Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications.
The Kruppel-like factor (KLF) family of transcription factors regulates diverse cell biological processes including proliferation, differentiation, survival and growth. Previous studies have shown that KLF15 inhibits cardiac hypertrophy by repressing the activity of pivotal cardiac transcription fac...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3346753?pdf=render |
| _version_ | 1818585255313932288 |
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| author | Joost J Leenders Wino J Wijnen Ingeborg van der Made Monika Hiller Melissa Swinnen Thierry Vandendriessche Marinee Chuah Yigal M Pinto Esther E Creemers |
| author_facet | Joost J Leenders Wino J Wijnen Ingeborg van der Made Monika Hiller Melissa Swinnen Thierry Vandendriessche Marinee Chuah Yigal M Pinto Esther E Creemers |
| author_sort | Joost J Leenders |
| collection | DOAJ |
| description | The Kruppel-like factor (KLF) family of transcription factors regulates diverse cell biological processes including proliferation, differentiation, survival and growth. Previous studies have shown that KLF15 inhibits cardiac hypertrophy by repressing the activity of pivotal cardiac transcription factors such as GATA4, MEF2 and myocardin. We set out this study to characterize the interaction of KLF15 with putative other transcription factors. We first show that KLF15 interacts with myocardin-related transcription factors (MRTFs) and strongly represses the transcriptional activity of MRTF-A and MRTF-B. Second, we identified a region within the C-terminal zinc fingers of KLF15 that contains the nuclear localization signal. Third, we investigated whether overexpression of KLF15 in the heart would have therapeutic potential. Using recombinant adeno-associated viruses (rAAV) we have overexpressed KLF15 specifically in the mouse heart and provide the first evidence that elevation of cardiac KLF15 levels prevents the development of cardiac hypertrophy in a model of Angiotensin II induced hypertrophy. |
| first_indexed | 2024-12-16T08:34:10Z |
| format | Article |
| id | doaj.art-1fd6139a87124b14b3bf8ee5a8095a4e |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-16T08:34:10Z |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-1fd6139a87124b14b3bf8ee5a8095a4e2022-12-21T22:37:49ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0175e3675410.1371/journal.pone.0036754Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications.Joost J LeendersWino J WijnenIngeborg van der MadeMonika HillerMelissa SwinnenThierry VandendriesscheMarinee ChuahYigal M PintoEsther E CreemersThe Kruppel-like factor (KLF) family of transcription factors regulates diverse cell biological processes including proliferation, differentiation, survival and growth. Previous studies have shown that KLF15 inhibits cardiac hypertrophy by repressing the activity of pivotal cardiac transcription factors such as GATA4, MEF2 and myocardin. We set out this study to characterize the interaction of KLF15 with putative other transcription factors. We first show that KLF15 interacts with myocardin-related transcription factors (MRTFs) and strongly represses the transcriptional activity of MRTF-A and MRTF-B. Second, we identified a region within the C-terminal zinc fingers of KLF15 that contains the nuclear localization signal. Third, we investigated whether overexpression of KLF15 in the heart would have therapeutic potential. Using recombinant adeno-associated viruses (rAAV) we have overexpressed KLF15 specifically in the mouse heart and provide the first evidence that elevation of cardiac KLF15 levels prevents the development of cardiac hypertrophy in a model of Angiotensin II induced hypertrophy.http://europepmc.org/articles/PMC3346753?pdf=render |
| spellingShingle | Joost J Leenders Wino J Wijnen Ingeborg van der Made Monika Hiller Melissa Swinnen Thierry Vandendriessche Marinee Chuah Yigal M Pinto Esther E Creemers Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. PLoS ONE |
| title | Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. |
| title_full | Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. |
| title_fullStr | Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. |
| title_full_unstemmed | Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. |
| title_short | Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications. |
| title_sort | repression of cardiac hypertrophy by klf15 underlying mechanisms and therapeutic implications |
| url | http://europepmc.org/articles/PMC3346753?pdf=render |
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