Effects of serum starvation and vascular endothelial growth factor stimulation on the expression of Notch signalling pathway components
Brain arteriovenous malformation (BAVM) is an abnormality in the cerebral vascular system. Although the upregulation of the Notch signalling pathway is a deterministic factor in BAVM, the mechanism by which this pathway is upregulated in patients with BAVM is uncertain. The effects of serum starvati...
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| Veröffentlicht in: | Science progress (1916) 2021-07, Vol.104 (3), p.368504211028387-368504211028387 |
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| creator | Li, Liming Liu, Xiaqing Zhao, Mingguang Guo, Peng Zhang, Haifeng |
| description | Brain arteriovenous malformation (BAVM) is an abnormality in the cerebral vascular system. Although the upregulation of the Notch signalling pathway is a deterministic factor in BAVM, the mechanism by which this pathway is upregulated in patients with BAVM is uncertain. The effects of serum starvation and vascular endothelial growth factor (VEGF) stimulation on the Notch signalling pathway in brain microvascular endothelial cells (MECs) and mouse embryonic stem (mES)/embryoid body (EB)-derived endothelial cells were investigated in this study. The duration of serum starvation and VEGF concentration were changed, cell viability was measured, and reasonable time and concentration gradients were selected for subsequent studies. Protein and mRNA expression levels of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells were detected using western blotting and real-time PCR, respectively. Expression levels of the Notch1, Notch4, Jagged1, delta-like ligand 4 (Dll4) and Hes1 proteins and mRNAs were upregulated by lower VEGF concentrations and shorter-term serum starvation but inhibited by higher VEGF concentrations and longer-term serum starvation. This study revealed effects of changes in the duration of serum starvation and VEGF concentration on the expression of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells, potentially contributing to BAVM formation. |
| doi_str_mv | 10.1177/00368504211028387 |
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Although the upregulation of the Notch signalling pathway is a deterministic factor in BAVM, the mechanism by which this pathway is upregulated in patients with BAVM is uncertain. The effects of serum starvation and vascular endothelial growth factor (VEGF) stimulation on the Notch signalling pathway in brain microvascular endothelial cells (MECs) and mouse embryonic stem (mES)/embryoid body (EB)-derived endothelial cells were investigated in this study. The duration of serum starvation and VEGF concentration were changed, cell viability was measured, and reasonable time and concentration gradients were selected for subsequent studies. Protein and mRNA expression levels of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells were detected using western blotting and real-time PCR, respectively. Expression levels of the Notch1, Notch4, Jagged1, delta-like ligand 4 (Dll4) and Hes1 proteins and mRNAs were upregulated by lower VEGF concentrations and shorter-term serum starvation but inhibited by higher VEGF concentrations and longer-term serum starvation. This study revealed effects of changes in the duration of serum starvation and VEGF concentration on the expression of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells, potentially contributing to BAVM formation.</description><identifier>ISSN: 0036-8504</identifier><identifier>EISSN: 2047-7163</identifier><identifier>DOI: 10.1177/00368504211028387</identifier><identifier>PMID: 34231445</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Arteriovenous Malformations - metabolism ; Brain ; Cell viability ; Concentration gradient ; Endothelial cells ; Endothelial Cells - metabolism ; Gene expression ; Growth factors ; Humans ; Jagged1 protein ; Mice ; Microvasculature ; Notch1 protein ; Proteins ; Receptor, Notch1 - genetics ; Receptor, Notch1 - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Messenger - pharmacology ; Signal Transduction ; Signaling ; Stimulation ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism ; Vascular system ; Western blotting</subject><ispartof>Science progress (1916), 2021-07, Vol.104 (3), p.368504211028387-368504211028387</ispartof><rights>The Author(s) 2021</rights><rights>2021. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/ ) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage ). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2021 2021 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c419t-144bd6a1b99f081419203db05a32caa6becdf7f7e5beeb64c2baeb8c11dd4eec3</cites><orcidid>0000-0002-2796-362X ; 0000-0002-2524-7590</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/PMC10450735/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10450735/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,21966,27853,27924,27925,44945,45333,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34231445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Liming</creatorcontrib><creatorcontrib>Liu, Xiaqing</creatorcontrib><creatorcontrib>Zhao, Mingguang</creatorcontrib><creatorcontrib>Guo, Peng</creatorcontrib><creatorcontrib>Zhang, Haifeng</creatorcontrib><title>Effects of serum starvation and vascular endothelial growth factor stimulation on the expression of Notch signalling pathway components</title><title>Science progress (1916)</title><addtitle>Sci Prog</addtitle><description>Brain arteriovenous malformation (BAVM) is an abnormality in the cerebral vascular system. Although the upregulation of the Notch signalling pathway is a deterministic factor in BAVM, the mechanism by which this pathway is upregulated in patients with BAVM is uncertain. The effects of serum starvation and vascular endothelial growth factor (VEGF) stimulation on the Notch signalling pathway in brain microvascular endothelial cells (MECs) and mouse embryonic stem (mES)/embryoid body (EB)-derived endothelial cells were investigated in this study. The duration of serum starvation and VEGF concentration were changed, cell viability was measured, and reasonable time and concentration gradients were selected for subsequent studies. Protein and mRNA expression levels of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells were detected using western blotting and real-time PCR, respectively. Expression levels of the Notch1, Notch4, Jagged1, delta-like ligand 4 (Dll4) and Hes1 proteins and mRNAs were upregulated by lower VEGF concentrations and shorter-term serum starvation but inhibited by higher VEGF concentrations and longer-term serum starvation. This study revealed effects of changes in the duration of serum starvation and VEGF concentration on the expression of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells, potentially contributing to BAVM formation.</description><subject>Animals</subject><subject>Arteriovenous Malformations - metabolism</subject><subject>Brain</subject><subject>Cell viability</subject><subject>Concentration gradient</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Jagged1 protein</subject><subject>Mice</subject><subject>Microvasculature</subject><subject>Notch1 protein</subject><subject>Proteins</subject><subject>Receptor, Notch1 - genetics</subject><subject>Receptor, Notch1 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Messenger - pharmacology</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stimulation</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Vascular system</subject><subject>Western blotting</subject><issn>0036-8504</issn><issn>2047-7163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><recordid>eNp1kcFu1TAQRS1ERR-FD2CDLLFhk9aOnThZIVS1gFSVDayjiTNOUjlxsJ3X9gv47fr1lUJBSJYszZx7Z-xLyBvOjjlX6oQxUVYFkznnLK9EpZ6RTc6kyhQvxXOy2fWzHXBIXoZwxRgveFm9IIdC5oJLWWzIzzNjUMdAnaEB_TrREMFvIY5upjB3dAtBrxY8xblzcUA7gqW9d9dxoAZ0dD4pxikh95J0EkTxZvEYwn3F0EsX9UDD2M9g7Tj3dIE4XMMt1W5a3IxzDK_IgQEb8PXDfUS-n599O_2cXXz99OX040WmJa9jlpZuuxJ4W9eGVTzVcia6lhUgcg1Qtqg7o4zCokVsS6nzFrCtNOddJxG1OCIf9r7L2k7Y6TTbg20WP07gbxsHY_O0M49D07ttw5ksmBJFcnj_4ODdjxVDbKYxaLQWZnRraPJC1ryupRQJffcXeuVWnz5hR6mKqRRNlSi-p7R3IXg0j9tw1uxybv7JOWne_vmMR8WvYBNwvAcC9Ph77P8d7wDED7U4</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Li, Liming</creator><creator>Liu, Xiaqing</creator><creator>Zhao, Mingguang</creator><creator>Guo, Peng</creator><creator>Zhang, Haifeng</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AFRWT</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>F28</scope><scope>FR3</scope><scope>JQ2</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2796-362X</orcidid><orcidid>https://orcid.org/0000-0002-2524-7590</orcidid></search><sort><creationdate>20210701</creationdate><title>Effects of serum starvation and vascular endothelial growth factor stimulation on the expression of Notch signalling pathway components</title><author>Li, Liming ; Liu, Xiaqing ; Zhao, Mingguang ; Guo, Peng ; Zhang, Haifeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-144bd6a1b99f081419203db05a32caa6becdf7f7e5beeb64c2baeb8c11dd4eec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Arteriovenous Malformations - metabolism</topic><topic>Brain</topic><topic>Cell viability</topic><topic>Concentration gradient</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Jagged1 protein</topic><topic>Mice</topic><topic>Microvasculature</topic><topic>Notch1 protein</topic><topic>Proteins</topic><topic>Receptor, Notch1 - genetics</topic><topic>Receptor, Notch1 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Messenger - pharmacology</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Stimulation</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascular system</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Liming</creatorcontrib><creatorcontrib>Liu, Xiaqing</creatorcontrib><creatorcontrib>Zhao, Mingguang</creatorcontrib><creatorcontrib>Guo, Peng</creatorcontrib><creatorcontrib>Zhang, Haifeng</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Science progress (1916)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Liming</au><au>Liu, Xiaqing</au><au>Zhao, Mingguang</au><au>Guo, Peng</au><au>Zhang, Haifeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of serum starvation and vascular endothelial growth factor stimulation on the expression of Notch signalling pathway components</atitle><jtitle>Science progress (1916)</jtitle><addtitle>Sci Prog</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>104</volume><issue>3</issue><spage>368504211028387</spage><epage>368504211028387</epage><pages>368504211028387-368504211028387</pages><issn>0036-8504</issn><eissn>2047-7163</eissn><abstract>Brain arteriovenous malformation (BAVM) is an abnormality in the cerebral vascular system. Although the upregulation of the Notch signalling pathway is a deterministic factor in BAVM, the mechanism by which this pathway is upregulated in patients with BAVM is uncertain. The effects of serum starvation and vascular endothelial growth factor (VEGF) stimulation on the Notch signalling pathway in brain microvascular endothelial cells (MECs) and mouse embryonic stem (mES)/embryoid body (EB)-derived endothelial cells were investigated in this study. The duration of serum starvation and VEGF concentration were changed, cell viability was measured, and reasonable time and concentration gradients were selected for subsequent studies. Protein and mRNA expression levels of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells were detected using western blotting and real-time PCR, respectively. Expression levels of the Notch1, Notch4, Jagged1, delta-like ligand 4 (Dll4) and Hes1 proteins and mRNAs were upregulated by lower VEGF concentrations and shorter-term serum starvation but inhibited by higher VEGF concentrations and longer-term serum starvation. This study revealed effects of changes in the duration of serum starvation and VEGF concentration on the expression of Notch signalling pathway components in both MECs and mES/EB-derived endothelial cells, potentially contributing to BAVM formation.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>34231445</pmid><doi>10.1177/00368504211028387</doi><orcidid>https://orcid.org/0000-0002-2796-362X</orcidid><orcidid>https://orcid.org/0000-0002-2524-7590</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arteriovenous Malformations - metabolism Brain Cell viability Concentration gradient Endothelial cells Endothelial Cells - metabolism Gene expression Growth factors Humans Jagged1 protein Mice Microvasculature Notch1 protein Proteins Receptor, Notch1 - genetics Receptor, Notch1 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Messenger - pharmacology Signal Transduction Signaling Stimulation Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism Vascular system Western blotting |
| title | Effects of serum starvation and vascular endothelial growth factor stimulation on the expression of Notch signalling pathway components |
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