AAV1-mediated shRNA Knockdown of SASH1 in Rat Bronchus Attenuates Hypoxia-Induced Pulmonary Artery Remodeling

2020 ◽  
Author(s):  
Hong Liu ◽  
Ning Wang ◽  
Jun Li ◽  
Wenting Wang ◽  
Wei Han ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Artery Remodeling ◽  
Shrna Knockdown ◽  
Pulmonary Artery Remodeling

scholarly journals The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021 ◽  
Vol 22 (9) ◽  
pp. 4980
Author(s):  
Inés Roger ◽  
Javier Milara ◽  
Paula Montero ◽  
Julio Cortijo
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Clinical Manifestations ◽  
Different Types ◽  
Artery Remodeling ◽  
Stat Pathway ◽  
Pulmonary Artery Remodeling

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular, and cellular processes involved in PH. Chronic inflammation contributes to pulmonary artery remodeling and PH, among other vascular disorders, and many inflammatory mediators signal through the JAK/STAT pathway. Recent evidence indicates that the JAK/STAT pathway is overactivated in the pulmonary arteries of patients with PH of different types. In addition, different profibrotic cytokines such as IL-6, IL-13, and IL-11 and growth factors such as PDGF, VEGF, and TGFβ1 are activators of the JAK/STAT pathway and inducers of pulmonary remodeling, thus participating in the development of PH. The understanding of the participation and modulation of the JAK/STAT pathway in PH could be an attractive strategy for developing future treatments. There have been no studies to date focused on the JAK/STAT pathway and PH. In this review, we focus on the analysis of the expression and distribution of different JAK/STAT isoforms in the pulmonary arteries of patients with different types of PH. Furthermore, molecular canonical and noncanonical JAK/STAT pathway transactivation will be discussed in the context of vascular remodeling and PH. The consequences of JAK/STAT activation for endothelial cells and pulmonary artery smooth muscle cells’ proliferation, migration, senescence, and transformation into mesenchymal/myofibroblast cells will be described and discussed, together with different promising drugs targeting the JAK/STAT pathway in vitro and in vivo.

scholarly journals Adventitial Alterations Are the Main Features in Pulmonary Artery Remodeling due to Long-Term Chronic Intermittent Hypobaric Hypoxia in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Julio Brito ◽  
Patricia Siques ◽  
Silvia M. Arribas ◽  
Angel L. López de Pablo ◽  
M. Carmen González ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Inflammatory Cells ◽  
Cell Number ◽  
Hypoxic Conditions ◽  
Artery Remodeling ◽  
Medial Hypertrophy ◽  
The Right ◽  
Pulmonary Artery Remodeling

Long-term chronic intermittent exposure to altitude hypoxia is a labor phenomenon requiring further research. Using a rat model, we examined whether this type of exposure differed from chronic exposure in terms of pulmonary artery remodeling and other features. Rats were subjected to chronic hypoxia (CH,n=9) and long-term intermittent hypoxia (CIH2x2; 2 days of hypoxia/2 days of normoxia,n=10) in a chamber (428 Torr, 4,600 m of altitude) for 46 days and compared to rats under normoxia (NX,n=10). Body weight, hematocrit, and right ventricle ratio were measured. Pulmonary artery remodeling was assessed using confocal microscopy of tissues stained with a nuclear dye (DAPI) and CD11b antibody. Both hypoxic conditions exhibited increased hematocrit and hypertrophy of the right ventricle, tunica adventitia, and tunica media, with no changes in lumen size. The medial hypertrophy area (larger in CH) depicted a significant increase in smooth muscle cell number. Additionally, CIH2x2 increased the adventitial hypertrophy area, with an increased cellularity and a larger prevalence of clustered inflammatory cells. In conclusion, CIH2x2 elicits milder effects on pulmonary artery medial layer muscularization and subsequent right ventricular hypertrophy than CH. However, CIH2x2 induces greater and characteristic alterations of the adventitial layer.

scholarly journals Pulmonary artery remodeling in transposition of the great arteries: relevance for neoaortic root dilatation

2003 ◽  
Vol 126 (4) ◽  
pp. 1053-1060 ◽  
Author(s):  
Shirin Lalezari ◽  
Mark G Hazekamp ◽  
Margot M Bartelings ◽  
Paul H Schoof ◽  
Adriana C Gittenberger-de Groot
Keyword(s):  
Pulmonary Artery ◽  
Artery Remodeling ◽  
Pulmonary Artery Remodeling

Heparin Reduces Overcirculation-Induced Pulmonary Artery Remodeling Through P38 MAPK in Piglet

2015 ◽  
Vol 99 (5) ◽  
pp. 1677-1684 ◽  
Author(s):  
Gaofeng Zhao ◽  
Jingjing Seng ◽  
John Beagle ◽  
Olga Syrkina ◽  
Charles A. Hales
Keyword(s):  
Pulmonary Artery ◽  
P38 Mapk ◽  
Artery Remodeling ◽  
Pulmonary Artery Remodeling
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