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      Influence of Biochemical Cues in Human Corneal Stromal Cell Phenotype

      1 , 2 , 1 , 2
      Current Eye Research
      Informa UK Limited

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          Abstract

          To identify biochemical cues that could promote a keratocyte-like phenotype in human corneal stromal cells that had become fibroblastic when expanded in serum-supplemented media while also examining the effect on cell proliferation and migration.

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          Most cited references41

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          Transcriptional control by the TGF-beta/Smad signaling system.

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            Keratocyte and fibroblast phenotypes in the repairing cornea.

            M. Fini (1999)
            In mammals, tissue damage is usually repaired by activation of a fibrotic response which saves the life of the organism, but which can never restore function to the damaged organ. In addition, fibrotic responses form the basis for diverse pathologies, including many that occur in the eye. It is intriguing, therefore, to observe the occasional circumstances in which repair in mammals appears to take on a regenerative character, such as during fetal wound healing or in certain types of corneal wounds. The thesis of this chapter is that the choice between regeneration or fibrosis lies in the control of fibroblast phenotype. The cornea of the eye has several features which make it a particularly useful model for the study of fibroblast phenotype. Studies discussed herein, identify failure to activate the transcription factor NF-kappaB as a control mechanism for inhibiting fibroblast activation in the cornea. Evidence is further presented for the view that transition in fibroblast phenotype in repair tissue is not simply a matter of differential gene expression, but is a developmental event which reflects changes in the hard wiring of signalling pathways by which the cell responds to environmental input.
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              Myofibroblasts differentiate from fibroblasts when plated at low density.

              Myofibroblasts, defined by their expression of smooth muscle alpha-actin, appear at corneal and dermal incisions and promote wound contraction. We report here that cultured fibroblasts differentiate into myofibroblasts by a cell density-dependent mechanism. Fibroblasts seeded at low density (5 cells per mm2) produced a cell culture population consisting of 70-80% myofibroblasts, 5-7 days after seeding. In contrast, fibroblasts seeded at high density (500 cells per mm2) produced cultures with only 5-10% myofibroblasts. When the myofibroblast-enriched cultures were subsequently passaged at high density, the smooth muscle alpha-actin phenotype was lost within 3 days. Furthermore, initially 60% of the low density-cultured cells incorporated BrdUrd compared to 30% of cells passaged at high density. Media from myofibroblast-enriched cultures had more latent and active transforming growth factor beta (TGF-beta) than did media from fibroblast-enriched cultures. Although there was a trend towards increased numbers of myofibroblasts after addition of exogenous TGF-beta, the results did not reach statistical significance. We conclude that myofibroblast differentiation can be induced in fibroblasts by plating at low density. We propose a cell density-dependent model of myofibroblast differentiation during wounding and healing in which at least two factors interact: loss of cell contact and the presence of TGF-beta.
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                Author and article information

                Journal
                Current Eye Research
                Current Eye Research
                Informa UK Limited
                0271-3683
                1460-2202
                October 22 2018
                February 2019
                October 29 2018
                February 2019
                : 44
                : 2
                : 135-146
                Affiliations
                [1 ] Department of Mechanical and Manufacturing Engineering, School of Engineering, Trinity College Dublin, University of Dublin, Dublin, Ireland
                [2 ] Trinity Centre for Bioengineering, Trinity Biomedical Science Institute, Trinity College Dublin, University of Dublin, Dublin, Ireland
                Article
                10.1080/02713683.2018.1536216
                30335528
                57105189-a957-4a0c-91d0-274948098675
                © 2019
                History

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