Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension
Abstract To explore the role of FoxO1 and apoptosis in a rat model of chronic thromboembolic pulmonary hypertension (CTEPH). Rats were randomly divided into a sham group (n = 45) and an experimental group (n = 45). Autologous blood clots were injected into rats three times to induce CTEPH. Rats were...
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| Format: | Article |
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Nature Portfolio
2017-05-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-017-02007-5 |
| _version_ | 1819200188005220352 |
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| author | Chaosheng Deng Zhanghua Zhong Dawen Wu Yunfei Chen Ningfang Lian Haibo Ding Qiaoxian Zhang Qichang Lin Shuang Wu |
| author_facet | Chaosheng Deng Zhanghua Zhong Dawen Wu Yunfei Chen Ningfang Lian Haibo Ding Qiaoxian Zhang Qichang Lin Shuang Wu |
| author_sort | Chaosheng Deng |
| collection | DOAJ |
| description | Abstract To explore the role of FoxO1 and apoptosis in a rat model of chronic thromboembolic pulmonary hypertension (CTEPH). Rats were randomly divided into a sham group (n = 45) and an experimental group (n = 45). Autologous blood clots were injected into rats three times to induce CTEPH. Rats were further divided into three subgroups: a 1-week subgroup (n = 15), a 2-week subgroup (n = 15), and a 4-week subgroup (n = 15). Mean pulmonary arterial pressure (mPAP) and histopathology were evaluated at each time point. FoxO1, Bad, and Bcl-2 levels were examined at each time point using reverse transcription PCR and western blotting. The mPAP and vessel wall area/total area (WA/TA) ratio in the experimental group gradually increased in a time-dependent manner (P < 0.05). Both the mRNA and protein levels of FoxO1 decreased in the CTEPH rats compared to in the sham group. In addition, embolization led to the up-regulation of Bad and the down-regulation of Bcl-2 (P < 0.05). FoxO1 and apoptosis play an important role in the pathogenesis of CTEPH. Apoptosis-resistant pulmonary artery endothelial cells may play an important role in remodeling of the rat pulmonary artery. |
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| format | Article |
| id | doaj.art-d5d19a3198554d49b1614cbb868a2ac9 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-12-23T03:28:15Z |
| publishDate | 2017-05-01 |
| publisher | Nature Portfolio |
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| series | Scientific Reports |
| spelling | doaj.art-d5d19a3198554d49b1614cbb868a2ac92022-12-21T18:01:47ZengNature PortfolioScientific Reports2045-23222017-05-017111010.1038/s41598-017-02007-5Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertensionChaosheng Deng0Zhanghua Zhong1Dawen Wu2Yunfei Chen3Ningfang Lian4Haibo Ding5Qiaoxian Zhang6Qichang Lin7Shuang Wu8Division of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityDivision of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical UniversityAbstract To explore the role of FoxO1 and apoptosis in a rat model of chronic thromboembolic pulmonary hypertension (CTEPH). Rats were randomly divided into a sham group (n = 45) and an experimental group (n = 45). Autologous blood clots were injected into rats three times to induce CTEPH. Rats were further divided into three subgroups: a 1-week subgroup (n = 15), a 2-week subgroup (n = 15), and a 4-week subgroup (n = 15). Mean pulmonary arterial pressure (mPAP) and histopathology were evaluated at each time point. FoxO1, Bad, and Bcl-2 levels were examined at each time point using reverse transcription PCR and western blotting. The mPAP and vessel wall area/total area (WA/TA) ratio in the experimental group gradually increased in a time-dependent manner (P < 0.05). Both the mRNA and protein levels of FoxO1 decreased in the CTEPH rats compared to in the sham group. In addition, embolization led to the up-regulation of Bad and the down-regulation of Bcl-2 (P < 0.05). FoxO1 and apoptosis play an important role in the pathogenesis of CTEPH. Apoptosis-resistant pulmonary artery endothelial cells may play an important role in remodeling of the rat pulmonary artery.https://doi.org/10.1038/s41598-017-02007-5 |
| spellingShingle | Chaosheng Deng Zhanghua Zhong Dawen Wu Yunfei Chen Ningfang Lian Haibo Ding Qiaoxian Zhang Qichang Lin Shuang Wu Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension Scientific Reports |
| title | Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| title_full | Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| title_fullStr | Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| title_full_unstemmed | Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| title_short | Role of FoxO1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| title_sort | role of foxo1 and apoptosis in pulmonary vascular remolding in a rat model of chronic thromboembolic pulmonary hypertension |
| url | https://doi.org/10.1038/s41598-017-02007-5 |
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