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Adipose-derived regenerative cell therapy inhibits the progression of monocrotaline-induced pulmonary hypertension in rats.
MedLine Citation:
PMID:  24853385     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
MAIN METHODS: Rats were assigned to Control and MCT groups without and with (M/A) intravenous transfusion of seven million ADRC on day 7. We echocardiographically evaluated pulmonary hypertension as pulmonary artery flow acceleration time (PAAT) and deceleration (PADc). Right ventricular (RV) systolic pressure was measured by catheterization on day 28 and then pathological changes in pulmonary vessels were assessed. We analyzed PAH-associated gene expression on day 14 using real-time RT-PCR.
KEY FINDINGS: Echocardiography and RV catheterization showed that ADRC therapy inhibited PH development (assessed as PAAT, PADc, and RV systolic pressure) at day 28 (MCT vs. M/A, p<0.05). Pulmonary vascular remodeling was also inhibited (vessel wall thickness: MCT vs. M/A, p<0.01). Messenger RNA levels of endothelin (ET) A and B receptors, ET-1 and transforming growth factor (TGF)-β increased in the lungs by MCT were suppressed by ADRC (MCT vs. M/A, p<0.05).
SIGNIFICANCE: The development of PH was inhibited by ADRC through suppressing changes in the expression of genes associated with ET and TGF-β systems. We believe that ADRC therapy could serve as a novel strategy for treating PH.
Authors:
Masamichi Eguchi; Satoshi Ikeda; Saburo Kusumoto; Daisuke Sato; Yuji Koide; Hiroaki Kawano; Koji Maemura
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-5-19
Journal Detail:
Title:  Life sciences     Volume:  -     ISSN:  1879-0631     ISO Abbreviation:  Life Sci.     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-5-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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