Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis
Inflammatory responses involving microglia and astrocytes contribute to the pathogenesis of neurodegenerative diseases (NDs). In addition, inflammation is tightly linked to iron metabolism dysregulation. However, it is not clear whether the brain inflammation-induced iron metabolism dysregulation co...
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| Veröffentlicht in: | Cell death & disease 2017-03, Vol.8 (3), p.e2676-e2676 |
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| creator | You, Lin-Hao Yan, Cai-Zhen Zheng, Bing-Jie Ci, Yun-Zhe Chang, Shi-Yang Yu, Peng Gao, Guo-Fen Li, Hai-Yan Dong, Tian-Yu Chang, Yan-Zhong |
| description | Inflammatory responses involving microglia and astrocytes contribute to the pathogenesis of neurodegenerative diseases (NDs). In addition, inflammation is tightly linked to iron metabolism dysregulation. However, it is not clear whether the brain inflammation-induced iron metabolism dysregulation contributes to the NDs pathogenesis. Herein, we demonstrate that the expression of the systemic iron regulatory hormone, hepcidin, is induced by lipopolysaccharide (LPS) through the IL-6/STAT3 pathway in the cortex and hippocampus. In this paradigm, activated glial cells are the source of IL-6, which was essential in the iron overload-activated apoptosis of neurons. Disrupting astrocyte hepcidin expression prevented the apoptosis of neurons, which were able to maintain levels of FPN1 adequate to avoid iron accumulation. Together, our data are consistent with a model whereby inflammation initiates an intercellular signaling cascade in which activated microglia, through IL-6 signaling, stimulate astrocytes to release hepcidin which, in turn, signals to neurons, via hepcidin, to prevent their iron release. Such a pathway is relevant to NDs in that it links inflammation, microglia and astrocytes to neuronal damage. |
| doi_str_mv | 10.1038/cddis.2017.93 |
| format | Article |
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In addition, inflammation is tightly linked to iron metabolism dysregulation. However, it is not clear whether the brain inflammation-induced iron metabolism dysregulation contributes to the NDs pathogenesis. Herein, we demonstrate that the expression of the systemic iron regulatory hormone, hepcidin, is induced by lipopolysaccharide (LPS) through the IL-6/STAT3 pathway in the cortex and hippocampus. In this paradigm, activated glial cells are the source of IL-6, which was essential in the iron overload-activated apoptosis of neurons. Disrupting astrocyte hepcidin expression prevented the apoptosis of neurons, which were able to maintain levels of FPN1 adequate to avoid iron accumulation. Together, our data are consistent with a model whereby inflammation initiates an intercellular signaling cascade in which activated microglia, through IL-6 signaling, stimulate astrocytes to release hepcidin which, in turn, signals to neurons, via hepcidin, to prevent their iron release. Such a pathway is relevant to NDs in that it links inflammation, microglia and astrocytes to neuronal damage.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2017.93</identifier><identifier>PMID: 28300826</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/2 ; 13/51 ; 14/34 ; 631/378/1689/364 ; 631/378/340 ; 631/80/82/23 ; 631/80/86 ; 64/60 ; 82/80 ; 96/2 ; Animals ; Antibodies ; Apoptosis ; Apoptosis - drug effects ; Astrobiology ; Astrocytes - drug effects ; Astrocytes - metabolism ; Astrocytes - pathology ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cells, Cultured ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Encephalitis - metabolism ; Encephalitis - pathology ; Hepcidins - metabolism ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Immunology ; Inflammatory diseases ; Interleukin-6 - metabolism ; Iron - metabolism ; Life Sciences ; Lipopolysaccharides - pharmacology ; Male ; Mice ; Mice, Inbred BALB C ; Microglia - drug effects ; Microglia - metabolism ; Microglia - pathology ; Neurons ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Original ; original-article ; Rats ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism</subject><ispartof>Cell death & disease, 2017-03, Vol.8 (3), p.e2676-e2676</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Mar 2017</rights><rights>Copyright © 2017 The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-c5b62b3f390268dcf434df950f3bb0fe614879760025e3160896c208db1270a43</citedby><cites>FETCH-LOGICAL-c520t-c5b62b3f390268dcf434df950f3bb0fe614879760025e3160896c208db1270a43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386583/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386583/$$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/28300826$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>You, Lin-Hao</creatorcontrib><creatorcontrib>Yan, Cai-Zhen</creatorcontrib><creatorcontrib>Zheng, Bing-Jie</creatorcontrib><creatorcontrib>Ci, Yun-Zhe</creatorcontrib><creatorcontrib>Chang, Shi-Yang</creatorcontrib><creatorcontrib>Yu, Peng</creatorcontrib><creatorcontrib>Gao, Guo-Fen</creatorcontrib><creatorcontrib>Li, Hai-Yan</creatorcontrib><creatorcontrib>Dong, Tian-Yu</creatorcontrib><creatorcontrib>Chang, Yan-Zhong</creatorcontrib><title>Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Inflammatory responses involving microglia and astrocytes contribute to the pathogenesis of neurodegenerative diseases (NDs). In addition, inflammation is tightly linked to iron metabolism dysregulation. However, it is not clear whether the brain inflammation-induced iron metabolism dysregulation contributes to the NDs pathogenesis. Herein, we demonstrate that the expression of the systemic iron regulatory hormone, hepcidin, is induced by lipopolysaccharide (LPS) through the IL-6/STAT3 pathway in the cortex and hippocampus. In this paradigm, activated glial cells are the source of IL-6, which was essential in the iron overload-activated apoptosis of neurons. Disrupting astrocyte hepcidin expression prevented the apoptosis of neurons, which were able to maintain levels of FPN1 adequate to avoid iron accumulation. Together, our data are consistent with a model whereby inflammation initiates an intercellular signaling cascade in which activated microglia, through IL-6 signaling, stimulate astrocytes to release hepcidin which, in turn, signals to neurons, via hepcidin, to prevent their iron release. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>You, Lin-Hao</au><au>Yan, Cai-Zhen</au><au>Zheng, Bing-Jie</au><au>Ci, Yun-Zhe</au><au>Chang, Shi-Yang</au><au>Yu, Peng</au><au>Gao, Guo-Fen</au><au>Li, Hai-Yan</au><au>Dong, Tian-Yu</au><au>Chang, Yan-Zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2017-03-16</date><risdate>2017</risdate><volume>8</volume><issue>3</issue><spage>e2676</spage><epage>e2676</epage><pages>e2676-e2676</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Inflammatory responses involving microglia and astrocytes contribute to the pathogenesis of neurodegenerative diseases (NDs). In addition, inflammation is tightly linked to iron metabolism dysregulation. However, it is not clear whether the brain inflammation-induced iron metabolism dysregulation contributes to the NDs pathogenesis. Herein, we demonstrate that the expression of the systemic iron regulatory hormone, hepcidin, is induced by lipopolysaccharide (LPS) through the IL-6/STAT3 pathway in the cortex and hippocampus. In this paradigm, activated glial cells are the source of IL-6, which was essential in the iron overload-activated apoptosis of neurons. Disrupting astrocyte hepcidin expression prevented the apoptosis of neurons, which were able to maintain levels of FPN1 adequate to avoid iron accumulation. Together, our data are consistent with a model whereby inflammation initiates an intercellular signaling cascade in which activated microglia, through IL-6 signaling, stimulate astrocytes to release hepcidin which, in turn, signals to neurons, via hepcidin, to prevent their iron release. Such a pathway is relevant to NDs in that it links inflammation, microglia and astrocytes to neuronal damage.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28300826</pmid><doi>10.1038/cddis.2017.93</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/2 13/51 14/34 631/378/1689/364 631/378/340 631/80/82/23 631/80/86 64/60 82/80 96/2 Animals Antibodies Apoptosis Apoptosis - drug effects Astrobiology Astrocytes - drug effects Astrocytes - metabolism Astrocytes - pathology Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Cells, Cultured Cerebral Cortex - drug effects Cerebral Cortex - metabolism Cerebral Cortex - pathology Encephalitis - metabolism Encephalitis - pathology Hepcidins - metabolism Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Immunology Inflammatory diseases Interleukin-6 - metabolism Iron - metabolism Life Sciences Lipopolysaccharides - pharmacology Male Mice Mice, Inbred BALB C Microglia - drug effects Microglia - metabolism Microglia - pathology Neurons Neurons - drug effects Neurons - metabolism Neurons - pathology Original original-article Rats Signal Transduction - drug effects STAT3 Transcription Factor - metabolism |
| title | Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis |
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