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      • Record: found
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      Human Corneal Endothelial Cells Expanded In Vitro Are a Powerful Resource for Tissue Engineering

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          Abstract

          Human corneal endothelial cells have two major functions: barrier function mediated by proteins such as ZO-1 and pump function mediated by Na-K-ATPase which help to maintain visual function. However, human corneal endothelial cells are notorious for their limited proliferative capability in vivo and are therefore prone to corneal endothelial dysfunction that eventually may lead to blindness. At present, the only method to cure corneal endothelial dysfunction is by transplantation of a cadaver donor cornea with normal corneal endothelial cells. Due to the global shortage of donor corneas, it is vital to engineer corneal tissue in vitro that could potentially be transplanted clinically. In this review, we summarize the advances in understanding the behavior of human corneal endothelial cells, their current engineering strategy in vitro and their potential applications.

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          Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.

          In-kyung Park, Dalong Qian, Mark J. Kiel … (2003)
          A central issue in stem cell biology is to understand the mechanisms that regulate the self-renewal of haematopoietic stem cells (HSCs), which are required for haematopoiesis to persist for the lifetime of the animal. We found that adult and fetal mouse and adult human HSCs express the proto-oncogene Bmi-1. The number of HSCs in the fetal liver of Bmi-1-/- mice was normal. In postnatal Bmi-1-/- mice, the number of HSCs was markedly reduced. Transplanted fetal liver and bone marrow cells obtained from Bmi-1-/- mice were able to contribute only transiently to haematopoiesis. There was no detectable self-renewal of adult HSCs, indicating a cell autonomous defect in Bmi-1-/- mice. A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice. Expression of p16Ink4a and p19Arf in normal HSCs resulted in proliferative arrest and p53-dependent cell death, respectively. Our results indicate that Bmi-1 is essential for the generation of self-renewing adult HSCs.
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            The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus.

            J J Jacobs, K. Kieboom, S. Marino … (1999)
            The bmi-1 gene was first isolated as an oncogene that cooperates with c-myc in the generation of mouse lymphomas. We subsequently identified Bmi-1 as a transcriptional repressor belonging to the mouse Polycomb group. The Polycomb group comprises an important, conserved set of proteins that are required to maintain stable repression of specific target genes, such as homeobox-cluster genes, during development. In mice, the absence of bmi-1 expression results in neurological defects and severe proliferative defects in lymphoid cells, whereas bmi-1 overexpression induces lymphomas. Here we show that bmi-1-deficient primary mouse embryonic fibroblasts are impaired in progression into the S phase of the cell cycle and undergo premature senescence. In these fibroblasts and in bmi-1-deficient lymphocytes, the expression of the tumour suppressors p16 and p19Arf, which are encoded by ink4a, is raised markedly. Conversely, overexpression of bmi-1 allows fibroblast immortalization, downregulates expression of p16 and p19Arf and, in combination with H-ras, leads to neoplastic transformation. Removal of ink4a dramatically reduces the lymphoid and neurological defects seen in bmi-1-deficient mice, indicating that ink4a is a critical in vivo target for Bmi-1. Our results connect transcriptional repression by Polycomb-group proteins with cell-cycle control and senescence.
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              Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation.

              Anna V. Molofsky, Ricardo Pardal, Toshihide Iwashita … (2003)
              Stem cells persist throughout life by self-renewing in numerous tissues including the central and peripheral nervous systems. This raises the issue of whether there is a conserved mechanism to effect self-renewing divisions. Deficiency in the polycomb family transcriptional repressor Bmi-1 leads to progressive postnatal growth retardation and neurological defects. Here we show that Bmi-1 is required for the self-renewal of stem cells in the peripheral and central nervous systems but not for their survival or differentiation. The reduced self-renewal of Bmi-1-deficient neural stem cells leads to their postnatal depletion. In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation. p16Ink4a deficiency partially reverses the self-renewal defect in Bmi-1-/- neural stem cells. This conserved requirement for Bmi-1 to promote self-renewal and to repress p16Ink4a expression suggests that a common mechanism regulates the self-renewal and postnatal persistence of diverse types of stem cell. Restricted neural progenitors from the gut and forebrain proliferate normally in the absence of Bmi-1. Thus, Bmi-1 dependence distinguishes stem cell self-renewal from restricted progenitor proliferation in these tissues.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Med Sci
                Journal ID (iso-abbrev): Int J Med Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Medical Sciences
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1449-1907
                Publication date Collection: 2017
                Publication date (Electronic): 7 February 2017
                Volume: 14
                Issue: 2
                Pages: 128-135
                Affiliations
                [1 ]Department of Ophthalmology, Yan' An Hospital of Kunming City, Kunming, 650051, China;
                [2 ]Department of Ophthalmology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China;
                [3 ]Department of Ophthalmology, the Second People's Hospital of Yunnan Province, Kunming, 650021, China;
                [4 ]Public Health, the University of Arizona, Tucson, Arizona, 85709, USA;
                [5 ]Research and Development Department, TissueTech, Inc., 7000 SW 97th Avenue, Suite 212, Miami, FL 33173, USA;
                [6 ]Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China;
                [7 ]Shenzhen Eye Hospital, School of Optometry & Ophthalmology of Shenzhen University, Shenzhen Key Laboratory of Department of Ophthalmology, Shenzhen, 518000, China.
                Author notes
                ✉ Corresponding author: Ping Guo: Shenzhen Eye Hospital, Zetian Road 18, Room 421, Futian District, Shenzhen, 518000, China. Tel 08613924659029; Fax 08675523959500; Email: 2607212858@ 123456qq.com

                * These authors contributed equally to this manuscript.

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: ijmsv14p0128
                DOI: 10.7150/ijms.17624
                PMC ID: 5332841
                PubMed ID: 28260988
                SO-VID: e9117f85-7e39-4579-ba77-9a65904bfb9d
                Copyright © © Ivyspring International Publisher
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 18 September 2016
                Date accepted : 28 December 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Medicine
                Keywords: cornea,endothelial,progenitor,regenerative medical application.
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: cornea, endothelial, progenitor, regenerative medical application.

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