CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats
The present study is aimed at investigating the molecular mechanism of C1q/TNF-related protein 9 (CTRP9) and providing a new perspective in arteriovenous shunt-induced pulmonary arterial hypertension (PAH). PAH was established by an arteriovenous shunt placement performed in rats. Adenovirus(Ad)-CTR...
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Language: | English |
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Wiley
2021-01-01
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Series: | Cardiovascular Therapeutics |
Online Access: | http://dx.doi.org/10.1155/2021/4971300 |
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author | Hua Guan Xiaofeng Yang Tao Shi Yongjian Zhang Aoqi Xiang Yongxin Li |
author_facet | Hua Guan Xiaofeng Yang Tao Shi Yongjian Zhang Aoqi Xiang Yongxin Li |
author_sort | Hua Guan |
collection | DOAJ |
description | The present study is aimed at investigating the molecular mechanism of C1q/TNF-related protein 9 (CTRP9) and providing a new perspective in arteriovenous shunt-induced pulmonary arterial hypertension (PAH). PAH was established by an arteriovenous shunt placement performed in rats. Adenovirus(Ad)-CTRP9 and Ad-green fluorescent protein viral particles were injected into the rats through the tail vein. Following 12 weeks, the mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) were measured and morphological analysis was conducted to confirm the establishment of the PAH model. The systemic elevation of CTRP9 maintained pulmonary vascular homeostasis and protected the rats from dysfunctional and abnormal remodeling. CTRP9 attenuated the pulmonary vascular remodeling in the shunt group by decreasing the mPAP and RVSP, which was associated with suppressed inflammation, apoptosis, and extracellular matrix injury. In addition, CTRP9 dramatically increased the phosphorylation of AKT and p38-MAPK in the lung tissues of shunt-operated animals. These findings suggest a previously unrecognized effect of CTRP9 in pulmonary vascular homeostasis during PAH pathogenesis. |
format | Article |
id | doaj-art-c0b12b00dc544aee863ba4db0bc79ac9 |
institution | Kabale University |
issn | 1755-5922 |
language | English |
publishDate | 2021-01-01 |
publisher | Wiley |
record_format | Article |
series | Cardiovascular Therapeutics |
spelling | doaj-art-c0b12b00dc544aee863ba4db0bc79ac92025-02-03T06:46:18ZengWileyCardiovascular Therapeutics1755-59222021-01-01202110.1155/2021/4971300CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in RatsHua Guan0Xiaofeng Yang1Tao Shi2Yongjian Zhang3Aoqi Xiang4Yongxin Li5Shaanxi Key Laboratory of Ischemic Cardiovascular Diseases & Institute of Basic and Translational MedicineDepartment of Pathogenic Microbiology and ImmunologyDepartment of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryShaanxi Key Laboratory of Ischemic Cardiovascular Diseases & Institute of Basic and Translational MedicineDepartment of Cardiovascular SurgeryThe present study is aimed at investigating the molecular mechanism of C1q/TNF-related protein 9 (CTRP9) and providing a new perspective in arteriovenous shunt-induced pulmonary arterial hypertension (PAH). PAH was established by an arteriovenous shunt placement performed in rats. Adenovirus(Ad)-CTRP9 and Ad-green fluorescent protein viral particles were injected into the rats through the tail vein. Following 12 weeks, the mean pulmonary arterial pressure (mPAP) and right ventricular systolic pressure (RVSP) were measured and morphological analysis was conducted to confirm the establishment of the PAH model. The systemic elevation of CTRP9 maintained pulmonary vascular homeostasis and protected the rats from dysfunctional and abnormal remodeling. CTRP9 attenuated the pulmonary vascular remodeling in the shunt group by decreasing the mPAP and RVSP, which was associated with suppressed inflammation, apoptosis, and extracellular matrix injury. In addition, CTRP9 dramatically increased the phosphorylation of AKT and p38-MAPK in the lung tissues of shunt-operated animals. These findings suggest a previously unrecognized effect of CTRP9 in pulmonary vascular homeostasis during PAH pathogenesis.http://dx.doi.org/10.1155/2021/4971300 |
spellingShingle | Hua Guan Xiaofeng Yang Tao Shi Yongjian Zhang Aoqi Xiang Yongxin Li CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats Cardiovascular Therapeutics |
title | CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats |
title_full | CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats |
title_fullStr | CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats |
title_full_unstemmed | CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats |
title_short | CTRP9 Mitigates the Progression of Arteriovenous Shunt-Induced Pulmonary Artery Hypertension in Rats |
title_sort | ctrp9 mitigates the progression of arteriovenous shunt induced pulmonary artery hypertension in rats |
url | http://dx.doi.org/10.1155/2021/4971300 |
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