Artery Research

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Volume 22, Issue C, June 2018, Pages 49 - 56

Prostaglandin E1 for preventing the progress of pulmonary arterial hypertension in rat model

Authors
Jae Chul Leea, b, *, Soo Young Choec, Chan Yeong Heoa, Sun Ju Jeongd, **
aDepartment of Plastic and Reconstructive Surgery, Seoul National University Bundang Hospital, Gyeonggi-do, Republic of Korea
bDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Republic of Korea
cDepartment of Biology, School of Life Sciences, Chungbuk National University, Cheongju 361-763, Republic of Korea
dDepartment of Nursing, Suwon Women’s University, Suwon, Republic of Korea
*Corresponding author. Department of Plastic and Reconstructive Surgery, Seoul National University Bundang Hospital, 82, Gumi-ro 173 Beon-Gil, Bundang-Gu, Seongnam-si, Gyeonggi-do 463707, Republic of Korea. Fax: +82 31 738 0271. E-mail address: beas100@snu.ac.kr (J.C. Lee)
**Corresponding author. Department of Nursing, Suwon Women’s University Suwon, Onjung-ro 72, Gweonseon-gu, Suwon-si, Gyeonggi-do 16632, Republic of Korea. Fax: +82 31 738 0208. E-mail address: sunjuright@swc.ac.kr (S.J. Jeong).
Corresponding Authors
Jae Chul Lee, Sun Ju Jeong
Received 15 January 2018, Revised 2 April 2018, Accepted 2 May 2018, Available Online 26 May 2018.
DOI
10.1016/j.artres.2018.05.001How to use a DOI?
Keywords
Heart; Lung; Prostaglandin E1; Pulmonary artery hypertension; Right ventricular
Abstract

Pulmonary artery hypertension (PAH) is a progressive chronic disease with a high mortality rate. Increased pulmonary vascular resistance and over-proliferation of pulmonary artery endothelial cells lead to remodeling of pulmonary vasculature. Several anti-PAH therapies targeting various pathways involved in PAH progression have been approved by the FDA. However, many of the currently available anti-PAH drugs suffer from a number of limitations, including short biological half-life, and poor pulmonary selectivity. Prostaglandin E1 (PGE1) is a compound with vasodilatory, anti-inflammatory, anti-aggregatory, and anti-proliferative properties. Recently, PGE1 is known to accumulate in sites of inflammation or vascular lesions and thus enhance the effects of the drugs and alleviate the side effects. Therefore, we hypothesized that long-term effect of PGE1 could reduce ma adaptive structural remodeling of the lung and heart and prevent ventricular arrhythmias in monocrotaline (MCT)-induced rat model of PAH. Our results revealed that PGE1 reduced ventricular hypertrophy, protein expressions of endothelin-1 (ET-1) and endothelin receptor A (ERA), and the expression of fibrosis. These results support the notion that PGE1 can improve the functional properties of RV, highlighting its potential benefits for heart and lung impairment.

Copyright
© 2018 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

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<Previous Article In Issue
Next Article In Issue>
Journal
Artery Research
Volume-Issue
22 - C
Pages
49 - 56
Publication Date
2018/05/26
ISSN (Online)
1876-4401
ISSN (Print)
1872-9312
DOI
10.1016/j.artres.2018.05.001How to use a DOI?
Copyright
© 2018 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

Cite this article

risenwbib
TY  - JOUR
AU  - Jae Chul Lee
AU  - Soo Young Choe
AU  - Chan Yeong Heo
AU  - Sun Ju Jeong
PY  - 2018
DA  - 2018/05/26
TI  - Prostaglandin E1 for preventing the progress of pulmonary arterial hypertension in rat model
JO  - Artery Research
SP  - 49
EP  - 56
VL  - 22
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2018.05.001
DO  - 10.1016/j.artres.2018.05.001
ID  - Lee2018
ER  -