CXCR4/CXCL12 axis counteracts hematopoietic stem cell exhaustion through selective protection against oxidative stress
Hematopoietic stem cells (HSCs) undergo self-renewal to maintain hematopoietic homeostasis for lifetime, which is regulated by the bone marrow (BM) microenvironment. The chemokine receptor CXCR4 and its ligand CXCL12 are critical factors supporting quiescence and BM retention of HSCs. Here, we repor...
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| Veröffentlicht in: | Scientific reports 2016-11, Vol.6 (1), p.37827-37827, Article 37827 |
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| creator | Zhang, Yanyan Dépond, Mallorie He, Liang Foudi, Adlen Kwarteng, Edward Owusu Lauret, Evelyne Plo, Isabelle Desterke, Christophe Dessen, Philippe Fujii, Nobutaka Opolon, Paule Herault, Olivier Solary, Eric Vainchenker, William Joulin, Virginie Louache, Fawzia Wittner, Monika |
| description | Hematopoietic stem cells (HSCs) undergo self-renewal to maintain hematopoietic homeostasis for lifetime, which is regulated by the bone marrow (BM) microenvironment. The chemokine receptor CXCR4 and its ligand CXCL12 are critical factors supporting quiescence and BM retention of HSCs. Here, we report an unknown function of CXCR4/CXCL12 axis in the protection of HSCs against oxidative stress. Disruption of CXCR4 receptor in mice leads to increased endogenous production of reactive oxygen species (ROS), resulting in p38 MAPK activation, increased DNA double-strand breaks and apoptosis leading to marked reduction in HSC repopulating potential. Increased ROS levels are directly responsible for exhaustion of the HSC pool and are not linked to loss of quiescence of CXCR4-deficient HSCs. Furthermore, we report that CXCL12 has a direct rescue effect on oxidative stress-induced HSC damage at the mitochondrial level. These data highlight the importance of CXCR4/CXCL12 axis in the regulation of lifespan of HSCs by limiting ROS generation and genotoxic stress. |
| doi_str_mv | 10.1038/srep37827 |
| format | Article |
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The chemokine receptor CXCR4 and its ligand CXCL12 are critical factors supporting quiescence and BM retention of HSCs. Here, we report an unknown function of CXCR4/CXCL12 axis in the protection of HSCs against oxidative stress. Disruption of CXCR4 receptor in mice leads to increased endogenous production of reactive oxygen species (ROS), resulting in p38 MAPK activation, increased DNA double-strand breaks and apoptosis leading to marked reduction in HSC repopulating potential. Increased ROS levels are directly responsible for exhaustion of the HSC pool and are not linked to loss of quiescence of CXCR4-deficient HSCs. Furthermore, we report that CXCL12 has a direct rescue effect on oxidative stress-induced HSC damage at the mitochondrial level. These data highlight the importance of CXCR4/CXCL12 axis in the regulation of lifespan of HSCs by limiting ROS generation and genotoxic stress.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep37827</identifier><identifier>PMID: 27886253</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/532/1542 ; 631/80/84 ; Apoptosis ; Biochemistry, Molecular Biology ; Bone marrow ; Cell self-renewal ; CXCL12 protein ; CXCR4 protein ; DNA damage ; Genes ; Genotoxicity ; Homeostasis ; Humanities and Social Sciences ; Life Sciences ; Life span ; MAP kinase ; Mitochondria ; multidisciplinary ; Oxidative stress ; Reactive oxygen species ; Rodents ; Science ; Stem cell transplantation ; Stem cells</subject><ispartof>Scientific reports, 2016-11, Vol.6 (1), p.37827-37827, Article 37827</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Nov 2016</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2016, The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-cb614050726ddc2196713008c9d99a67034ce3f46e2aaabee08c8b4366e7bf073</citedby><cites>FETCH-LOGICAL-c541t-cb614050726ddc2196713008c9d99a67034ce3f46e2aaabee08c8b4366e7bf073</cites><orcidid>0000-0001-8029-8473 ; 0000-0002-5915-6910 ; 0000-0003-4705-202X ; 0000-0002-8629-1341 ; 0000-0003-3330-4062 ; 0000-0002-4799-5071 ; 0000-0002-7419-1124</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122894/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122894/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27886253$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-01472381$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yanyan</creatorcontrib><creatorcontrib>Dépond, Mallorie</creatorcontrib><creatorcontrib>He, Liang</creatorcontrib><creatorcontrib>Foudi, Adlen</creatorcontrib><creatorcontrib>Kwarteng, Edward Owusu</creatorcontrib><creatorcontrib>Lauret, Evelyne</creatorcontrib><creatorcontrib>Plo, Isabelle</creatorcontrib><creatorcontrib>Desterke, Christophe</creatorcontrib><creatorcontrib>Dessen, Philippe</creatorcontrib><creatorcontrib>Fujii, Nobutaka</creatorcontrib><creatorcontrib>Opolon, Paule</creatorcontrib><creatorcontrib>Herault, Olivier</creatorcontrib><creatorcontrib>Solary, Eric</creatorcontrib><creatorcontrib>Vainchenker, William</creatorcontrib><creatorcontrib>Joulin, Virginie</creatorcontrib><creatorcontrib>Louache, Fawzia</creatorcontrib><creatorcontrib>Wittner, Monika</creatorcontrib><title>CXCR4/CXCL12 axis counteracts hematopoietic stem cell exhaustion through selective protection against oxidative stress</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Hematopoietic stem cells (HSCs) undergo self-renewal to maintain hematopoietic homeostasis for lifetime, which is regulated by the bone marrow (BM) microenvironment. The chemokine receptor CXCR4 and its ligand CXCL12 are critical factors supporting quiescence and BM retention of HSCs. Here, we report an unknown function of CXCR4/CXCL12 axis in the protection of HSCs against oxidative stress. Disruption of CXCR4 receptor in mice leads to increased endogenous production of reactive oxygen species (ROS), resulting in p38 MAPK activation, increased DNA double-strand breaks and apoptosis leading to marked reduction in HSC repopulating potential. Increased ROS levels are directly responsible for exhaustion of the HSC pool and are not linked to loss of quiescence of CXCR4-deficient HSCs. Furthermore, we report that CXCL12 has a direct rescue effect on oxidative stress-induced HSC damage at the mitochondrial level. These data highlight the importance of CXCR4/CXCL12 axis in the regulation of lifespan of HSCs by limiting ROS generation and genotoxic stress.</description><subject>631/532/1542</subject><subject>631/80/84</subject><subject>Apoptosis</subject><subject>Biochemistry, Molecular Biology</subject><subject>Bone marrow</subject><subject>Cell self-renewal</subject><subject>CXCL12 protein</subject><subject>CXCR4 protein</subject><subject>DNA damage</subject><subject>Genes</subject><subject>Genotoxicity</subject><subject>Homeostasis</subject><subject>Humanities and Social Sciences</subject><subject>Life Sciences</subject><subject>Life span</subject><subject>MAP kinase</subject><subject>Mitochondria</subject><subject>multidisciplinary</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Science</subject><subject>Stem cell transplantation</subject><subject>Stem 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axis counteracts hematopoietic stem cell exhaustion through selective protection against oxidative stress</title><author>Zhang, Yanyan ; Dépond, Mallorie ; He, Liang ; Foudi, Adlen ; Kwarteng, Edward Owusu ; Lauret, Evelyne ; Plo, Isabelle ; Desterke, Christophe ; Dessen, Philippe ; Fujii, Nobutaka ; Opolon, Paule ; Herault, Olivier ; Solary, Eric ; Vainchenker, William ; Joulin, Virginie ; Louache, Fawzia ; Wittner, Monika</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-cb614050726ddc2196713008c9d99a67034ce3f46e2aaabee08c8b4366e7bf073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>631/532/1542</topic><topic>631/80/84</topic><topic>Apoptosis</topic><topic>Biochemistry, Molecular Biology</topic><topic>Bone marrow</topic><topic>Cell self-renewal</topic><topic>CXCL12 protein</topic><topic>CXCR4 protein</topic><topic>DNA damage</topic><topic>Genes</topic><topic>Genotoxicity</topic><topic>Homeostasis</topic><topic>Humanities and Social Sciences</topic><topic>Life Sciences</topic><topic>Life span</topic><topic>MAP kinase</topic><topic>Mitochondria</topic><topic>multidisciplinary</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Science</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yanyan</creatorcontrib><creatorcontrib>Dépond, Mallorie</creatorcontrib><creatorcontrib>He, Liang</creatorcontrib><creatorcontrib>Foudi, Adlen</creatorcontrib><creatorcontrib>Kwarteng, Edward Owusu</creatorcontrib><creatorcontrib>Lauret, Evelyne</creatorcontrib><creatorcontrib>Plo, Isabelle</creatorcontrib><creatorcontrib>Desterke, Christophe</creatorcontrib><creatorcontrib>Dessen, Philippe</creatorcontrib><creatorcontrib>Fujii, Nobutaka</creatorcontrib><creatorcontrib>Opolon, Paule</creatorcontrib><creatorcontrib>Herault, Olivier</creatorcontrib><creatorcontrib>Solary, Eric</creatorcontrib><creatorcontrib>Vainchenker, William</creatorcontrib><creatorcontrib>Joulin, Virginie</creatorcontrib><creatorcontrib>Louache, Fawzia</creatorcontrib><creatorcontrib>Wittner, Monika</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium 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Liang</au><au>Foudi, Adlen</au><au>Kwarteng, Edward Owusu</au><au>Lauret, Evelyne</au><au>Plo, Isabelle</au><au>Desterke, Christophe</au><au>Dessen, Philippe</au><au>Fujii, Nobutaka</au><au>Opolon, Paule</au><au>Herault, Olivier</au><au>Solary, Eric</au><au>Vainchenker, William</au><au>Joulin, Virginie</au><au>Louache, Fawzia</au><au>Wittner, Monika</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXCR4/CXCL12 axis counteracts hematopoietic stem cell exhaustion through selective protection against oxidative stress</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-11-25</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>37827</spage><epage>37827</epage><pages>37827-37827</pages><artnum>37827</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Hematopoietic stem cells (HSCs) undergo self-renewal to maintain hematopoietic homeostasis for lifetime, which is regulated by the bone marrow (BM) microenvironment. The chemokine receptor CXCR4 and its ligand CXCL12 are critical factors supporting quiescence and BM retention of HSCs. Here, we report an unknown function of CXCR4/CXCL12 axis in the protection of HSCs against oxidative stress. Disruption of CXCR4 receptor in mice leads to increased endogenous production of reactive oxygen species (ROS), resulting in p38 MAPK activation, increased DNA double-strand breaks and apoptosis leading to marked reduction in HSC repopulating potential. Increased ROS levels are directly responsible for exhaustion of the HSC pool and are not linked to loss of quiescence of CXCR4-deficient HSCs. Furthermore, we report that CXCL12 has a direct rescue effect on oxidative stress-induced HSC damage at the mitochondrial level. These data highlight the importance of CXCR4/CXCL12 axis in the regulation of lifespan of HSCs by limiting ROS generation and genotoxic stress.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27886253</pmid><doi>10.1038/srep37827</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-8029-8473</orcidid><orcidid>https://orcid.org/0000-0002-5915-6910</orcidid><orcidid>https://orcid.org/0000-0003-4705-202X</orcidid><orcidid>https://orcid.org/0000-0002-8629-1341</orcidid><orcidid>https://orcid.org/0000-0003-3330-4062</orcidid><orcidid>https://orcid.org/0000-0002-4799-5071</orcidid><orcidid>https://orcid.org/0000-0002-7419-1124</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/532/1542 631/80/84 Apoptosis Biochemistry, Molecular Biology Bone marrow Cell self-renewal CXCL12 protein CXCR4 protein DNA damage Genes Genotoxicity Homeostasis Humanities and Social Sciences Life Sciences Life span MAP kinase Mitochondria multidisciplinary Oxidative stress Reactive oxygen species Rodents Science Stem cell transplantation Stem cells |
| title | CXCR4/CXCL12 axis counteracts hematopoietic stem cell exhaustion through selective protection against oxidative stress |
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