HRT1 modulates vascular smooth muscle cell proliferation and apoptosis
The Notch signaling pathway plays vital roles in vascular development and homeostasis. However, the functional role of HRT1, a primary downstream effector of Notch signaling in VSMC, is poorly characterized. In the present study, we postulated that HRT1 plays fundamental roles in modulating VSMC fat...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2003-08, Vol.308 (3), p.596-601 |
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| creator | Wang, Wenli Prince, Chengyu Z Hu, Xing Pollman, Matthew J |
| description | The Notch signaling pathway plays vital roles in vascular development and homeostasis. However, the functional role of HRT1, a primary downstream effector of Notch signaling in VSMC, is poorly characterized. In the present study, we postulated that HRT1 plays fundamental roles in modulating VSMC fate. To test the hypothesis that HRT1 is coupled to growth regulation, we generated VSMC lines constitutively overexpressing HRT1 (HRT1SMC) and demonstrated an exaggerated growth behavior compared to its control cell line. The lack of cell cycle arrest at confluence in HRT1SMC was associated with an attenuated up-regulation of the cell cycle inhibitor, p21
WAF1/CIP1. We further established that both transient and constitutive HRT1 signaling promoted VSMC survival in response to serum deprivation and pro-apoptotic Fas ligand. Resistance to apoptosis was associated with the induction of Akt expression/activity, a well-described anti-apoptotic mediator. Overall, these findings provide initial evidence that HRT1 functions as a critical determinant of VSMC proliferation and survival. |
| doi_str_mv | 10.1016/S0006-291X(03)01453-0 |
| format | Article |
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WAF1/CIP1. We further established that both transient and constitutive HRT1 signaling promoted VSMC survival in response to serum deprivation and pro-apoptotic Fas ligand. Resistance to apoptosis was associated with the induction of Akt expression/activity, a well-described anti-apoptotic mediator. Overall, these findings provide initial evidence that HRT1 functions as a critical determinant of VSMC proliferation and survival.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/S0006-291X(03)01453-0</identifier><identifier>PMID: 12914792</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; Cell Division ; Cell Line ; Cell Survival ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - metabolism ; HRT1 ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Proliferation ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Repressor Proteins - physiology ; Signal Transduction ; VSMC</subject><ispartof>Biochemical and biophysical research communications, 2003-08, Vol.308 (3), p.596-601</ispartof><rights>2003 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-c7636b2f4b0db2549c1114561f8147aab62eb659abe82d8b30a44713175548fa3</citedby><cites>FETCH-LOGICAL-c361t-c7636b2f4b0db2549c1114561f8147aab62eb659abe82d8b30a44713175548fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-291X(03)01453-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12914792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Wenli</creatorcontrib><creatorcontrib>Prince, Chengyu Z</creatorcontrib><creatorcontrib>Hu, Xing</creatorcontrib><creatorcontrib>Pollman, Matthew J</creatorcontrib><title>HRT1 modulates vascular smooth muscle cell proliferation and apoptosis</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The Notch signaling pathway plays vital roles in vascular development and homeostasis. However, the functional role of HRT1, a primary downstream effector of Notch signaling in VSMC, is poorly characterized. In the present study, we postulated that HRT1 plays fundamental roles in modulating VSMC fate. To test the hypothesis that HRT1 is coupled to growth regulation, we generated VSMC lines constitutively overexpressing HRT1 (HRT1SMC) and demonstrated an exaggerated growth behavior compared to its control cell line. The lack of cell cycle arrest at confluence in HRT1SMC was associated with an attenuated up-regulation of the cell cycle inhibitor, p21
WAF1/CIP1. We further established that both transient and constitutive HRT1 signaling promoted VSMC survival in response to serum deprivation and pro-apoptotic Fas ligand. Resistance to apoptosis was associated with the induction of Akt expression/activity, a well-described anti-apoptotic mediator. Overall, these findings provide initial evidence that HRT1 functions as a critical determinant of VSMC proliferation and survival.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Basic Helix-Loop-Helix Transcription Factors</subject><subject>Cell Division</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - metabolism</subject><subject>HRT1</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Proliferation</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Rats</subject><subject>Repressor Proteins - physiology</subject><subject>Signal Transduction</subject><subject>VSMC</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotlZ_grIn0cPqzOZjuyeRYq1QELSCt5DNZjGy29Rkt-C_N_1Aj54yhGdm3nkIOUe4QUBx-woAIs0KfL8Ceg3IOE3hgAwRCkgzBHZIhr_IgJyE8AmAyERxTAYYP1leZEMynb0sMGld1TeqMyFZq6Bj6ZPQOtd9JG0fdGMSbZomWXnX2Np41Vm3TNSyStTKrToXbDglR7VqgjnbvyPyNn1YTGbp_PnxaXI_TzUV2KU6F1SUWc1KqMqMs0JjjMQF1uOYR6lSZKYUvFClGWfVuKSgGMuRYs45G9eKjsjlbm7M8tWb0MnWhk04tTSuDzKnXHAQPIJ8B2rvQvCmlitvW-W_JYLcCJRbgXJjRwKVW4GxGJGL_YK-bE3117U3FoG7HWDimWtrvAzamqU2lfVGd7Jy9p8VP5hXf6I</recordid><startdate>20030829</startdate><enddate>20030829</enddate><creator>Wang, Wenli</creator><creator>Prince, Chengyu Z</creator><creator>Hu, Xing</creator><creator>Pollman, Matthew J</creator><general>Elsevier Inc</general><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>20030829</creationdate><title>HRT1 modulates vascular smooth muscle cell proliferation and apoptosis</title><author>Wang, Wenli ; Prince, Chengyu Z ; Hu, Xing ; Pollman, Matthew J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-c7636b2f4b0db2549c1114561f8147aab62eb659abe82d8b30a44713175548fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Basic Helix-Loop-Helix Transcription Factors</topic><topic>Cell Division</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclins - metabolism</topic><topic>HRT1</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Proliferation</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Rats</topic><topic>Repressor Proteins - physiology</topic><topic>Signal Transduction</topic><topic>VSMC</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Wenli</creatorcontrib><creatorcontrib>Prince, Chengyu Z</creatorcontrib><creatorcontrib>Hu, Xing</creatorcontrib><creatorcontrib>Pollman, Matthew J</creatorcontrib><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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Wenli</au><au>Prince, Chengyu Z</au><au>Hu, Xing</au><au>Pollman, Matthew J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HRT1 modulates vascular smooth muscle cell proliferation and apoptosis</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003-08-29</date><risdate>2003</risdate><volume>308</volume><issue>3</issue><spage>596</spage><epage>601</epage><pages>596-601</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The Notch signaling pathway plays vital roles in vascular development and homeostasis. However, the functional role of HRT1, a primary downstream effector of Notch signaling in VSMC, is poorly characterized. In the present study, we postulated that HRT1 plays fundamental roles in modulating VSMC fate. To test the hypothesis that HRT1 is coupled to growth regulation, we generated VSMC lines constitutively overexpressing HRT1 (HRT1SMC) and demonstrated an exaggerated growth behavior compared to its control cell line. The lack of cell cycle arrest at confluence in HRT1SMC was associated with an attenuated up-regulation of the cell cycle inhibitor, p21
WAF1/CIP1. We further established that both transient and constitutive HRT1 signaling promoted VSMC survival in response to serum deprivation and pro-apoptotic Fas ligand. Resistance to apoptosis was associated with the induction of Akt expression/activity, a well-described anti-apoptotic mediator. Overall, these findings provide initial evidence that HRT1 functions as a critical determinant of VSMC proliferation and survival.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12914792</pmid><doi>10.1016/S0006-291X(03)01453-0</doi><tpages>6</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2003-08, Vol.308 (3), p.596-601 |
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| subjects | Animals Apoptosis Basic Helix-Loop-Helix Transcription Factors Cell Division Cell Line Cell Survival Cells, Cultured Cyclin-Dependent Kinase Inhibitor p21 Cyclins - metabolism HRT1 Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Proliferation Protein-Serine-Threonine Kinases Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Rats Repressor Proteins - physiology Signal Transduction VSMC |
| title | HRT1 modulates vascular smooth muscle cell proliferation and apoptosis |
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