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      Antagonizing Effects of Aspartic Acid against Ultraviolet A-Induced Downregulation of the Stemness of Human Adipose Tissue-Derived Mesenchymal Stem Cells

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          Abstract

          Ultraviolet A (UVA) irradiation is responsible for a variety of changes in cell biology. The purpose of this study was to investigate effects of aspartic acid on UVA irradiation-induced damages in the stemness properties of human adipose tissue-derived mesenchymal stem cells (hAMSCs). Furthermore, we elucidated the UVA-antagonizing mechanisms of aspartic acid. The results of this study showed that aspartic acid attenuated the UVA-induced reduction of the proliferative potential and stemness of hAMSCs, as evidenced by increased proliferative activity in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and upregulation of stemness-related genes OCT4, NANOG, and SOX2 in response to the aspartic acid treatment. UVA-induced reduction in the mRNA level of hypoxia-inducible factor (HIF)-1α was also significantly recovered by aspartic acid. In addition, the antagonizing effects of aspartic acid against the UVA effects were found to be mediated by reduced production of PGE2 through the inhibition of JNK and p42/44 MAPK. Taken together, these findings show that aspartic acid improves reduced stemness of hAMSCs induced by UVA and its effects are mediated by upregulation of HIF-1α via the inhibition of PGE2-cAMP signaling. In addition, aspartic acid may be used as an antagonizing agent to mitigate the effects of UVA.

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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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            SASP mediates chemoresistance and tumor-initiating-activity of mesothelioma cells.

            M Cioce, C Canino, F Facciolo … (2012)
            Here we show that pemetrexed-treated mesothelioma cells undergo accelerated senescence. This is characterized by the secretion of proinflammatory and mitogenic cytokines, reminiscent of an SASP (senescence-associated secretory phenotype). Conditioned media from senescent MPM (malignant pleural mesothelioma) cells trigger the emergence of EMT (epithelial-to-mesenchymal)-like, clonogenic and chemoresistant cell subpopulations, expressing high levels of ALDH (aldehyde dehydrogenase) activity (ALDH(bright) cells). We show by fluorescence-activated cell sorting of purified ALDH(bright) and ALDH(low) cells, that both cell-autonomous and cell-non-autonomous mechanisms converge to maintain the SASP-induced, EMT-like cell subpopulations. Chemoresistant ALDH(bright) cells exist within primary MPM specimens and enrichment for ALDH(bright) cells correlates with an earlier tumor onset into NOD/SCID mice. We show that RAS(v12) expression induces SASP-like changes in untransformed human mesothelial cells, and that p53 ablation increases the effect of RAS(v12) expression. We identify STAT3 activation as a crucial event downstream to SASP signaling. In fact, small hairpin RNA-mediated ablation of STAT3 deeply attenuates the induction of EMT genes and the increase of ALDH(bright) cells induced by SASP-cytokines. This strongly affects the chemoresistance of MPM cells in vitro and leads to anticancer effects in vivo.
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              FM19G11, a new hypoxia-inducible factor (HIF) modulator, affects stem cell differentiation status.

              Santos Fustero, Slaven Erceg, Irma Victoria Rivas Manzano … (2010)
              The biology of the alpha subunits of hypoxia-inducible factors (HIFalpha) has expanded from their role in angiogenesis to their current position in the self-renewal and differentiation of stem cells. The results reported in this article show the discovery of FM19G11, a novel chemical entity that inhibits HIFalpha proteins that repress target genes of the two alpha subunits, in various tumor cell lines as well as in adult and embryonic stem cell models from rodents and humans, respectively. FM19G11 inhibits at nanomolar range the transcriptional and protein expression of Oct4, Sox2, Nanog, and Tgf-alpha undifferentiating factors, in adult rat and human embryonic stem cells, FM19G11 activity occurs in ependymal progenitor stem cells from rats (epSPC), a cell model reported for spinal cord regeneration, which allows the progression of oligodendrocyte cell differentiation in a hypoxic environment, has created interest in its characterization for pharmacological research. Experiments using small interfering RNA showed a significant depletion in Sox2 protein only in the case of HIF2alpha silencing, but not in HIF1alpha-mediated ablation. Moreover, chromatin immunoprecipitation data, together with the significant presence of functional hypoxia response element consensus sequences in the promoter region of Sox2, strongly validated that this factor behaves as a target gene of HIF2alpha in epSPCs. FM19G11 causes a reduction of overall histone acetylation with significant repression of p300, a histone acetyltransferase required as a co-factor for HIF-transcription activation. Arrays carried out in the presence and absence of the inhibitor showed the predominant involvement of epigenetic-associated events mediated by the drug.
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                Author and article information

                Contributors
                Georgios Simos: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 24 April 2015
                Publication date Collection: 2015
                Volume: 10
                Issue: 4
                Electronic Location Identifier: e0124417
                Affiliations
                [1 ]Department of Convergence Biomedical Science & Engineering, Eulji University, Seongnam City, Gyunggi Do, Republic of Korea
                [2 ]Skincure Life Science Institute, Seongnam City, Gyunggi Do, Republic of Korea
                [3 ]Department of Genetic Engineering, Sungkyunkwan University, Suwon-Si, Gyeonggi-Do, Republic of Korea
                [4 ]Viral Disease Division, Animal and Plant Quarantine Agency, 175 Anyang-Ro, Manan-Gu, Anyang-Si, Gyeonggi-Do, Republic of Korea
                [5 ]Biospectrum Life Science Institute, Seongnam City, Gyunggi Do, Republic of Korea
                [6 ]Department of Senior Healthcare, BK21 plus program, Graduated school, Eulji University, Seongnam City, Gyunggi Do, Republic of Korea
                [7 ]Department of Physical Therapy, College of Health Science, Eulji University, Seongnam City, Gyunggi Do, Republic of Korea
                [8 ]Department of Dermatological Health Management, College of Health Science, Eulji University, Seongnam City, Gyunggi Do, Korea
                University of Thessaly, Faculty of Medicine, GREECE
                Author notes

                Competing Interests: Kwangseon Jung and Eunsun Jung are employed by Skincure Life Science Institute and Biospectrum Life Science Institute, respectively. However, there are no further patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

                Conceived and designed the experiments: KJ JYC Jongsung Lee. Performed the experiments: KJ JYC YJS Jienny Lee SWS SJ EJ MK. Analyzed the data: KJ JYC YJS EJ MK. Contributed reagents/materials/analysis tools: EJ MK Jongsung Lee. Wrote the paper: KJ JYC YJS Jongsung Lee.

                Article
                Publisher ID: PONE-D-14-57299
                DOI: 10.1371/journal.pone.0124417
                PMC ID: 4409053
                PubMed ID: 25909857
                SO-VID: dcee6fb7-170b-4b7c-ba1b-835b805a71c1
                Copyright statement: Copyright @ 2015
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                Date received : 21 December 2014
                Date accepted : 2 March 2015
                Page count
                Figures: 7, Tables: 0, Pages: 14
                Funding
                This study was supported by a grant from the Korean Health Technology R & D Project, Ministry of Health and Welfare, Republic of Korea (Grant Number: HN13C0072). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Co-author Kwangseon Jung is employed by Skincure Life Science Institute. Skincure Life Science Institute provided support in the form of salary for author KJ, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific role of this author is articulated in the ‘author contributions’ section. Co-author Eunsun Jung is employed by Biospectrum Life Science Institute. Biospectrum Life Science Institute provided support in the form of salary for author EJ, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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