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      Stemness and differentiation potential-recovery effects of sinapic acid against ultraviolet-A-induced damage through the regulation of p38 MAPK and NF-κB

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          Abstract

          Ultraviolet A (UVA) irradiation exerts negative effects on stemness and differentiation potential of stem cells. This study aimed to explore the effect of sinapic acid on UVA-irradiation-induced damages to stemness and differentiation potential of human-adipose-tissue-derived mesenchymal stem cells (hAMSCs) and its UVA-antagonist mechanisms. Sinapic acid attenuated UVA-induced reduction in the proliferative potential and stemness by upregulating OCT4, SOX2, and NANOG. In addition, sinapic acid significantly recovered UVA-induced reduction in expression level of hypoxia-inducible factor (HIF)-1α. The antagonist effect of sinapic acid against stemness damage was mediated by reduceing PGE 2 production through inhibition of p38 MAPK and NF-κB. Moreover, sinapic acid attenuated UVA-induced reduction in differentiation potential by downregulating the expression of macrophage migration inhibitory factor (MIF) and Kruppel-like factor (KLF) 2 gene while activating AMP-activated protein kinase (AMPK). UVA-induced inhibition of adipogenic differentiation was mediated by reducing MIF production through suppression of NF-κB. Taken together, these findings suggest that sinapic acid may ameliorate UVA-irradiation-induced reduced stemness and differentiation potential of hAMSCs. Therefore, sinapic acid might have potential as an antagonist agent to attenuate damages caused by UVA.

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          Macrophage migration inhibitory factor: a regulator of innate immunity

          Thierry Calandra, Thierry Roger (2003)
          Key Points Cytokines are essential effector molecules of innate immunity that initiate and coordinate the cellular and humoral responses aimed, for example, at the eradication of microbial pathogens. Discovered in the late 1960s as a product of activated T cells, the cytokine macrophage migration inhibitory factor (MIF) has been discovered recently to carry out important functions as a mediator of the innate immune system. Constitutively expressed by a broad spectrum of cells and tissues, including monocytes and macrophages, MIF is rapidly released after exposure to microbial products and pro-inflammatory mediators, and in response to stress. After it is released, MIF induces pro-inflammatory biological responses that act as a regulator of immune responses. MIF activates the extracellular signal-regulated kinase 1 (ERK1)/ERK2–mitogen-activated protein kinase pathway, inhibits the activity of JUN activation domain-binding protein 1 (JAB1) — a co-activator of the activator protein 1 (AP1) — upregulates the expression of Toll-like receptor 4 to promote the recognition of endotoxin-expressing bacterial pathogens, sustains pro-inflammatory function by inhibiting p53-dependent apoptosis of macrophages and counter-regulates the immunosuppressive effects of glucocorticoids on immune cells. As a pro-inflammatory mediator, MIF has been shown to be implicated in the pathogenesis of severe sepsis and septic shock, acute respiratory distress syndrome, and several other inflammatory and autoimmune diseases, including rheumatoid arthritis, glomerulonephritis and inflammatory bowel diseases. Given its crucial role as a regulator of innate and acquired immunity, pharmacological or immunological modulation of MIF activity might offer new treatment opportunities for the management of acute and chronic inflammatory diseases.
          Article 0 comments Cited 482 times – based on 0 reviews     Review now
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            HIF-2alpha regulates Oct-4: effects of hypoxia on stem cell function, embryonic development, and tumor growth.

            Kelly Covello, James Kehler, Hongwei Yu … (2006)
            The division, differentiation, and function of stem cells and multipotent progenitors are influenced by complex signals in the microenvironment, including oxygen availability. Using a genetic "knock-in" strategy, we demonstrate that targeted replacement of the oxygen-regulated transcription factor HIF-1alpha with HIF-2alpha results in expanded expression of HIF-2alpha-specific target genes including Oct-4, a transcription factor essential for maintaining stem cell pluripotency. We show that HIF-2alpha, but not HIF-1alpha, binds to the Oct-4 promoter and induces Oct-4 expression and transcriptional activity, thereby contributing to impaired development in homozygous Hif-2alpha KI/KI embryos, defective hematopoietic stem cell differentiation in embryoid bodies, and large embryonic stem cell (ES)-derived tumors characterized by altered cellular differentiation. Furthermore, loss of HIF-2alpha severely reduces the number of embryonic primordial germ cells, which require Oct-4 expression for survival and/or maintenance. These results identify Oct-4 as a HIF-2alpha-specific target gene and indicate that HIF-2alpha can regulate stem cell function and/or differentiation through activation of Oct-4, which in turn contributes to HIF-2alpha's tumor promoting activity.
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              MIF: a new cytokine link between rheumatoid arthritis and atherosclerosis.

              Michelle Leech, Jürgen Bernhagen, E Morand (2006)
              Macrophage migration inhibitory factor (MIF) is well established as a key cytokine in immuno-inflammatory diseases such as rheumatoid arthritis. Inflammation is now also recognized as having a crucial role in atherosclerosis, and recent evidence indicates that MIF could also be important in this disease. Here, we review the role of MIF in rheumatoid arthritis and atherosclerosis, discuss the ways in which MIF and its relationship with glucocorticoids could link these diseases, and consider the potential of MIF as a new therapeutic target for small-molecule and antibody-based anti-cytokine drugs.
              Article 0 comments Cited 87 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yong Seek Park: yongseek@khu.ac.kr
                Jongsung Lee: bioneer@skku.edu
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 19 April 2017
                Publication date PMC-release: 19 April 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 909
                Affiliations
                [1 ]GRID grid.264381.a, Department of Genetic Engineering, , College of Biotechnology and Bioengineering, Sungkyunkwan University, ; Suwon City, 164-19 Gyunggi Do Republic of Korea
                [2 ]GRID grid.255588.7, Department of Dental Hygiene, , College of Health Science, Eulji University, ; Seongnam City, 131-35 Gyunggi Do Republic of Korea
                [3 ]GRID grid.412172.3, Department of Bio and Chemical Engineering, , Hongik University, ; 300-16 Sejong City, Republic of Korea
                [4 ]GRID grid.289247.2, Department of Microbiology, , School of Medicine, Kyung Hee University, ; 024-53 Seoul, Republic of Korea
                [5 ]Skincure Life Science Institute, Seongnam City, 132-16 Gyunggi Do Republic of Korea
                Article
                Publisher ID: 1089
                DOI: 10.1038/s41598-017-01089-5
                PMC ID: 5430417
                PubMed ID: 28424532
                SO-VID: 30cde35f-9b06-461a-b838-77d51d7ce157
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 19 December 2016
                Date accepted : 23 March 2017
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

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