The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis
Background Sulforaphane (SUL), a kind of isothiocyanate, has recently been focused due to its strong pro-apoptotic effect on cancer cells as well as tumor vascular endothelial cells (ECs). And recently, we demonstrated the induction of autophagy by colon cancer cells as a protective mechanism agains...
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| Veröffentlicht in: | Angiogenesis (London) 2010-09, Vol.13 (3), p.227-238 |
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| creator | Nishikawa, Takeshi Tsuno, Nelson H. Okaji, Yurai Sunami, Eiji Shuno, Yasutaka Sasaki, Kazuhito Hongo, Kumiko Kaneko, Manabu Hiyoshi, Masaya Kawai, Kazushige Kitayama, Joji Takahashi, Koki Nagawa, Hirokazu |
| description | Background
Sulforaphane (SUL), a kind of isothiocyanate, has recently been focused due to its strong pro-apoptotic effect on cancer cells as well as tumor vascular endothelial cells (ECs). And recently, we demonstrated the induction of autophagy by colon cancer cells as a protective mechanism against SUL. In the present study, we aimed to investigate the possible role of autophagy induction by ECs as a defense mechanism against SUL.
Methods
Human umbilical vein endothelial cells (HUVECs) were used as the in vitro model of angiogenic ECs. The induction of autophagy was evaluated by the detection of acidic vesicular organelles (AVOs) by flow-cytometry, after the staining with acridine orange, as well as the detection of light chain 3(LC3) by Western blot. Finally, the functional implication of autophagy inhibition and SUL treatment in ECs was investigated by their ability to form vascular-like structures on Matrigel.
Results
Treatment of HUVECs with relatively low concentrations of SUL for 16 h resulted in the evident formation of AVOs and the recruitment of LC3 to autophagosomes, the pathognomonic features of autophagy. Co-treatment of cells with the specific autophagy inhibitor (3-methyladenine) potentiated the proapoptotic effect of SUL. And inhibition of autophagy potentiated the inhibitory effect of SUL on the ability of ECs to form capillary-like structures.
Conclusion
Similar to cancer cells, ECs induced autophagy in response to the pro-apoptotic agent, SUL, and the inhibition of autophagy potentiated the pro-apoptotic effect. These findings open premises for the use of autophagy inhibitors in combination with anti–angiogenic agents. |
| doi_str_mv | 10.1007/s10456-010-9180-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_755172150</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>755172150</sourcerecordid><originalsourceid>FETCH-LOGICAL-c466t-d10286f74bfb21cb2ed27ad10790dcc8706131aea2f916cf35aa5675d7cb0e3f3</originalsourceid><addsrcrecordid>eNp1kcFrHCEYxaW0NJu0f0AvZQiUnGw_nVHHY1naJBDIJT2L4-isYVan6hz2v6_LbhsI9KR8_t77Hj6EPhH4SgDEt0ygYxwDASxJD5i-QRvCRIsFBfkWbUByibkUcIEuc34GqIO-e48uKHDZia7bIPu0s40POz_44mNoomv0WuKy09OhWWKxoXhdbG50vWAdJh8nG7xprHPWlHwU5HV2MemqCbYZDtVuXI0PU6OXuJSYff6A3jk9Z_vxfF6hXz9_PG3v8MPj7f32-wM2HecFjwRoz53oBjdQYgZqRyp0nQoJozG9AE5aoq2mThJuXMu0ZlywUZgBbOvaK3Rz8l1S_L3aXNTeZ2PnuSaLa1aCMSIoYVDJ61fkc1xTqOEq1PaV6mSFyAkyKeacrFNL8nudDoqAOjagTg2o2oA6NqBo1Xw-G6_D3o7_FH-_vAJfzoDORs8u6WB8fuFaypkQRyN64nJ9CpNNLwn_v_0PeMKfQA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>753817249</pqid></control><display><type>article</type><title>The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis</title><source>MEDLINE</source><source>SpringerLink</source><creator>Nishikawa, Takeshi ; Tsuno, Nelson H. ; Okaji, Yurai ; Sunami, Eiji ; Shuno, Yasutaka ; Sasaki, Kazuhito ; Hongo, Kumiko ; Kaneko, Manabu ; Hiyoshi, Masaya ; Kawai, Kazushige ; Kitayama, Joji ; Takahashi, Koki ; Nagawa, Hirokazu</creator><creatorcontrib>Nishikawa, Takeshi ; Tsuno, Nelson H. ; Okaji, Yurai ; Sunami, Eiji ; Shuno, Yasutaka ; Sasaki, Kazuhito ; Hongo, Kumiko ; Kaneko, Manabu ; Hiyoshi, Masaya ; Kawai, Kazushige ; Kitayama, Joji ; Takahashi, Koki ; Nagawa, Hirokazu</creatorcontrib><description>Background
Sulforaphane (SUL), a kind of isothiocyanate, has recently been focused due to its strong pro-apoptotic effect on cancer cells as well as tumor vascular endothelial cells (ECs). And recently, we demonstrated the induction of autophagy by colon cancer cells as a protective mechanism against SUL. In the present study, we aimed to investigate the possible role of autophagy induction by ECs as a defense mechanism against SUL.
Methods
Human umbilical vein endothelial cells (HUVECs) were used as the in vitro model of angiogenic ECs. The induction of autophagy was evaluated by the detection of acidic vesicular organelles (AVOs) by flow-cytometry, after the staining with acridine orange, as well as the detection of light chain 3(LC3) by Western blot. Finally, the functional implication of autophagy inhibition and SUL treatment in ECs was investigated by their ability to form vascular-like structures on Matrigel.
Results
Treatment of HUVECs with relatively low concentrations of SUL for 16 h resulted in the evident formation of AVOs and the recruitment of LC3 to autophagosomes, the pathognomonic features of autophagy. Co-treatment of cells with the specific autophagy inhibitor (3-methyladenine) potentiated the proapoptotic effect of SUL. And inhibition of autophagy potentiated the inhibitory effect of SUL on the ability of ECs to form capillary-like structures.
Conclusion
Similar to cancer cells, ECs induced autophagy in response to the pro-apoptotic agent, SUL, and the inhibition of autophagy potentiated the pro-apoptotic effect. These findings open premises for the use of autophagy inhibitors in combination with anti–angiogenic agents.</description><identifier>ISSN: 0969-6970</identifier><identifier>EISSN: 1573-7209</identifier><identifier>DOI: 10.1007/s10456-010-9180-2</identifier><identifier>PMID: 20694744</identifier><identifier>CODEN: AGIOFT</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Angiogenesis Inhibitors - pharmacology ; Apoptosis - drug effects ; Autophagy - drug effects ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Blood and lymphatic vessels ; Blotting, Western ; Cancer Research ; Cardiology ; Cardiology. Vascular system ; Cardiovascular system ; Caspases - metabolism ; Cell Biology ; Cell Proliferation - drug effects ; Colony-Forming Units Assay ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endothelial Cells - cytology ; Endothelial Cells - drug effects ; Endothelial Cells - enzymology ; Flow Cytometry ; Humans ; Isothiocyanates ; Medical sciences ; Microtubule-Associated Proteins - metabolism ; Neovascularization, Physiologic - drug effects ; Oncology ; Ophthalmology ; Organelles - drug effects ; Organelles - metabolism ; Original Paper ; Pharmacology. Drug treatments ; Thiocyanates - pharmacology ; Umbilical Veins - cytology ; Vasodilator agents. Cerebral vasodilators</subject><ispartof>Angiogenesis (London), 2010-09, Vol.13 (3), p.227-238</ispartof><rights>Springer Science+Business Media B.V. 2010</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-d10286f74bfb21cb2ed27ad10790dcc8706131aea2f916cf35aa5675d7cb0e3f3</citedby><cites>FETCH-LOGICAL-c466t-d10286f74bfb21cb2ed27ad10790dcc8706131aea2f916cf35aa5675d7cb0e3f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10456-010-9180-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10456-010-9180-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23265772$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20694744$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishikawa, Takeshi</creatorcontrib><creatorcontrib>Tsuno, Nelson H.</creatorcontrib><creatorcontrib>Okaji, Yurai</creatorcontrib><creatorcontrib>Sunami, Eiji</creatorcontrib><creatorcontrib>Shuno, Yasutaka</creatorcontrib><creatorcontrib>Sasaki, Kazuhito</creatorcontrib><creatorcontrib>Hongo, Kumiko</creatorcontrib><creatorcontrib>Kaneko, Manabu</creatorcontrib><creatorcontrib>Hiyoshi, Masaya</creatorcontrib><creatorcontrib>Kawai, Kazushige</creatorcontrib><creatorcontrib>Kitayama, Joji</creatorcontrib><creatorcontrib>Takahashi, Koki</creatorcontrib><creatorcontrib>Nagawa, Hirokazu</creatorcontrib><title>The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis</title><title>Angiogenesis (London)</title><addtitle>Angiogenesis</addtitle><addtitle>Angiogenesis</addtitle><description>Background
Sulforaphane (SUL), a kind of isothiocyanate, has recently been focused due to its strong pro-apoptotic effect on cancer cells as well as tumor vascular endothelial cells (ECs). And recently, we demonstrated the induction of autophagy by colon cancer cells as a protective mechanism against SUL. In the present study, we aimed to investigate the possible role of autophagy induction by ECs as a defense mechanism against SUL.
Methods
Human umbilical vein endothelial cells (HUVECs) were used as the in vitro model of angiogenic ECs. The induction of autophagy was evaluated by the detection of acidic vesicular organelles (AVOs) by flow-cytometry, after the staining with acridine orange, as well as the detection of light chain 3(LC3) by Western blot. Finally, the functional implication of autophagy inhibition and SUL treatment in ECs was investigated by their ability to form vascular-like structures on Matrigel.
Results
Treatment of HUVECs with relatively low concentrations of SUL for 16 h resulted in the evident formation of AVOs and the recruitment of LC3 to autophagosomes, the pathognomonic features of autophagy. Co-treatment of cells with the specific autophagy inhibitor (3-methyladenine) potentiated the proapoptotic effect of SUL. And inhibition of autophagy potentiated the inhibitory effect of SUL on the ability of ECs to form capillary-like structures.
Conclusion
Similar to cancer cells, ECs induced autophagy in response to the pro-apoptotic agent, SUL, and the inhibition of autophagy potentiated the pro-apoptotic effect. These findings open premises for the use of autophagy inhibitors in combination with anti–angiogenic agents.</description><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy - drug effects</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood and lymphatic vessels</subject><subject>Blotting, Western</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>Caspases - metabolism</subject><subject>Cell Biology</subject><subject>Cell Proliferation - drug effects</subject><subject>Colony-Forming Units Assay</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - enzymology</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Isothiocyanates</subject><subject>Medical sciences</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Oncology</subject><subject>Ophthalmology</subject><subject>Organelles - drug effects</subject><subject>Organelles - metabolism</subject><subject>Original Paper</subject><subject>Pharmacology. Drug treatments</subject><subject>Thiocyanates - pharmacology</subject><subject>Umbilical Veins - cytology</subject><subject>Vasodilator agents. Cerebral vasodilators</subject><issn>0969-6970</issn><issn>1573-7209</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kcFrHCEYxaW0NJu0f0AvZQiUnGw_nVHHY1naJBDIJT2L4-isYVan6hz2v6_LbhsI9KR8_t77Hj6EPhH4SgDEt0ygYxwDASxJD5i-QRvCRIsFBfkWbUByibkUcIEuc34GqIO-e48uKHDZia7bIPu0s40POz_44mNoomv0WuKy09OhWWKxoXhdbG50vWAdJh8nG7xprHPWlHwU5HV2MemqCbYZDtVuXI0PU6OXuJSYff6A3jk9Z_vxfF6hXz9_PG3v8MPj7f32-wM2HecFjwRoz53oBjdQYgZqRyp0nQoJozG9AE5aoq2mThJuXMu0ZlywUZgBbOvaK3Rz8l1S_L3aXNTeZ2PnuSaLa1aCMSIoYVDJ61fkc1xTqOEq1PaV6mSFyAkyKeacrFNL8nudDoqAOjagTg2o2oA6NqBo1Xw-G6_D3o7_FH-_vAJfzoDORs8u6WB8fuFaypkQRyN64nJ9CpNNLwn_v_0PeMKfQA</recordid><startdate>20100901</startdate><enddate>20100901</enddate><creator>Nishikawa, Takeshi</creator><creator>Tsuno, Nelson H.</creator><creator>Okaji, Yurai</creator><creator>Sunami, Eiji</creator><creator>Shuno, Yasutaka</creator><creator>Sasaki, Kazuhito</creator><creator>Hongo, Kumiko</creator><creator>Kaneko, Manabu</creator><creator>Hiyoshi, Masaya</creator><creator>Kawai, Kazushige</creator><creator>Kitayama, Joji</creator><creator>Takahashi, Koki</creator><creator>Nagawa, Hirokazu</creator><general>Springer Netherlands</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</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>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20100901</creationdate><title>The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis</title><author>Nishikawa, Takeshi ; Tsuno, Nelson H. ; Okaji, Yurai ; Sunami, Eiji ; Shuno, Yasutaka ; Sasaki, Kazuhito ; Hongo, Kumiko ; Kaneko, Manabu ; Hiyoshi, Masaya ; Kawai, Kazushige ; Kitayama, Joji ; Takahashi, Koki ; Nagawa, Hirokazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-d10286f74bfb21cb2ed27ad10790dcc8706131aea2f916cf35aa5675d7cb0e3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Autophagy - drug effects</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood and lymphatic vessels</topic><topic>Blotting, Western</topic><topic>Cancer Research</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular system</topic><topic>Caspases - metabolism</topic><topic>Cell Biology</topic><topic>Cell Proliferation - drug effects</topic><topic>Colony-Forming Units Assay</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - enzymology</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Isothiocyanates</topic><topic>Medical sciences</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Oncology</topic><topic>Ophthalmology</topic><topic>Organelles - drug effects</topic><topic>Organelles - metabolism</topic><topic>Original Paper</topic><topic>Pharmacology. Drug treatments</topic><topic>Thiocyanates - pharmacology</topic><topic>Umbilical Veins - cytology</topic><topic>Vasodilator agents. Cerebral vasodilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishikawa, Takeshi</creatorcontrib><creatorcontrib>Tsuno, Nelson H.</creatorcontrib><creatorcontrib>Okaji, Yurai</creatorcontrib><creatorcontrib>Sunami, Eiji</creatorcontrib><creatorcontrib>Shuno, Yasutaka</creatorcontrib><creatorcontrib>Sasaki, Kazuhito</creatorcontrib><creatorcontrib>Hongo, Kumiko</creatorcontrib><creatorcontrib>Kaneko, Manabu</creatorcontrib><creatorcontrib>Hiyoshi, Masaya</creatorcontrib><creatorcontrib>Kawai, Kazushige</creatorcontrib><creatorcontrib>Kitayama, Joji</creatorcontrib><creatorcontrib>Takahashi, Koki</creatorcontrib><creatorcontrib>Nagawa, Hirokazu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Angiogenesis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishikawa, Takeshi</au><au>Tsuno, Nelson H.</au><au>Okaji, Yurai</au><au>Sunami, Eiji</au><au>Shuno, Yasutaka</au><au>Sasaki, Kazuhito</au><au>Hongo, Kumiko</au><au>Kaneko, Manabu</au><au>Hiyoshi, Masaya</au><au>Kawai, Kazushige</au><au>Kitayama, Joji</au><au>Takahashi, Koki</au><au>Nagawa, Hirokazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis</atitle><jtitle>Angiogenesis (London)</jtitle><stitle>Angiogenesis</stitle><addtitle>Angiogenesis</addtitle><date>2010-09-01</date><risdate>2010</risdate><volume>13</volume><issue>3</issue><spage>227</spage><epage>238</epage><pages>227-238</pages><issn>0969-6970</issn><eissn>1573-7209</eissn><coden>AGIOFT</coden><abstract>Background
Sulforaphane (SUL), a kind of isothiocyanate, has recently been focused due to its strong pro-apoptotic effect on cancer cells as well as tumor vascular endothelial cells (ECs). And recently, we demonstrated the induction of autophagy by colon cancer cells as a protective mechanism against SUL. In the present study, we aimed to investigate the possible role of autophagy induction by ECs as a defense mechanism against SUL.
Methods
Human umbilical vein endothelial cells (HUVECs) were used as the in vitro model of angiogenic ECs. The induction of autophagy was evaluated by the detection of acidic vesicular organelles (AVOs) by flow-cytometry, after the staining with acridine orange, as well as the detection of light chain 3(LC3) by Western blot. Finally, the functional implication of autophagy inhibition and SUL treatment in ECs was investigated by their ability to form vascular-like structures on Matrigel.
Results
Treatment of HUVECs with relatively low concentrations of SUL for 16 h resulted in the evident formation of AVOs and the recruitment of LC3 to autophagosomes, the pathognomonic features of autophagy. Co-treatment of cells with the specific autophagy inhibitor (3-methyladenine) potentiated the proapoptotic effect of SUL. And inhibition of autophagy potentiated the inhibitory effect of SUL on the ability of ECs to form capillary-like structures.
Conclusion
Similar to cancer cells, ECs induced autophagy in response to the pro-apoptotic agent, SUL, and the inhibition of autophagy potentiated the pro-apoptotic effect. These findings open premises for the use of autophagy inhibitors in combination with anti–angiogenic agents.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>20694744</pmid><doi>10.1007/s10456-010-9180-2</doi><tpages>12</tpages></addata></record> |
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| subjects | Angiogenesis Inhibitors - pharmacology Apoptosis - drug effects Autophagy - drug effects Biological and medical sciences Biomedical and Life Sciences Biomedicine Blood and lymphatic vessels Blotting, Western Cancer Research Cardiology Cardiology. Vascular system Cardiovascular system Caspases - metabolism Cell Biology Cell Proliferation - drug effects Colony-Forming Units Assay Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endothelial Cells - cytology Endothelial Cells - drug effects Endothelial Cells - enzymology Flow Cytometry Humans Isothiocyanates Medical sciences Microtubule-Associated Proteins - metabolism Neovascularization, Physiologic - drug effects Oncology Ophthalmology Organelles - drug effects Organelles - metabolism Original Paper Pharmacology. Drug treatments Thiocyanates - pharmacology Umbilical Veins - cytology Vasodilator agents. Cerebral vasodilators |
| title | The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis |
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