Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis
Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2021, Vol.2021 (1), p.3119953-3119953 |
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| container_title | Oxidative medicine and cellular longevity |
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| creator | Wu, Qi Chen, Yuanyang Wang, Zhiwei Cai, Xin Che, Yanjia Zheng, Sihao Yuan, Shun Zhong, Xiaohan |
| description | Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia. |
| doi_str_mv | 10.1155/2021/3119953 |
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Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2021/3119953</identifier><identifier>PMID: 34900084</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>AMP-Activated Protein Kinases - metabolism ; Animals ; Antibodies ; Becaplermin - pharmacology ; Biotechnology ; Cardiovascular disease ; Carotid Arteries - pathology ; Cell culture ; Cell Dedifferentiation - drug effects ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cells, Cultured ; Coronary vessels ; Dynamins - metabolism ; Flow cytometry ; Hyperplasia ; Hyperplasia - metabolism ; Hyperplasia - pathology ; Kinases ; Laboratory animals ; Male ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - metabolism ; Medical prognosis ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondrial Dynamics - drug effects ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Phosphorylation ; Proliferating Cell Nuclear Antigen - genetics ; Proliferating Cell Nuclear Antigen - metabolism ; Rats ; Reactive Oxygen Species - metabolism ; Smooth muscle ; Vein & artery diseases ; Xanthones - pharmacology</subject><ispartof>Oxidative medicine and cellular longevity, 2021, Vol.2021 (1), p.3119953-3119953</ispartof><rights>Copyright © 2021 Qi Wu et al.</rights><rights>Copyright © 2021 Qi Wu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Qi Wu et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-9fdea121cdb39ecd225bf9bb1a3c724f338e31abba406677c851c8dd313177723</citedby><cites>FETCH-LOGICAL-c448t-9fdea121cdb39ecd225bf9bb1a3c724f338e31abba406677c851c8dd313177723</cites><orcidid>0000-0001-5643-9344</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/PMC8664531/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8664531/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34900084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Daiber, Andreas</contributor><creatorcontrib>Wu, Qi</creatorcontrib><creatorcontrib>Chen, Yuanyang</creatorcontrib><creatorcontrib>Wang, Zhiwei</creatorcontrib><creatorcontrib>Cai, Xin</creatorcontrib><creatorcontrib>Che, Yanjia</creatorcontrib><creatorcontrib>Zheng, Sihao</creatorcontrib><creatorcontrib>Yuan, Shun</creatorcontrib><creatorcontrib>Zhong, Xiaohan</creatorcontrib><title>Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia.</description><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Becaplermin - pharmacology</subject><subject>Biotechnology</subject><subject>Cardiovascular disease</subject><subject>Carotid Arteries - pathology</subject><subject>Cell culture</subject><subject>Cell Dedifferentiation - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Coronary vessels</subject><subject>Dynamins - metabolism</subject><subject>Flow cytometry</subject><subject>Hyperplasia</subject><subject>Hyperplasia - metabolism</subject><subject>Hyperplasia - pathology</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Qi</au><au>Chen, Yuanyang</au><au>Wang, Zhiwei</au><au>Cai, Xin</au><au>Che, Yanjia</au><au>Zheng, Sihao</au><au>Yuan, Shun</au><au>Zhong, Xiaohan</au><au>Daiber, Andreas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><issue>1</issue><spage>3119953</spage><epage>3119953</epage><pages>3119953-3119953</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>34900084</pmid><doi>10.1155/2021/3119953</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5643-9344</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AMP-Activated Protein Kinases - metabolism Animals Antibodies Becaplermin - pharmacology Biotechnology Cardiovascular disease Carotid Arteries - pathology Cell culture Cell Dedifferentiation - drug effects Cell Movement - drug effects Cell Proliferation - drug effects Cells, Cultured Coronary vessels Dynamins - metabolism Flow cytometry Hyperplasia Hyperplasia - metabolism Hyperplasia - pathology Kinases Laboratory animals Male Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Medical prognosis Mice Mice, Inbred C57BL Mitochondria Mitochondrial Dynamics - drug effects Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Phosphorylation Proliferating Cell Nuclear Antigen - genetics Proliferating Cell Nuclear Antigen - metabolism Rats Reactive Oxygen Species - metabolism Smooth muscle Vein & artery diseases Xanthones - pharmacology |
| title | Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis |
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