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      Arg-Gly-Asp-modified elastin-like polypeptide regulates cell proliferation and cell cycle proteins via the phosphorylation of Erk and Akt in pancreatic β-cell.

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          Abstract

          Objective

          Enhancement of β-cell proliferation plays an important role in maintaining β-cell mass and function, and in improving pancreatic β-cell survival before transplantation. Extracellular matrix (ECM) components increase the adhesion and proliferation of β-cells, and the RGD-modified elastin-like polypeptide (RGD-ELP, REP) has been described as a bioactive matrix. In this study, we investigated whether REP could enhance β-cell adhesion and proliferation and elucidated the signaling pathways involved.

          Methods

          We investigated the effect of REP on cell adhesion, proliferation and insulin secretion via assays using Rin-m and rat islets. Crystal violet, CCK-8, and BrdU assay, FACS, western blot, real time q-PCR analyses and insulin ELISA were examined. To explain the associated mechanisms, phosphorylation of Akt and extracellular signal-regulated kinase (Erk) were measured.

          Results

          REP more increased the adhesion, proliferation and survival of Rin-m cells compared to elastin-like poly peptide (ELP) without RGD-motif. The enhancement of β-cell proliferation by REP was associated with increased cyclin D1, cyclin D2 and cdk6, and decreased p27 levels. When β-cells were cultured on REP, Erk and the phosphatidylinositol 3-kinase (PI3-kinase) downstream effector, Akt was stimulated. Treatment with the Erk pathway inhibitor and PI3-kinase inhibitor decreased REP-induced β-cell adhesion and proliferation, and regulated REP-induced cell cycle proteins. Additionally, REP increased the mRNA and protein levels of insulin and its transcription factor, PDX-1, and insulin secretion.

          Conclusions

          Our results demonstrate that the up-regulation of the PI3K/Akt and Erk signaling pathways and the regulation of cell cycle proteins by REP could serve as effective strategies for improving pancreatic β-cell adhesion and proliferation.

          Abstract

          Tissue engineering; Biomedical materials; Cell biology; Biotechnology; Diabetes; Insulin; <beta>-cell adhesion; <beta>-cell proliferation; RGD-modified elastin-like polypeptide; Cell cycle

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          Most cited references33

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          Of extracellular matrix, scaffolds, and signaling: tissue architecture regulates development, homeostasis, and cancer.

          Celeste Nelson, Mina Bissell (2006)
          The microenvironment influences gene expression so that the behavior of a cell is largely determined by its interactions with the extracellular matrix, neighboring cells, and soluble local and systemic cues. We describe the essential roles of context and organ structure in directing mammary gland development and differentiated function and in determining the response to oncogenic insults, including mutations. We expand on the concept of "dynamic reciprocity" to present an integrated view of development, cancer, and aging and posit that genes are like the keys on a piano: Although they are essential, it is the context that makes the music.
          Article 0 comments Cited 288 times – based on 0 reviews     Review now
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            Focal adhesions: transmembrane junctions between the extracellular matrix and the cytoskeleton.

            K. Burridge, K Fath, T. Kelly … (1988)
            Article 0 comments Cited 165 times – based on 0 reviews     Review now
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              Cyclins D2 and D1 are essential for postnatal pancreatic beta-cell growth.

              Jake A Kushner, Maria A Ciemerych, Ewa Sicinska … (2005)
              Regulation of adult beta-cell mass in pancreatic islets is essential to preserve sufficient insulin secretion in order to appropriately regulate glucose homeostasis. In many tissues mitogens influence development by stimulating D-type cyclins (D1, D2, or D3) and activating cyclin-dependent kinases (CDK4 or CDK6), which results in progression through the G(1) phase of the cell cycle. Here we show that cyclins D2 and D1 are essential for normal postnatal islet growth. In adult murine islets basal cyclin D2 mRNA expression was easily detected, while cyclin D1 was expressed at lower levels and cyclin D3 was nearly undetectable. Prenatal islet development occurred normally in cyclin D2(-/-) or cyclin D1(+/-) D2(-/-) mice. However, beta-cell proliferation, adult mass, and glucose tolerance were decreased in adult cyclin D2(-/-) mice, causing glucose intolerance that progressed to diabetes by 12 months of age. Although cyclin D1(+/-) mice never developed diabetes, life-threatening diabetes developed in 3-month-old cyclin D1(-/+) D2(-/-) mice as beta-cell mass decreased after birth. Thus, cyclins D2 and D1 were essential for beta-cell expansion in adult mice. Strategies to tightly regulate D-type cyclin activity in beta cells could prevent or cure diabetes.
              Article 0 comments Cited 102 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Kyeong-Min Lee
                Journal
                Journal ID (nlm-ta): Heliyon
                Journal ID (iso-abbrev): Heliyon
                Title: Heliyon
                Publisher: Elsevier
                ISSN (Electronic): 2405-8440
                Publication date PMC-release: 14 September 2020
                Publication date Collection: September 2020
                Publication date (Electronic): 14 September 2020
                Volume: 6
                Issue: 9
                Electronic Location Identifier: e04918
                Affiliations
                [a ]Division of Biotechnology, Daegu Gyeongbuk Institute of Science and Technology, Daegu, Republic of Korea
                [b ]Division of Electronics & Information System, Daegu Gyeongbuk Institute of Science and Technology, Daegu, Republic of Korea
                [c ]New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu, Republic of Korea
                Author notes
                [∗ ]Corresponding author. leekm1009@ 123456dgist.ac.kr
                [1]

                Contributed equally.

                Article
                Publisher ID: S2405-8440(20)31761-8 Publisher ID: e04918
                DOI: 10.1016/j.heliyon.2020.e04918
                PMC ID: 7501433
                SO-VID: ead718d1-984c-4c99-8fe6-42b29dc1f111
                Copyright © © 2020 The Author(s)
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 13 May 2020
                Date revision received : 14 August 2020
                Date accepted : 8 September 2020
                Categories
                Subject: Research Article

                Keywords: tissue engineering,biomedical materials,cell biology,biotechnology,diabetes,insulin,β-cell adhesion,β-cell proliferation,rgd-modified elastin-like polypeptide,cell cycle
                Data availability:
                Keywords: tissue engineering, biomedical materials, cell biology, biotechnology, diabetes, insulin, β-cell adhesion, β-cell proliferation, rgd-modified elastin-like polypeptide, cell cycle

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