can regulate epithelial cell proliferation and cell density via a ZONAB/ZO-1–based pathway. Although this regulatory process may also involve regulation of transcription by ZONAB, our data suggest that one mechanism by which ZONAB and ZO-1 influence proliferation is by regulating the nuclear accumulation of CDK4.
              Article 0 comments Cited 93 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Med
                Journal ID (iso-abbrev): Int. J. Mol. Med
                Journal ID (publisher-id): IJMM
                Title: International Journal of Molecular Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1107-3756
                ISSN (Electronic): 1791-244X
                Publication date (Print): July 2018
                Publication date (Electronic): 22 March 2018
                Publication date PMC-release: 22 March 2018
                Volume: 42
                Issue: 1
                Pages: 71-80
                Affiliations
                [1 ]Department of Ophthalmology, The First Affiliated Hospital of University of South China
                [2 ]Medical College, University of South China, Hengyang, Hunan 421001
                [3 ]Department of Ophthalmology, The First Affiliated Hospital of Nanchang University, Jiangxi Province Clinical Ophthalmology Institute, Nanchang, Jiangxi 330006
                [4 ]Department of Cardiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China
                Author notes
                Correspondence to: Professor Gang Tan, Department of Ophthalmology, The First Affiliated Hospital of University of South China, 69 Chuanshan Road, Hengyang, Hunan 421001, P.R. China, E-mail: tangang99@ 123456hotmail.com
                [*]

                Contributed equally

                Article
                Publisher ID: ijmm-42-01-0071
                DOI: 10.3892/ijmm.2018.3580
                PMC ID: 5979832
                PubMed ID: 29568941
                SO-VID: 826a471f-d6ef-47c7-845f-5bac68c7fedb
                Copyright © Copyright: © He et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 27 October 2017
                Date accepted : 05 March 2018
                Categories
                Subject: Articles

                Keywords: bradykinin,zonula occludens-1,zo-1-associated nucleic-acid-binding protein,corneal endothelial cells,proliferation
                Data availability:
                Keywords: bradykinin, zonula occludens-1, zo-1-associated nucleic-acid-binding protein, corneal endothelial cells, proliferation

                Comments

                Comment on this article