For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
11
views
57
references
 Top references
cited by
15
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      314
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Human Amnion-Derived Mesenchymal Stem Cells Protect Human Bone Marrow Mesenchymal Stem Cells against Oxidative Stress-Mediated Dysfunction via ERK1/2 MAPK Signaling

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Epidemiological evidence suggests that bone is especially sensitive to oxidative stress, causing bone loss in the elderly. Previous studies indicated that human amnion-derived mesenchymal stem cells (HAMSCs), obtained from human amniotic membranes, exerted osteoprotective effects in vivo. However, the potential of HAMSCs as seed cells against oxidative stress-mediated dysfunction is unknown. In this study, we systemically investigated their antioxidative and osteogenic effects in vitro. Here, we demonstrated that HAMSCs signi cantly promoted the proliferation and osteoblastic differentiation of H 2O 2-induced human bone marrow mesenchymal stem cells (HBMSCs), and down-regulated the reactive oxygen species (ROS) level. Further, our results suggest that activation of the ERK1/2 MAPK signal transduction pathway is essential for both HAMSCs-mediated osteogenic and protective effects against oxidative stress-induced dysfunction in HBMSCs. U0126, a highly selective inhibitor of extracellular ERK1/2 MAPK signaling, significantly suppressed the antioxidative and osteogenic effects in HAMSCs. In conclusion, by modulating HBMSCs, HAMSCs show a strong potential in treating oxidative stress- mediated bone deficiency.

          Related collections

          Most cited references57

          • Record: found
          • Abstract: found
          • Article: not found

          Mammalian sirtuins: biological insights and disease relevance.

          Marcia Haigis, David A Sinclair (2010)
          Aging is accompanied by a decline in the healthy function of multiple organ systems, leading to increased incidence and mortality from diseases such as type II diabetes mellitus, neurodegenerative diseases, cancer, and cardiovascular disease. Historically, researchers have focused on investigating individual pathways in isolated organs as a strategy to identify the root cause of a disease, with hopes of designing better drugs. Studies of aging in yeast led to the discovery of a family of conserved enzymes known as the sirtuins, which affect multiple pathways that increase the life span and the overall health of organisms. Since the discovery of the first known mammalian sirtuin, SIRT1, 10 years ago, there have been major advances in our understanding of the enzymology of sirtuins, their regulation, and their ability to broadly improve mammalian physiology and health span. This review summarizes and discusses the advances of the past decade and the challenges that will confront the field in the coming years.
          Article 0 comments Cited 656 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.

            Christopher B Davis, J Raingeaud, Chris Dickens … (1995)
            Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.
            Article 0 comments Cited 437 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Oxidative stress modulates osteoblastic differentiation of vascular and bone cells.

              N. Mody, F Parhami, T A Sarafian … (2001)
              Oxidative stress may regulate cellular function in multiple pathological conditions, including atherosclerosis. One feature of the atherosclerotic plaque is calcium mineral deposition, which appears to result from the differentiation of vascular osteoblastic cells, calcifying vascular cells (CVC). To determine the role of oxidative stress in regulating the activity of CVC, we treated these cells with hydrogen peroxide (H(2)O(2)) or xanthine/xanthine oxidase (XXO) and assessed their effects on intracellular oxidative stress, differentiation, and mineralization. These agents increased intracellular oxidative stress as determined by 2,7 dichlorofluorescein fluorescence, and enhanced osteoblastic differentiation of vascular cells, based on alkaline phosphatase activity and mineralization. In contrast, H(2)O(2) and XXO resulted in inhibition of differentiation markers in bone osteoblastic cells, MC3T3-E1, and marrow stromal cells, M2-10B4, while increasing oxidative stress. In addition, minimally oxidized low-density lipoprotein (MM-LDL), previously shown to enhance vascular cell and inhibit bone cell differentiation, also increased intracellular oxidative stress in the three cell types. These effects of XXO and MM-LDL were counteracted by the antioxidants Trolox and pyrrolidinedithiocarbamate. These results suggest that oxidative stress modulates differentiation of vascular and bone cells oppositely, which may explain the parallel buildup and loss of calcification, seen in vascular calcification and osteoporosis, respectively.
              Article 0 comments Cited 164 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Cells
                Journal ID (iso-abbrev): Mol. Cells
                Journal ID (publisher-id): ksmcb
                Title: Molecules and Cells
                Publisher: Korean Society for Molecular and Cellular Biology
                ISSN (Print): 1016-8478
                ISSN (Electronic): 0219-1032
                Publication date (Print): 31 March 2016
                Publication date (Electronic): 07 January 2016
                Publication date PMC-release: 07 January 2016
                Volume: 39
                Issue: 3
                Pages: 186-194
                Affiliations
                [1 ]Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing 210029, Jiangsu, People’s Republic of China
                Author notes
                [2]

                These authors contributed equally to this work.

                [* ]Correspondence: njcn@ 123456njmu.edu.cn
                Article
                Publisher ID: molce-39-3-186
                DOI: 10.14348/molcells.2016.2159
                PMC ID: 4794600
                PubMed ID: 26743906
                SO-VID: 2c358a26-2d6b-4ef1-a9d4-0116e423bef2
                Copyright © © The Korean Society for Molecular and Cellular Biology. All rights reserved.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

                History
                Date received : 03 June 2015
                Date revision received : 17 November 2015
                Date accepted : 23 November 2015
                Categories
                Subject: Article

                Keywords: erk1/2 mapk signal transduction pathway,human amnion mesenchymal stem cells (hamscs),human bone marrow mesenchymal stem cells (hbmscs),oxidative stress,reactive oxygen species (ros)
                Data availability:
                Keywords: erk1/2 mapk signal transduction pathway, human amnion mesenchymal stem cells (hamscs), human bone marrow mesenchymal stem cells (hbmscs), oxidative stress, reactive oxygen species (ros)

                Comments

                Comment on this article

                scite_

                Similar content314

                See all similar

                Cited by15

                See all cited by

                Most referenced authors652

                See all reference authors