Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis
OBJECTIVES—Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2007-07, Vol.27 (7), p.1535-1541 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
| container_volume | 27 |
| creator | Kada, Nanae Suzuki, Toru Aizawa, Kenichi Matsumura, Takayoshi Ishibashi, Naoto Suzuki, Naomi Takeda, Norifumi Munemasa, Yoshiko Sawaki, Daigo Ishikawa, Takashi Nagai, Ryozo |
| description | OBJECTIVES—Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely neointima formation, effects of ACR on neointima formation and the involved mechanisms were investigated.
METHODS AND RESULTS—ACR was administered to cuff-injured mice which showed inhibition of neointima formation. Investigation of involved mechanisms at the cellular and molecular levels showed that ACR induces apoptosis of neointimal cells and this to be mediated by selective induction of retinoic-acid receptor β (RARβ) which shows growth inhibitory and proapoptotic effects on smooth muscle cells.
CONCLUSION—We show that ACR inhibits neointima formation by inducing RARβ which in turn inhibits cell growth and induces apoptosis. The retinoid, ACR, may be potentially exploitable for treatment and prevention of neointima formation. |
| doi_str_mv | 10.1161/ATVBAHA.106.134114 |
| format | Article |
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METHODS AND RESULTS—ACR was administered to cuff-injured mice which showed inhibition of neointima formation. Investigation of involved mechanisms at the cellular and molecular levels showed that ACR induces apoptosis of neointimal cells and this to be mediated by selective induction of retinoic-acid receptor β (RARβ) which shows growth inhibitory and proapoptotic effects on smooth muscle cells.
CONCLUSION—We show that ACR inhibits neointima formation by inducing RARβ which in turn inhibits cell growth and induces apoptosis. The retinoid, ACR, may be potentially exploitable for treatment and prevention of neointima formation.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.106.134114</identifier><identifier>PMID: 17478760</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cells, Cultured ; Disease Models, Animal ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Drug toxicity and drugs side effects treatment ; Femoral Artery - drug effects ; Femoral Artery - physiology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - growth & development ; Pharmacology. Drug treatments ; Receptors, Retinoic Acid ; Retinoids - pharmacology ; Sensitivity and Specificity ; Toxicity: blood ; Toxicity: digestive system ; Tunica Intima - drug effects ; Tunica Intima - metabolism</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2007-07, Vol.27 (7), p.1535-1541</ispartof><rights>2007 American Heart Association, Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4547-f86c2c922ca2f5f91038424ffe8a091d54e5791ab6953c432aa3cbd58ecd4fee3</citedby><cites>FETCH-LOGICAL-c4547-f86c2c922ca2f5f91038424ffe8a091d54e5791ab6953c432aa3cbd58ecd4fee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18867812$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17478760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kada, Nanae</creatorcontrib><creatorcontrib>Suzuki, Toru</creatorcontrib><creatorcontrib>Aizawa, Kenichi</creatorcontrib><creatorcontrib>Matsumura, Takayoshi</creatorcontrib><creatorcontrib>Ishibashi, Naoto</creatorcontrib><creatorcontrib>Suzuki, Naomi</creatorcontrib><creatorcontrib>Takeda, Norifumi</creatorcontrib><creatorcontrib>Munemasa, Yoshiko</creatorcontrib><creatorcontrib>Sawaki, Daigo</creatorcontrib><creatorcontrib>Ishikawa, Takashi</creatorcontrib><creatorcontrib>Nagai, Ryozo</creatorcontrib><title>Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVES—Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely neointima formation, effects of ACR on neointima formation and the involved mechanisms were investigated.
METHODS AND RESULTS—ACR was administered to cuff-injured mice which showed inhibition of neointima formation. Investigation of involved mechanisms at the cellular and molecular levels showed that ACR induces apoptosis of neointimal cells and this to be mediated by selective induction of retinoic-acid receptor β (RARβ) which shows growth inhibitory and proapoptotic effects on smooth muscle cells.
CONCLUSION—We show that ACR inhibits neointima formation by inducing RARβ which in turn inhibits cell growth and induces apoptosis. The retinoid, ACR, may be potentially exploitable for treatment and prevention of neointima formation.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Femoral Artery - drug effects</subject><subject>Femoral Artery - physiology</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - growth & development</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, Retinoic Acid</subject><subject>Retinoids - pharmacology</subject><subject>Sensitivity and Specificity</subject><subject>Toxicity: blood</subject><subject>Toxicity: digestive system</subject><subject>Tunica Intima - drug effects</subject><subject>Tunica Intima - metabolism</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkdtu1DAQhi0Eogd4AS5QbuAuy9jxIblMK0pXqkCqFm4t72RCDNl4sRNVfXtcbarKGs1B3z_S_GbsA4cN55p_aXe_rtrbdsNBb3glOZev2DlXQpZSV_p1rsE0pdJSnLGLlP4AgBQC3rIzbqSpjYZzhi0-4uixuKfZT8F3xXYa_N7PqfhOwU-zP7jiJsSDm32Yit0Qw_J7eKaxaDFL7gnpOIdYXNHsyu3ULUhd0R5DHiaf3rE3vRsTvV_zJft583V3fVve_fi2vW7vSpRKmrKvNQpshEAnetU3HKpaCtn3VDtoeKckKdNwt9eNqlBWwrkK952qCTvZE1WX7PNp7zGGfwul2R58QhpHN1FYkjWgJTegMihOIMaQUqTeHmO-Mz5aDvbJWrtam3ttT9Zm0cd1-7I_UPciWb3MwKcVcAnd2Ec3oU8vXF1rU3OROXniHsI4U0x_x-WBoh3IjfNgnz6p0qBKAWDyAyhzgKn-A7dfkhU</recordid><startdate>200707</startdate><enddate>200707</enddate><creator>Kada, Nanae</creator><creator>Suzuki, Toru</creator><creator>Aizawa, Kenichi</creator><creator>Matsumura, Takayoshi</creator><creator>Ishibashi, Naoto</creator><creator>Suzuki, Naomi</creator><creator>Takeda, Norifumi</creator><creator>Munemasa, Yoshiko</creator><creator>Sawaki, Daigo</creator><creator>Ishikawa, Takashi</creator><creator>Nagai, Ryozo</creator><general>American Heart Association, Inc</general><general>Lippincott</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>7X8</scope></search><sort><creationdate>200707</creationdate><title>Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis</title><author>Kada, Nanae ; Suzuki, Toru ; Aizawa, Kenichi ; Matsumura, Takayoshi ; Ishibashi, Naoto ; Suzuki, Naomi ; Takeda, Norifumi ; Munemasa, Yoshiko ; Sawaki, Daigo ; Ishikawa, Takashi ; Nagai, Ryozo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4547-f86c2c922ca2f5f91038424ffe8a091d54e5791ab6953c432aa3cbd58ecd4fee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Femoral Artery - drug effects</topic><topic>Femoral Artery - physiology</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - growth & development</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, Retinoic Acid</topic><topic>Retinoids - pharmacology</topic><topic>Sensitivity and Specificity</topic><topic>Toxicity: blood</topic><topic>Toxicity: digestive system</topic><topic>Tunica Intima - drug effects</topic><topic>Tunica Intima - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kada, Nanae</creatorcontrib><creatorcontrib>Suzuki, Toru</creatorcontrib><creatorcontrib>Aizawa, Kenichi</creatorcontrib><creatorcontrib>Matsumura, Takayoshi</creatorcontrib><creatorcontrib>Ishibashi, Naoto</creatorcontrib><creatorcontrib>Suzuki, Naomi</creatorcontrib><creatorcontrib>Takeda, Norifumi</creatorcontrib><creatorcontrib>Munemasa, Yoshiko</creatorcontrib><creatorcontrib>Sawaki, Daigo</creatorcontrib><creatorcontrib>Ishikawa, Takashi</creatorcontrib><creatorcontrib>Nagai, Ryozo</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>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kada, Nanae</au><au>Suzuki, Toru</au><au>Aizawa, Kenichi</au><au>Matsumura, Takayoshi</au><au>Ishibashi, Naoto</au><au>Suzuki, Naomi</au><au>Takeda, Norifumi</au><au>Munemasa, Yoshiko</au><au>Sawaki, Daigo</au><au>Ishikawa, Takashi</au><au>Nagai, Ryozo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2007-07</date><risdate>2007</risdate><volume>27</volume><issue>7</issue><spage>1535</spage><epage>1541</epage><pages>1535-1541</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVES—Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely neointima formation, effects of ACR on neointima formation and the involved mechanisms were investigated.
METHODS AND RESULTS—ACR was administered to cuff-injured mice which showed inhibition of neointima formation. Investigation of involved mechanisms at the cellular and molecular levels showed that ACR induces apoptosis of neointimal cells and this to be mediated by selective induction of retinoic-acid receptor β (RARβ) which shows growth inhibitory and proapoptotic effects on smooth muscle cells.
CONCLUSION—We show that ACR inhibits neointima formation by inducing RARβ which in turn inhibits cell growth and induces apoptosis. The retinoid, ACR, may be potentially exploitable for treatment and prevention of neointima formation.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>17478760</pmid><doi>10.1161/ATVBAHA.106.134114</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2007-07, Vol.27 (7), p.1535-1541 |
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| subjects | Animals Apoptosis - drug effects Apoptosis - physiology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cells, Cultured Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Drug toxicity and drugs side effects treatment Femoral Artery - drug effects Femoral Artery - physiology Immunohistochemistry In Situ Nick-End Labeling Male Medical sciences Mice Mice, Inbred C57BL Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - growth & development Pharmacology. Drug treatments Receptors, Retinoic Acid Retinoids - pharmacology Sensitivity and Specificity Toxicity: blood Toxicity: digestive system Tunica Intima - drug effects Tunica Intima - metabolism |
| title | Acyclic Retinoid Inhibits Neointima Formation Through Retinoic Acid Receptor Beta-Induced Apoptosis |
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