Celastrol attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling
Vascular calcification is an important risk factor for the mortality and morbidity in chronic kidney disease (CKD). Unfortunately, until now there is no certain medication targeting vascular calcification in CKD. In this study, we explored the inhibitory effect of celastrol on high calcium–induced v...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-11, Vol.24 (21), p.12476-12490 |
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| creator | Su, Zhongping Zong, Pengyu Chen, Ji Yang, Shuo Shen, Yihui Lu, Yan Yang, Chuanxi Kong, Xiangqing Sheng, Yanhui Sun, Wei |
| description | Vascular calcification is an important risk factor for the mortality and morbidity in chronic kidney disease (CKD). Unfortunately, until now there is no certain medication targeting vascular calcification in CKD. In this study, we explored the inhibitory effect of celastrol on high calcium–induced vascular calcification and the underlying molecular mechanisms. Cell proliferation assay showed that celastrol inhibited aortic valve interstitial cell (VIC) and vascular smooth muscle cell (VSMC) proliferation when its concentration was higher than 0.6 μmol/L. 0.8 μmol/L celastrol inhibited the expression of osteogenic genes and calcium deposition induced by high‐calcium medium in both AVICs and VSMCs. In mouse vascular calcification model induced by adenine combined with vitamin D, alizarin red and immunostaining showed that celastrol inhibited pro‐calcification gene expression and calcium deposition in aortic wall and aortic valve tissues. At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p‐Smad1/5) and non‐phosphorylated β‐catenin (n‐p‐β‐catenin) induced by high‐calcium medium both in vitro and in vivo. Also, BMP2 overexpression reversed the anti‐calcification effects of celastrol by recovering the decrease of p‐Smad1/5 and n‐p‐β‐catenin. Furthermore, celastrol prevented the up‐regulation of BMPRII and down‐regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium–induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD. |
| doi_str_mv | 10.1111/jcmm.15779 |
| format | Article |
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Unfortunately, until now there is no certain medication targeting vascular calcification in CKD. In this study, we explored the inhibitory effect of celastrol on high calcium–induced vascular calcification and the underlying molecular mechanisms. Cell proliferation assay showed that celastrol inhibited aortic valve interstitial cell (VIC) and vascular smooth muscle cell (VSMC) proliferation when its concentration was higher than 0.6 μmol/L. 0.8 μmol/L celastrol inhibited the expression of osteogenic genes and calcium deposition induced by high‐calcium medium in both AVICs and VSMCs. In mouse vascular calcification model induced by adenine combined with vitamin D, alizarin red and immunostaining showed that celastrol inhibited pro‐calcification gene expression and calcium deposition in aortic wall and aortic valve tissues. At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p‐Smad1/5) and non‐phosphorylated β‐catenin (n‐p‐β‐catenin) induced by high‐calcium medium both in vitro and in vivo. Also, BMP2 overexpression reversed the anti‐calcification effects of celastrol by recovering the decrease of p‐Smad1/5 and n‐p‐β‐catenin. Furthermore, celastrol prevented the up‐regulation of BMPRII and down‐regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium–induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15779</identifier><identifier>PMID: 32954678</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adenine ; Adenoviruses ; Alzheimer's disease ; Aortic valve ; BMP2/Smad1/5 signalling ; Calcification ; Calcification (ectopic) ; Calcium ; Catenin ; celastrol ; Cell proliferation ; Experiments ; Gene expression ; high calcium ; Kidney diseases ; Metabolism ; Mineralization ; Molecular modelling ; Morbidity ; Original ; Penicillin ; Proteins ; Risk factors ; Smooth muscle ; vascular and valvular calcification ; Veins & arteries ; Vitamin D</subject><ispartof>Journal of cellular and molecular medicine, 2020-11, Vol.24 (21), p.12476-12490</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. 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-c4489-b280590dd2ddda192b863fc053881fcdde812d1b0d25e63360b94795999b91d03</citedby><cites>FETCH-LOGICAL-c4489-b280590dd2ddda192b863fc053881fcdde812d1b0d25e63360b94795999b91d03</cites><orcidid>0000-0001-9823-6529</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/PMC7686965/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686965/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32954678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Zhongping</creatorcontrib><creatorcontrib>Zong, Pengyu</creatorcontrib><creatorcontrib>Chen, Ji</creatorcontrib><creatorcontrib>Yang, Shuo</creatorcontrib><creatorcontrib>Shen, Yihui</creatorcontrib><creatorcontrib>Lu, Yan</creatorcontrib><creatorcontrib>Yang, Chuanxi</creatorcontrib><creatorcontrib>Kong, Xiangqing</creatorcontrib><creatorcontrib>Sheng, Yanhui</creatorcontrib><creatorcontrib>Sun, Wei</creatorcontrib><title>Celastrol attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Vascular calcification is an important risk factor for the mortality and morbidity in chronic kidney disease (CKD). Unfortunately, until now there is no certain medication targeting vascular calcification in CKD. In this study, we explored the inhibitory effect of celastrol on high calcium–induced vascular calcification and the underlying molecular mechanisms. Cell proliferation assay showed that celastrol inhibited aortic valve interstitial cell (VIC) and vascular smooth muscle cell (VSMC) proliferation when its concentration was higher than 0.6 μmol/L. 0.8 μmol/L celastrol inhibited the expression of osteogenic genes and calcium deposition induced by high‐calcium medium in both AVICs and VSMCs. In mouse vascular calcification model induced by adenine combined with vitamin D, alizarin red and immunostaining showed that celastrol inhibited pro‐calcification gene expression and calcium deposition in aortic wall and aortic valve tissues. At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p‐Smad1/5) and non‐phosphorylated β‐catenin (n‐p‐β‐catenin) induced by high‐calcium medium both in vitro and in vivo. Also, BMP2 overexpression reversed the anti‐calcification effects of celastrol by recovering the decrease of p‐Smad1/5 and n‐p‐β‐catenin. Furthermore, celastrol prevented the up‐regulation of BMPRII and down‐regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium–induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD.</description><subject>Adenine</subject><subject>Adenoviruses</subject><subject>Alzheimer's disease</subject><subject>Aortic valve</subject><subject>BMP2/Smad1/5 signalling</subject><subject>Calcification</subject><subject>Calcification (ectopic)</subject><subject>Calcium</subject><subject>Catenin</subject><subject>celastrol</subject><subject>Cell proliferation</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>high calcium</subject><subject>Kidney diseases</subject><subject>Metabolism</subject><subject>Mineralization</subject><subject>Molecular 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attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling</title><author>Su, Zhongping ; Zong, Pengyu ; Chen, Ji ; Yang, Shuo ; Shen, Yihui ; Lu, Yan ; Yang, Chuanxi ; Kong, Xiangqing ; Sheng, Yanhui ; Sun, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4489-b280590dd2ddda192b863fc053881fcdde812d1b0d25e63360b94795999b91d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenine</topic><topic>Adenoviruses</topic><topic>Alzheimer's disease</topic><topic>Aortic valve</topic><topic>BMP2/Smad1/5 signalling</topic><topic>Calcification</topic><topic>Calcification (ectopic)</topic><topic>Calcium</topic><topic>Catenin</topic><topic>celastrol</topic><topic>Cell proliferation</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>high calcium</topic><topic>Kidney 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calcification via inhibiting BMP2/Smad1/5 signalling</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-11</date><risdate>2020</risdate><volume>24</volume><issue>21</issue><spage>12476</spage><epage>12490</epage><pages>12476-12490</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Vascular calcification is an important risk factor for the mortality and morbidity in chronic kidney disease (CKD). Unfortunately, until now there is no certain medication targeting vascular calcification in CKD. In this study, we explored the inhibitory effect of celastrol on high calcium–induced vascular calcification and the underlying molecular mechanisms. Cell proliferation assay showed that celastrol inhibited aortic valve interstitial cell (VIC) and vascular smooth muscle cell (VSMC) proliferation when its concentration was higher than 0.6 μmol/L. 0.8 μmol/L celastrol inhibited the expression of osteogenic genes and calcium deposition induced by high‐calcium medium in both AVICs and VSMCs. In mouse vascular calcification model induced by adenine combined with vitamin D, alizarin red and immunostaining showed that celastrol inhibited pro‐calcification gene expression and calcium deposition in aortic wall and aortic valve tissues. At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p‐Smad1/5) and non‐phosphorylated β‐catenin (n‐p‐β‐catenin) induced by high‐calcium medium both in vitro and in vivo. Also, BMP2 overexpression reversed the anti‐calcification effects of celastrol by recovering the decrease of p‐Smad1/5 and n‐p‐β‐catenin. Furthermore, celastrol prevented the up‐regulation of BMPRII and down‐regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium–induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32954678</pmid><doi>10.1111/jcmm.15779</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-9823-6529</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenine Adenoviruses Alzheimer's disease Aortic valve BMP2/Smad1/5 signalling Calcification Calcification (ectopic) Calcium Catenin celastrol Cell proliferation Experiments Gene expression high calcium Kidney diseases Metabolism Mineralization Molecular modelling Morbidity Original Penicillin Proteins Risk factors Smooth muscle vascular and valvular calcification Veins & arteries Vitamin D |
| title | Celastrol attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling |
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