scholarly journals Chronic skeletal unloading of the rat femur: Mechanisms and functional consequences of vascular remodeling

Bone ◽  
2013 ◽  
Vol 57 (2) ◽  
pp. 355-360 ◽  
Author(s):  
John N. Stabley ◽  
Rhonda D. Prisby ◽  
Bradley J. Behnke ◽  
Michael D. Delp
Keyword(s):  
Vascular Remodeling ◽  
Rat Femur ◽  
Skeletal Unloading ◽  
Functional Consequences

scholarly journals Functional consequences of the collagen/elastin switch in vascular remodeling in Hyperhomocysteinemia

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Mesia Moore Steed ◽  
Walter Rodriquez ◽  
Neetu Tyagi ◽  
Suresh C. Tyagi
Keyword(s):  
Vascular Remodeling ◽  
Functional Consequences

scholarly journals Functional consequences of the collagen/elastin switch in vascular remodeling in hyperhomocysteinemic wild-type, eNOS−/−, and iNOS−/− mice

2010 ◽  
Vol 299 (3) ◽  
pp. L301-L311 ◽  
Author(s):  
Mesia M. Steed ◽  
Neetu Tyagi ◽  
Utpal Sen ◽  
Dale A. Schuschke ◽  
Irving G. Joshua ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Flow Velocity ◽  
Vascular Remodeling ◽  
Gelatin Zymography ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Wild Type ◽  
Elastin Degradation ◽  
Functional Consequences ◽  
Nos Isoforms

A decrease in vascular elasticity and an increase in pulse wave velocity in hyperhomocysteinemic (HHcy) cystathionine-β-synthase heterozygote knockout (CBS−/+) mice has been observed. Nitric oxide (NO) is a potential regulator of matrix metalloproteinase (MMP) activity in MMP-NO-tissue inhibitor of metalloproteinase (TIMP) inhibitory tertiary complex. However, the contribution of the nitric oxide synthase (NOS) isoforms eNOS and iNOS in the activation of latent MMP is unclear. We hypothesize that the differential production of NO contributes to oxidative stress and increased oxidative/nitrative activation of MMP, resulting in vascular remodeling in response to HHcy. The overall goal is to elucidate the contribution of the NOS isoforms, endothelial and inducible, in the collagen/elastin switch. Experiments were performed on six groups of animals [wild-type (WT), eNOS−/−, and iNOS−/− with and without homocysteine (Hcy) treatment (0.67 g/l) for 8–12 wk]. In vivo echograph was performed to assess aortic timed flow velocity for indirect compliance measurement. Histological determination of collagen and elastin with trichrome and van Gieson stains, respectively, was performed. In situ measurement of superoxide generation using dihydroethidium was used. Differential expression of eNOS, iNOS, nitrotyrosine, MMP-2 and -9, and elastin were measured by quantitative PCR and Western blot analyses. The 2% gelatin zymography was used to assess MMP activity. The increase in O2− and robust activity of MMP-9 in eNOS−/−, WT+Hcy, and eNOS−/−+Hcy was accompanied by the gross disorganization and thickening of the ECM along with extensive collagen deposition and elastin degradation (collagen/elastin switch) resulting in a decrease in aortic timed flow velocity. Results show that an increase in iNOS activity is a key contributor to HHcy-mediated collagen/elastin switch and resulting decline in aortic compliance.

Morphometric analysis of pulmonary vascular remodeling in COPD

Pneumologie ◽  
2009 ◽  
Vol 63 (02) ◽  
Author(s):  
T Medebach ◽  
N Weissmann ◽  
HA Ghofrani ◽  
W Seeger ◽  
F Grimminger
Keyword(s):  
Morphometric Analysis ◽  
Vascular Remodeling ◽  
Pulmonary Vascular Remodeling

Model Characterization of Pulmonary Arterial Hypertension: Analysis of Lung Pathology with Respect to Human Disease

2020 ◽  
Author(s):  
◽  
Eptisam lambu
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Human Disease ◽  
Vascular Remodeling ◽  
Vascular Wall ◽  
Lung Pathology ◽  
Pulmonary Arterial ◽  
Lung Pathogenesis ◽  
Arterial Endothelial Cells

Pulmonary arterial hypertension (PAH) is a rare multifactorial disease characterized by abnormal high blood pressure in the pulmonary artery, or increased pulmonary vascular resistance (PVR), caused by obstruction in the small arteries of the lung. Increased PVR is also thought to be caused by abnormal vascular remodeling, due to thickening of the pulmonary vascular wall resulting from significant hypertrophy of pulmonary arterial smooth-muscle cells (PASMCs) and increased proliferation/impaired apoptosis of pulmonary arterial endothelial cells (PAECs). Herein, we investigated the mechanisms and explored molecular pathways mediating the lung pathogenesis in two PAH rat models: Monocrotaline (MCT) and Sugen5416/Hypoxia (SuHx). We analyzed these disease models to determine where the vasculature shows the most severe PAH pathology and which model best recapitulates the human disease. We investigated the role vascular remodeling, hypoxia, cell proliferation, apoptosis, DNA damage and inflammation play in the pathogenesis of PAH. Neither model recapitulated all features of the human disease, however each model presented with some of the pathology seen in PAH patients.

Sign in / Sign up

Export Citation Format

Share Document