Circ-100290 Positively Regulates Angiogenesis Induced by Conditioned Medium of Human Amnion-Derived Mesenchymal Stem Cells Through miR-449a/eNOS and miR-449a/VEGFA Axes
The powerful pro-angiogenic capacity of human amnion-derived mesenchymal stem cells (hAMSCs) could be a valuable therapeutic angiogenesis strategy for bone regeneration. However, the molecular mechanisms underlying this process remain largely unknown. Herein, we report upregulated expression of circ...
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| Veröffentlicht in: | International journal of biological sciences 2020-01, Vol.16 (12), p.2131-2144 |
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| creator | Tang, Zichun Wu, Xiaoyue Hu, Liping Xiao, Yijing Tan, Junling Zuo, Siyu Shen, Ming Yuan, Xiaoqin |
| description | The powerful pro-angiogenic capacity of human amnion-derived mesenchymal stem cells (hAMSCs) could be a valuable therapeutic angiogenesis strategy for bone regeneration. However, the molecular mechanisms underlying this process remain largely unknown. Herein, we report upregulated expression of circular RNA 100290 (circ-100290) and an enhanced angiogenic phenotype of human umbilical vein endothelial cells (HUVECs) incubated with conditioned medium from hAMSCs (hAMSC-CM), whereas downregulation of circ-100290 reversed the pro-angiogenic capacity of HUVECs induced by hAMSC-CM. Circ-100290/microRNA 449a (miR-449a)/endothelial nitric oxide synthase (eNOS) and circ-100290/miR-449a/vascular endothelial growth factor A (VEGFA) axes were predicted by a bioinformatics method and subsequently verified by luciferase reporter assays
. Gain- or loss-of-function assays were then performed using small interfering RNAs (siRNAs) targeting circ-100290, or a plasmid overexpressing circ-100290. As expected, downregulation of circ-100290 in HUVECs led to weakened tube formation and migration of HUVECs following hAMSC-CM treatment, along with decreased expression of eNOS and VEGFA. In contrast, upregulation of circ-100290 led to enhanced tube formation and migration of HUVECs following hAMSC-CM treatment, along with increased expression of eNOS and VEGFA. Furthermore, a miR-449a inhibitor could largely rescue the effect of circ-100290 silencing on HUVECs, whereas a miR-449a mimic could significantly rescue the effect of overexpressing circ-100290 on HUVECs. Functional assays using eNOS or VEGF receptor inhibitors indicated eNOS and VEGFA may be important targets of miR-449a. Finally, a Matrigel plug assay revealed weakened angiogenesis when circ-100290 was silenced in HUVECs, but enhanced angiogenesis when circ-100290 was overexpressed
. Our results suggest that circ-100290 might function via miR-449a/eNOS and miR-449a/VEGFA axes in the pro-angiogenic role of hAMSC-CM on HUVECs. |
| doi_str_mv | 10.7150/ijbs.39895 |
| format | Article |
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. Gain- or loss-of-function assays were then performed using small interfering RNAs (siRNAs) targeting circ-100290, or a plasmid overexpressing circ-100290. As expected, downregulation of circ-100290 in HUVECs led to weakened tube formation and migration of HUVECs following hAMSC-CM treatment, along with decreased expression of eNOS and VEGFA. In contrast, upregulation of circ-100290 led to enhanced tube formation and migration of HUVECs following hAMSC-CM treatment, along with increased expression of eNOS and VEGFA. Furthermore, a miR-449a inhibitor could largely rescue the effect of circ-100290 silencing on HUVECs, whereas a miR-449a mimic could significantly rescue the effect of overexpressing circ-100290 on HUVECs. Functional assays using eNOS or VEGF receptor inhibitors indicated eNOS and VEGFA may be important targets of miR-449a. Finally, a Matrigel plug assay revealed weakened angiogenesis when circ-100290 was silenced in HUVECs, but enhanced angiogenesis when circ-100290 was overexpressed
. Our results suggest that circ-100290 might function via miR-449a/eNOS and miR-449a/VEGFA axes in the pro-angiogenic role of hAMSC-CM on HUVECs.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.39895</identifier><identifier>PMID: 32549760</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Amnion ; Angiogenesis ; Assaying ; Axes (reference lines) ; Binding sites ; Bioinformatics ; Bone growth ; Circular RNA ; Endothelial cells ; Experiments ; Gene expression ; Growth factors ; Mesenchymal stem cells ; miRNA ; Molecular modelling ; Nitric oxide ; Nitric-oxide synthase ; Phenotypes ; Plasmids ; Proteins ; Regeneration ; Regeneration (physiology) ; Research Paper ; Ribonucleic acid ; RNA ; siRNA ; Stem cells ; Umbilical vein ; Vascular endothelial growth factor ; Wound healing</subject><ispartof>International journal of biological sciences, 2020-01, Vol.16 (12), p.2131-2144</ispartof><rights>The author(s).</rights><rights>Copyright Ivyspring International Publisher Pty Ltd 2020</rights><rights>2020. This work is published under https://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><rights>The author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-c7dedb5142221b2d4f5f4d53901b0d338a936734a4b494cb9f3380978cc0c1523</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294943/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294943/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32549760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Zichun</creatorcontrib><creatorcontrib>Wu, Xiaoyue</creatorcontrib><creatorcontrib>Hu, Liping</creatorcontrib><creatorcontrib>Xiao, Yijing</creatorcontrib><creatorcontrib>Tan, Junling</creatorcontrib><creatorcontrib>Zuo, Siyu</creatorcontrib><creatorcontrib>Shen, Ming</creatorcontrib><creatorcontrib>Yuan, Xiaoqin</creatorcontrib><title>Circ-100290 Positively Regulates Angiogenesis Induced by Conditioned Medium of Human Amnion-Derived Mesenchymal Stem Cells Through miR-449a/eNOS and miR-449a/VEGFA Axes</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>The powerful pro-angiogenic capacity of human amnion-derived mesenchymal stem cells (hAMSCs) could be a valuable therapeutic angiogenesis strategy for bone regeneration. However, the molecular mechanisms underlying this process remain largely unknown. Herein, we report upregulated expression of circular RNA 100290 (circ-100290) and an enhanced angiogenic phenotype of human umbilical vein endothelial cells (HUVECs) incubated with conditioned medium from hAMSCs (hAMSC-CM), whereas downregulation of circ-100290 reversed the pro-angiogenic capacity of HUVECs induced by hAMSC-CM. Circ-100290/microRNA 449a (miR-449a)/endothelial nitric oxide synthase (eNOS) and circ-100290/miR-449a/vascular endothelial growth factor A (VEGFA) axes were predicted by a bioinformatics method and subsequently verified by luciferase reporter assays
. Gain- or loss-of-function assays were then performed using small interfering RNAs (siRNAs) targeting circ-100290, or a plasmid overexpressing circ-100290. As expected, downregulation of circ-100290 in HUVECs led to weakened tube formation and migration of HUVECs following hAMSC-CM treatment, along with decreased expression of eNOS and VEGFA. In contrast, upregulation of circ-100290 led to enhanced tube formation and migration of HUVECs following hAMSC-CM treatment, along with increased expression of eNOS and VEGFA. Furthermore, a miR-449a inhibitor could largely rescue the effect of circ-100290 silencing on HUVECs, whereas a miR-449a mimic could significantly rescue the effect of overexpressing circ-100290 on HUVECs. Functional assays using eNOS or VEGF receptor inhibitors indicated eNOS and VEGFA may be important targets of miR-449a. Finally, a Matrigel plug assay revealed weakened angiogenesis when circ-100290 was silenced in HUVECs, but enhanced angiogenesis when circ-100290 was overexpressed
. Our results suggest that circ-100290 might function via miR-449a/eNOS and miR-449a/VEGFA axes in the pro-angiogenic role of hAMSC-CM on HUVECs.</description><subject>Amnion</subject><subject>Angiogenesis</subject><subject>Assaying</subject><subject>Axes (reference lines)</subject><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Bone growth</subject><subject>Circular RNA</subject><subject>Endothelial cells</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Mesenchymal stem cells</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Phenotypes</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Regeneration</subject><subject>Regeneration (physiology)</subject><subject>Research Paper</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>siRNA</subject><subject>Stem cells</subject><subject>Umbilical vein</subject><subject>Vascular endothelial growth factor</subject><subject>Wound healing</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9kstu1TAQhiMEoqWw4QGQJTYIKa1vuXiDFIXepEJRW9hajj05x0eJ3dpJxXkjHhOHllJYsLI98-mf-eU_y14TvF-RAh_YTRf3mahF8STbJZyLnNK6fvrovpO9iHGDMSuLGj_PdhgtuKhKvJv9aG3QOcGYCoy--GgnewvDFl3Aah7UBBE1bmX9ChxEG9GpM7MGg7otar0zifYuPT-BsfOIfI9O5lE51IwuNfKPEJLa0o7g9Ho7qgFdTjCiFoYhoqt18PNqjUZ7kadN1QF8Pr9Eypk_lW-Hx0cNar5DfJk969UQ4dX9uZd9PTq8ak_ys_Pj07Y5yzVnfMp1ZcB0BeGUUtJRw_ui56ZgApMOG8ZqJVhZMa54xwXXnehTDYuq1hprUlC2l324072euxGMBjcFNcjrYEcVttIrK__uOLuWK38rKyqSIksC7-4Fgr-ZIU5ytFEnw8qBn6OknPCKsQovs97-g278HFyyJ2khao6ZIP-nOF0-FZdlot7fUTr4GAP0DysTLJeYyCUm8ldMEvzmsckH9Hcu2E8s-ba5</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Tang, Zichun</creator><creator>Wu, Xiaoyue</creator><creator>Hu, Liping</creator><creator>Xiao, Yijing</creator><creator>Tan, Junling</creator><creator>Zuo, Siyu</creator><creator>Shen, Ming</creator><creator>Yuan, Xiaoqin</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Circ-100290 Positively Regulates Angiogenesis Induced by Conditioned Medium of Human Amnion-Derived Mesenchymal Stem Cells Through miR-449a/eNOS and miR-449a/VEGFA Axes</title><author>Tang, Zichun ; Wu, Xiaoyue ; Hu, Liping ; Xiao, Yijing ; Tan, Junling ; Zuo, Siyu ; Shen, Ming ; Yuan, Xiaoqin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-c7dedb5142221b2d4f5f4d53901b0d338a936734a4b494cb9f3380978cc0c1523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Amnion</topic><topic>Angiogenesis</topic><topic>Assaying</topic><topic>Axes (reference lines)</topic><topic>Binding sites</topic><topic>Bioinformatics</topic><topic>Bone growth</topic><topic>Circular RNA</topic><topic>Endothelial cells</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Mesenchymal stem cells</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Phenotypes</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Regeneration</topic><topic>Regeneration (physiology)</topic><topic>Research Paper</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>siRNA</topic><topic>Stem cells</topic><topic>Umbilical vein</topic><topic>Vascular endothelial growth factor</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Zichun</creatorcontrib><creatorcontrib>Wu, Xiaoyue</creatorcontrib><creatorcontrib>Hu, Liping</creatorcontrib><creatorcontrib>Xiao, Yijing</creatorcontrib><creatorcontrib>Tan, Junling</creatorcontrib><creatorcontrib>Zuo, Siyu</creatorcontrib><creatorcontrib>Shen, Ming</creatorcontrib><creatorcontrib>Yuan, Xiaoqin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Zichun</au><au>Wu, Xiaoyue</au><au>Hu, Liping</au><au>Xiao, Yijing</au><au>Tan, Junling</au><au>Zuo, Siyu</au><au>Shen, Ming</au><au>Yuan, Xiaoqin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circ-100290 Positively Regulates Angiogenesis Induced by Conditioned Medium of Human Amnion-Derived Mesenchymal Stem Cells Through miR-449a/eNOS and miR-449a/VEGFA Axes</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>16</volume><issue>12</issue><spage>2131</spage><epage>2144</epage><pages>2131-2144</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>The powerful pro-angiogenic capacity of human amnion-derived mesenchymal stem cells (hAMSCs) could be a valuable therapeutic angiogenesis strategy for bone regeneration. However, the molecular mechanisms underlying this process remain largely unknown. Herein, we report upregulated expression of circular RNA 100290 (circ-100290) and an enhanced angiogenic phenotype of human umbilical vein endothelial cells (HUVECs) incubated with conditioned medium from hAMSCs (hAMSC-CM), whereas downregulation of circ-100290 reversed the pro-angiogenic capacity of HUVECs induced by hAMSC-CM. Circ-100290/microRNA 449a (miR-449a)/endothelial nitric oxide synthase (eNOS) and circ-100290/miR-449a/vascular endothelial growth factor A (VEGFA) axes were predicted by a bioinformatics method and subsequently verified by luciferase reporter assays
. Gain- or loss-of-function assays were then performed using small interfering RNAs (siRNAs) targeting circ-100290, or a plasmid overexpressing circ-100290. As expected, downregulation of circ-100290 in HUVECs led to weakened tube formation and migration of HUVECs following hAMSC-CM treatment, along with decreased expression of eNOS and VEGFA. In contrast, upregulation of circ-100290 led to enhanced tube formation and migration of HUVECs following hAMSC-CM treatment, along with increased expression of eNOS and VEGFA. Furthermore, a miR-449a inhibitor could largely rescue the effect of circ-100290 silencing on HUVECs, whereas a miR-449a mimic could significantly rescue the effect of overexpressing circ-100290 on HUVECs. Functional assays using eNOS or VEGF receptor inhibitors indicated eNOS and VEGFA may be important targets of miR-449a. Finally, a Matrigel plug assay revealed weakened angiogenesis when circ-100290 was silenced in HUVECs, but enhanced angiogenesis when circ-100290 was overexpressed
. Our results suggest that circ-100290 might function via miR-449a/eNOS and miR-449a/VEGFA axes in the pro-angiogenic role of hAMSC-CM on HUVECs.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>32549760</pmid><doi>10.7150/ijbs.39895</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amnion Angiogenesis Assaying Axes (reference lines) Binding sites Bioinformatics Bone growth Circular RNA Endothelial cells Experiments Gene expression Growth factors Mesenchymal stem cells miRNA Molecular modelling Nitric oxide Nitric-oxide synthase Phenotypes Plasmids Proteins Regeneration Regeneration (physiology) Research Paper Ribonucleic acid RNA siRNA Stem cells Umbilical vein Vascular endothelial growth factor Wound healing |
| title | Circ-100290 Positively Regulates Angiogenesis Induced by Conditioned Medium of Human Amnion-Derived Mesenchymal Stem Cells Through miR-449a/eNOS and miR-449a/VEGFA Axes |
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