Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis
Accelerated atherosclerotic calcification is responsible for plaque burden, especially in diabetes. The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabe...
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| Veröffentlicht in: | Cell death & disease 2020-01, Vol.11 (1), p.22-22, Article 22 |
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| creator | Li, Peng Wang, Ying Liu, Xue Liu, Bin Wang, Zhao-yang Xie, Fei Qiao, Wen Liang, Er-shun Lu, Qing-hua Zhang, Ming-xiang |
| description | Accelerated atherosclerotic calcification is responsible for plaque burden, especially in diabetes. The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabetic atherosclerotic calcification and decreases vessel stiffening in mice through Runx2 suppression. Specifically, PARP-1 deficiency reduces diabetic arteriosclerotic calcification by regulating Stat1-mediated synthetic phenotype switching of vascular smooth muscle cells and macrophage polarization. Meanwhile, both vascular smooth muscle cells and macrophages manifested osteogenic differentiation in osteogenic media, which was attenuated by PARP-1/Stat1 inhibition. Notably, Stat1 acts as a positive transcription factor by directly binding to the promoter of Runx2 and promoting atherosclerotic calcification in diabetes. Our results identify a new function of PARP-1, in which metabolism disturbance-related stimuli activate the Runx2 expression mediated by Stat1 transcription to facilitate diabetic arteriosclerotic calcification. PARP-1 inhibition may therefore represent a useful therapy for this challenging complication. |
| doi_str_mv | 10.1038/s41419-019-2215-8 |
| format | Article |
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The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabetic atherosclerotic calcification and decreases vessel stiffening in mice through Runx2 suppression. Specifically, PARP-1 deficiency reduces diabetic arteriosclerotic calcification by regulating Stat1-mediated synthetic phenotype switching of vascular smooth muscle cells and macrophage polarization. Meanwhile, both vascular smooth muscle cells and macrophages manifested osteogenic differentiation in osteogenic media, which was attenuated by PARP-1/Stat1 inhibition. Notably, Stat1 acts as a positive transcription factor by directly binding to the promoter of Runx2 and promoting atherosclerotic calcification in diabetes. Our results identify a new function of PARP-1, in which metabolism disturbance-related stimuli activate the Runx2 expression mediated by Stat1 transcription to facilitate diabetic arteriosclerotic calcification. PARP-1 inhibition may therefore represent a useful therapy for this challenging complication.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-019-2215-8</identifier><identifier>PMID: 31924749</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 45/15 ; 631/136/142 ; 692/699/75/593/2193 ; 82/51 ; 82/80 ; Animals ; Antibodies ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis - enzymology ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Calcification ; Cbfa-1 protein ; Cell Biology ; Cell Culture ; Cell differentiation ; Clonal deletion ; Core Binding Factor Alpha 1 Subunit - metabolism ; Diabetes ; Diabetes Complications - enzymology ; Diabetes Complications - genetics ; Diabetes mellitus ; Immunology ; Life Sciences ; Macrophages ; Macrophages - metabolism ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Osteogenesis - genetics ; Phenanthrenes - pharmacology ; Phenotypes ; Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1 - genetics ; Poly (ADP-Ribose) Polymerase-1 - metabolism ; Poly(ADP-ribose) polymerase ; Poly(ADP-ribose) Polymerase 1 ; Poly(ADP-ribose) Polymerase Inhibitors - pharmacology ; Promoter Regions, Genetic ; Protein Binding ; Smooth muscle ; Stat1 protein ; STAT1 Transcription Factor - genetics ; STAT1 Transcription Factor - metabolism ; Vascular Calcification - enzymology ; Vascular Calcification - genetics</subject><ispartof>Cell death & disease, 2020-01, Vol.11 (1), p.22-22, Article 22</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-b55246c33a9756e36fac5f4ab2950ba50a3819885c26227de4a3381506eb9aae3</citedby><cites>FETCH-LOGICAL-c536t-b55246c33a9756e36fac5f4ab2950ba50a3819885c26227de4a3381506eb9aae3</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/PMC6954221/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954221/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31924749$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Peng</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Liu, Xue</creatorcontrib><creatorcontrib>Liu, Bin</creatorcontrib><creatorcontrib>Wang, Zhao-yang</creatorcontrib><creatorcontrib>Xie, Fei</creatorcontrib><creatorcontrib>Qiao, Wen</creatorcontrib><creatorcontrib>Liang, Er-shun</creatorcontrib><creatorcontrib>Lu, Qing-hua</creatorcontrib><creatorcontrib>Zhang, Ming-xiang</creatorcontrib><title>Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Accelerated atherosclerotic calcification is responsible for plaque burden, especially in diabetes. The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabetic atherosclerotic calcification and decreases vessel stiffening in mice through Runx2 suppression. Specifically, PARP-1 deficiency reduces diabetic arteriosclerotic calcification by regulating Stat1-mediated synthetic phenotype switching of vascular smooth muscle cells and macrophage polarization. Meanwhile, both vascular smooth muscle cells and macrophages manifested osteogenic differentiation in osteogenic media, which was attenuated by PARP-1/Stat1 inhibition. Notably, Stat1 acts as a positive transcription factor by directly binding to the promoter of Runx2 and promoting atherosclerotic calcification in diabetes. Our results identify a new function of PARP-1, in which metabolism disturbance-related stimuli activate the Runx2 expression mediated by Stat1 transcription to facilitate diabetic arteriosclerotic calcification. PARP-1 inhibition may therefore represent a useful therapy for this challenging complication.</description><subject>13/31</subject><subject>45/15</subject><subject>631/136/142</subject><subject>692/699/75/593/2193</subject><subject>82/51</subject><subject>82/80</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis - enzymology</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Calcification</subject><subject>Cbfa-1 protein</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell differentiation</subject><subject>Clonal deletion</subject><subject>Core Binding Factor Alpha 1 Subunit - metabolism</subject><subject>Diabetes</subject><subject>Diabetes Complications - 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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>Li, Peng</au><au>Wang, Ying</au><au>Liu, Xue</au><au>Liu, Bin</au><au>Wang, Zhao-yang</au><au>Xie, Fei</au><au>Qiao, Wen</au><au>Liang, Er-shun</au><au>Lu, Qing-hua</au><au>Zhang, Ming-xiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-01-10</date><risdate>2020</risdate><volume>11</volume><issue>1</issue><spage>22</spage><epage>22</epage><pages>22-22</pages><artnum>22</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Accelerated atherosclerotic calcification is responsible for plaque burden, especially in diabetes. The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabetic atherosclerotic calcification and decreases vessel stiffening in mice through Runx2 suppression. Specifically, PARP-1 deficiency reduces diabetic arteriosclerotic calcification by regulating Stat1-mediated synthetic phenotype switching of vascular smooth muscle cells and macrophage polarization. Meanwhile, both vascular smooth muscle cells and macrophages manifested osteogenic differentiation in osteogenic media, which was attenuated by PARP-1/Stat1 inhibition. Notably, Stat1 acts as a positive transcription factor by directly binding to the promoter of Runx2 and promoting atherosclerotic calcification in diabetes. Our results identify a new function of PARP-1, in which metabolism disturbance-related stimuli activate the Runx2 expression mediated by Stat1 transcription to facilitate diabetic arteriosclerotic calcification. PARP-1 inhibition may therefore represent a useful therapy for this challenging complication.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31924749</pmid><doi>10.1038/s41419-019-2215-8</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/31 45/15 631/136/142 692/699/75/593/2193 82/51 82/80 Animals Antibodies Apolipoproteins E - genetics Apolipoproteins E - metabolism Arteriosclerosis Atherosclerosis - enzymology Atherosclerosis - genetics Atherosclerosis - metabolism Biochemistry Biomedical and Life Sciences Calcification Cbfa-1 protein Cell Biology Cell Culture Cell differentiation Clonal deletion Core Binding Factor Alpha 1 Subunit - metabolism Diabetes Diabetes Complications - enzymology Diabetes Complications - genetics Diabetes mellitus Immunology Life Sciences Macrophages Macrophages - metabolism Mice Mice, Knockout Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Osteogenesis - genetics Phenanthrenes - pharmacology Phenotypes Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors Poly (ADP-Ribose) Polymerase-1 - genetics Poly (ADP-Ribose) Polymerase-1 - metabolism Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerase 1 Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Promoter Regions, Genetic Protein Binding Smooth muscle Stat1 protein STAT1 Transcription Factor - genetics STAT1 Transcription Factor - metabolism Vascular Calcification - enzymology Vascular Calcification - genetics |
| title | Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis |
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