For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
27
views
5
references
 Top references
cited by
3
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      701
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      HIF-2α - a mediator of stem cell altruism?

      research-article
      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Stem Cell Research & Therapy
      Publisher: BioMed Central

      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

          Human embryonic stem cells (hESCs) have been reported to confer cytoprotection in the context of tissue injury. This is somewhat counterintuitive given that microenvironmental factors such as hypoxia and oxidative stress may activate p53 and result in death and differentiation of these hESCs. In this article, we discuss a novel mechanism through which hESCs can be re-programmed (through exposure to hypoxia/oxidative stress) to transiently suppress p53, enhance 'stemness', and exist in a highly cytoprotective and undifferentiated state.

          Related collections

          Most cited references5

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

          HIF1α and HIF2α: sibling rivalry in hypoxic tumour growth and progression.

          Brian Keith, Randall Johnson, M. Celeste Simon (2011)
          Hypoxia-inducible factors (HIFs) are broadly expressed in human cancers, and HIF1α and HIF2α were previously suspected to promote tumour progression through largely overlapping functions. However, this relatively simple model has now been challenged in light of recent data from various approaches that reveal unique and sometimes opposing activities of these HIFα isoforms in both normal physiology and disease. These effects are mediated in part through the regulation of unique target genes, as well as through direct and indirect interactions with important oncoproteins and tumour suppressors, including MYC and p53. As HIF inhibitors are currently undergoing clinical evaluation as cancer therapeutics, a more thorough understanding of the unique roles performed by HIF1α and HIF2α in human neoplasia is warranted.
          Article 0 comments Cited 271 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            A hypoxic niche regulates glioblastoma stem cells through hypoxia inducible factor 2 alpha.

            Guido Reifenberger, Monica Nistér, Konstantinos Meletis … (2010)
            Glioma growth and progression depend on a specialized subpopulation of tumour cells, termed tumour stem cells. Thus, tumour stem cells represent a critical therapeutic target, but the molecular mechanisms that regulate them are poorly understood. Hypoxia plays a key role in tumour progression and in this study we provide evidence that the hypoxic tumour microenvironment also controls tumour stem cells. We define a detailed molecular signature of tumour stem cell genes, which are overexpressed by tumour cells in vascular and perinecrotic/hypoxic niches. Mechanistically, we show that hypoxia plays a key role in the regulation of the tumour stem cell phenotype through hypoxia-inducible factor 2alpha and subsequent induction of specific tumour stem cell signature genes, including mastermind-like protein 3 (Notch pathway), nuclear factor of activated T cells 2 (calcineurin pathway) and aspartate beta-hydroxylase domain-containing protein 2. Notably, a number of these genes belong to pathways regulating the stem cell phenotype. Consistently, tumour stem cell signature genes are overexpressed in newly formed gliomas and are associated with worse clinical prognosis. We propose that tumour stem cells are maintained within a hypoxic niche, providing a functional link between the well-established role of hypoxia in stem cell and tumour biology. The identification of molecular regulators of tumour stem cells in the hypoxic niche points to specific signalling mechanisms that may be used to target the glioblastoma stem cell population.
            Article 0 comments Cited 147 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hypoxia-driven pathways in bone development, regeneration and disease.

              Christa Maes, Geert Carmeliet, Ernestina Schipani (2012)
              Adaptation to hypoxia is a critical cellular event both in pathological settings, such as cancer and ischaemia, and in normal development and differentiation. Oxygen is thought to be not only an indispensable metabolic substrate for a variety of in vivo enzymatic reactions, including mitochondrial respiration, but also a key regulatory signal in tissue development and homeostasis by controlling a specific genetic program. Hypoxia-inducible transcription factors (HIFs) HIF-1 and HIF-2 are central mediators of the homeostatic response that enables cells to survive and differentiate in low-oxygen conditions. Genetically altered mice have been used to identify important roles for HIF-1 and HIF-2 as well as vascular endothelial growth factor (VEGF)-a potent angiogenic factor and a downstream target of the HIF pathway-in the regulation of skeletal development, bone homeostasis and haematopoiesis. In this Review, we summarize the current knowledge of HIF signalling in cartilage, bone and blood, and pay particular attention to the complex relationship between HIF and VEGF in these tissues revealed by data from research using animal models. The study of these models expands our understanding of the cell autonomous, paracrine and autocrine effects that mediate the homeostatic responses downstream of HIFs and VEGF.
              Article 0 comments Cited 87 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Eoin P Cummins
                Journal
                Journal ID (nlm-ta): Stem Cell Res Ther
                Journal ID (iso-abbrev): Stem Cell Res Ther
                Title: Stem Cell Research & Therapy
                Publisher: BioMed Central
                ISSN (Electronic): 1757-6512
                Publication date Collection: 2012
                Publication date (Electronic): 18 December 2012
                Publication date PMC-release: 18 December 2013
                Volume: 3
                Issue: 6
                Page: 52
                Affiliations
                [1 ]School of Medicine and Medical Science, The Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland
                Article
                Publisher ID: scrt143
                DOI: 10.1186/scrt143
                PMC ID: 3580482
                PubMed ID: 23253294
                SO-VID: 9cd3086d-750c-483d-8527-8da4b2c8aaae
                Copyright © Copyright ©2012 BioMed Central Ltd
                History
                Categories
                Subject: Commentary

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

                Comments

                Comment on this article

                scite_

                Similar content701

                See all similar

                Cited by3

                See all cited by

                Most referenced authors85

                See all reference authors