BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition
Components of bone morphogenetic protein (BMP) signalling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT). In particular, the importance of BMP type 2 receptor in these processes has been extensively analysed. However...
| Main Authors: | , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Oxford University Press
2024
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| Online Access: | https://hdl.handle.net/1721.1/156912 |
| _version_ | 1824458406669320192 |
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| author | Lee, Heon-Woo Adachi, Takaomi Pak, Boryeong Park, Saejeong Hu, Xiaoyue Choi, Woosoung Kowalski, Piotr S Chang, C Hong Clapham, Katharine R Lee, Aram Papangeli, Irinna Kim, Jongmin Han, Orjin Park, Jihwan Anderson, Daniel G Simons, Michael Jin, Suk-Won Chun, Hyung J |
| author2 | Koch Institute for Integrative Cancer Research at MIT |
| author_facet | Koch Institute for Integrative Cancer Research at MIT Lee, Heon-Woo Adachi, Takaomi Pak, Boryeong Park, Saejeong Hu, Xiaoyue Choi, Woosoung Kowalski, Piotr S Chang, C Hong Clapham, Katharine R Lee, Aram Papangeli, Irinna Kim, Jongmin Han, Orjin Park, Jihwan Anderson, Daniel G Simons, Michael Jin, Suk-Won Chun, Hyung J |
| author_sort | Lee, Heon-Woo |
| collection | MIT |
| description | Components of bone morphogenetic protein (BMP) signalling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT). In particular, the importance of BMP type 2 receptor in these processes has been extensively analysed. However, the contribution of BMP type 1 receptors (BMPR1s) to the onset of PAH and EndoMT remains poorly understood. BMPR1A, one of BMPR1s, was recently implicated in the pathogenesis of PAH, and was found to be down-regulated in the lungs of PAH patients, neither the downstream mechanism nor its contribution to EndoMT has been described. Therefore, we aim to delineate the role of endothelial BMPR1A in modulating EndoMT and pathogenesis of PAH. |
| first_indexed | 2024-09-23T16:08:30Z |
| format | Article |
| id | mit-1721.1/156912 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2025-02-19T04:25:23Z |
| publishDate | 2024 |
| publisher | Oxford University Press |
| record_format | dspace |
| spelling | mit-1721.1/1569122025-01-03T04:13:51Z BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition Lee, Heon-Woo Adachi, Takaomi Pak, Boryeong Park, Saejeong Hu, Xiaoyue Choi, Woosoung Kowalski, Piotr S Chang, C Hong Clapham, Katharine R Lee, Aram Papangeli, Irinna Kim, Jongmin Han, Orjin Park, Jihwan Anderson, Daniel G Simons, Michael Jin, Suk-Won Chun, Hyung J Koch Institute for Integrative Cancer Research at MIT Components of bone morphogenetic protein (BMP) signalling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT). In particular, the importance of BMP type 2 receptor in these processes has been extensively analysed. However, the contribution of BMP type 1 receptors (BMPR1s) to the onset of PAH and EndoMT remains poorly understood. BMPR1A, one of BMPR1s, was recently implicated in the pathogenesis of PAH, and was found to be down-regulated in the lungs of PAH patients, neither the downstream mechanism nor its contribution to EndoMT has been described. Therefore, we aim to delineate the role of endothelial BMPR1A in modulating EndoMT and pathogenesis of PAH. 2024-09-19T21:07:36Z 2024-09-19T21:07:36Z 2023-05-02 2024-09-19T20:56:58Z Article http://purl.org/eprint/type/JournalArticle https://hdl.handle.net/1721.1/156912 Heon-Woo Lee, Takaomi Adachi, Boryeong Pak, Saejeong Park, Xiaoyue Hu, Woosoung Choi, Piotr S Kowalski, C Hong Chang, Katharine R Clapham, Aram Lee, Irinna Papangeli, Jongmin Kim, Orjin Han, Jihwan Park, Daniel G Anderson, Michael Simons, Suk-Won Jin, Hyung J Chun, BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition, Cardiovascular Research, Volume 119, Issue 3, March 2023, Pages 813–825. en 10.1093/cvr/cvac159 Cardiovascular Research Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. application/pdf Oxford University Press Oxford University Press |
| spellingShingle | Lee, Heon-Woo Adachi, Takaomi Pak, Boryeong Park, Saejeong Hu, Xiaoyue Choi, Woosoung Kowalski, Piotr S Chang, C Hong Clapham, Katharine R Lee, Aram Papangeli, Irinna Kim, Jongmin Han, Orjin Park, Jihwan Anderson, Daniel G Simons, Michael Jin, Suk-Won Chun, Hyung J BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title | BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title_full | BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title_fullStr | BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title_full_unstemmed | BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title_short | BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition |
| title_sort | bmpr1a promotes id2 zeb1 interaction to suppress excessive endothelial to mesenchymal transition |
| url | https://hdl.handle.net/1721.1/156912 |
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