Left-Ventricular Hypertrophy in 18-Month-Old Donor Hearts Was Not Associated with Graft Dysfunction in the Early Phase of Reperfusion after Cardiac Transplantation: Gene Expression Profiling

2020 ◽  
Author(s):  
S. Korkmaz-Icöz ◽  
D. Akca ◽  
L. Shiliang ◽  
S. Loganathan ◽  
P. Brlecic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Left Ventricular Hypertrophy ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Early Phase ◽  
Cardiac Transplantation ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Graft Dysfunction ◽  
Old Donor

scholarly journals Left-ventricular hypertrophy in 18-month-old donor rat hearts was not associated with graft dysfunction in the early phase of reperfusion after cardiac transplantation–gene expression profiling

GeroScience ◽  
2021 ◽  
Author(s):  
Sevil Korkmaz-Icöz ◽  
Deniz Akca ◽  
Shiliang Li ◽  
Sivakkanan Loganathan ◽  
Paige Brlecic ◽  
...  
Keyword(s):  
Early Phase ◽  
Cardiac Transplantation ◽  
Diastolic Pressure ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Left Ventricular ◽  
Graft Dysfunction ◽  
Altered Expression ◽  
Old Donor

AbstractThe use of hearts with left-ventricular (LV) hypertrophy (LVH) could offer an opportunity to extend the donor pool for cardiac transplantation. We assessed the effects of LVH in 18-month-old spontaneously hypertensive stroke-prone (SHRSP) donor rats and following transplantation. In donors, cardiac function and structural alterations were assessed. Then, the hearts were transplanted into young normotensive-rats. We evaluated LV graft function 1 h after transplantation. The myocardial expression of 92 genes involved in apoptosis, inflammation, and oxidative-stress was profiled using PCR-array. Compared to controls, SHRSP-rats developed LVH, had increased LV systolic performance (slope of the end-diastolic pressure-volume (PV) relationship: 1.6±0.2 vs 0.8±0.1mmHg/μl, p<0.05) accompanied by diastolic dysfunction [prolonged time constant of LV pressure decay (Tau: 15.8±0.6 vs 12.3±0.5ms) and augmented diastolic stiffness (LV end-diastolic PV relationship: 0.103±0.012 vs 0.045±0.006mmHg/ml), p<0.05]. They presented ECG changes, myocardial fibrosis, and increased nitrotyrosine immunoreactivity and plasma troponin-T and creatine kinase-CM levels. After transplantation, even though the graft contractility was better in SHRSP rats compared to controls, the adverse impact of ischemia/reperfusion-injury on contractility was not altered (Ees ratio after versus before transplantation: 32% vs 29%, p>0.05). Whereas nitrotyrosine immunoreactivity was higher, myeloperoxidase-positive cell infiltration was decreased in the SHRSP+transplanted compared to control+transplanted. Among the tested genes, LVH was associated with altered expression of 38 genes in donors, while transplantation of these hearts resulted in the change of four genes. Alterations in 18-month-old donor hearts, as a consequence of hypertension and LVH, were not associated with graft dysfunction in the early phase of reperfusion after transplantation.

Natriuretic peptide gene expression in DOCA-salt hypertension after blockade of type B endothelin receptor

2002 ◽  
Vol 282 (3) ◽  
pp. H1127-H1134 ◽  
Author(s):  
Liliana G. Bianciotti ◽  
Adolfo J. de Bold
Keyword(s):  
Gene Expression ◽  
Left Ventricular Hypertrophy ◽  
Natriuretic Peptide ◽  
Left Atrial ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Mrna Levels ◽  
Collagen Iii ◽  
Salt Hypertension ◽  
Np Gene

We investigated the effect of long-term in vivo blockade of the ET-1 receptor subtype B (ETB) with A-192621, a selective ETBantagonist, on atrial and ventricular natriuretic peptide (NP) gene expression in deoxycorticosterone acetate (DOCA)-salt hypertension. In this model, stimulation of the cardiac natriuretic peptide (NP) and the endothelin system and suppression of the renin-angiotensin system is observed. DOCA-salt induced significant hypertension, cardiac hypertrophy and increased NP plasma and left atrial and right and left ventricular NP gene expression. ETB blockade per se produced hypertension and left ventricular hypertrophy but induced little change on the levels of ventricular NP and only increased left atrial natriuretic factor (ANF) mRNA levels. Combined ETBblockade/DOCA-salt treatment worsened hypertension, increased left ventricular hypertrophy and induced right ventricular hypertrophy. All animals so treated had increased ventricular NP gene expression. Collagen III and β-myosin heavy chain gene expression were enhanced in both the right and the left ventricle of DOCA-salt hypertensive rats. The results of this study suggest that the ETBreceptor does not participate directly in the modulation of atrial or ventricular NP gene expression and that this receptor mediates a protective cardiovascular function. ETB blockade can induce significant ventricular hypertrophy without an increase in ANF or brain NP gene expression.

Allograft Left Ventricular Hypertrophy after Cardiac Transplantation

2012 ◽  
Vol 18 (8) ◽  
pp. S76
Author(s):  
Kimberly Parks ◽  
Cristina Castrillo ◽  
Angela Canteli-Alvarez ◽  
Malissa Wood ◽  
Asma Mahmud ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Cardiac Transplantation ◽  
Ventricular Hypertrophy ◽  
Left Ventricular

Abstract P112: Decreased α-Myosin Expression is Associated with Left Ventricular Hypertrophy in Hypertensive Caribbean Vervets

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Chelsea C Weaver ◽  
Anthony Gutierrez ◽  
Jeffrey L Osborn
Keyword(s):  
Gene Expression ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Cardiac Fibrosis ◽  
Peripheral Resistance ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Protein Isoforms ◽  
Left Ventricular Myocardium ◽  
Human Heart Failure

Caribbean vervets ( Chlorocebus aethiops sabeus ) develop hypertension (HT; Systolic Blood Pressure ≥ 140 mmHg) in over 30% (125/345) of the outbred population. Elevated total peripheral resistance in HT increases cardiac afterload, which may lead to left ventricular hypertrophy (LVH) and cardiac remodeling. We hypothesize that prolonged spontaneous HT is associated with LVH, cardiac and aortic fibrosis, as well as differential transcription of myocardial contractile proteins. Vervets were characterized as HT (SBP = 170 ± 25.3 mmHg; n=125) or normotensive (NT, SBP = 99 ± 14.5 mmHg; n=148) using forearm plethysmography (ketamine sedated;15 mg/kg i.m.). Cardiomyocyte cross-sectional area was greater in HT compared to NT animals (HT 283 ± 52 μm 2 , n=9 vs NT 114 ± 8 μm 2 , n=10; p<0.01). Average collagen stained as a function of tissue area was similar in left ventricular myocardium of HT and NT animals (HT 14.17 ± 3.13% or 0.17/1.21 mm 2 , n=9 vs NT 12.22 ± 0.80% or 0.16/1.27 mm 2 , n=10; p>0.05). Aortic adventia collagen area was greater in HT compared to NT vervets (HT 66.12 ± 4.22% or 0.60/0.90 mm 2 , n=6 vs NT 54.53 ± 2.21% or 0.56/1.02 mm 2 , n=10; p<0.05). Total tissue collagen was estimated using a hydroxyproline assay. Collagen content was not different between HT and NT vervets for left ventricular myocardium (HT 194.02 ± 8.61 μg/mL, n=11 vs NT 201.70 ± 18.89 μg/mL, n=10; p=0.71) or aorta (HT 745.64 ± 44.49 μg/mL, n=11 vs NT 668.39 ± 31.06 μg/mL, n=11; p=0.17). Myosin gene expression (α and β) was estimated using RT-PCR of mRNA in left ventricular myocardium of NT (SBP = 98.91 ±10.89 mmHg; n=20) and HT (SBP = 171.51 ± 30.28 mmHg; n=17) vervets. α-myosin was downregulated in HT compared to NT vervets (HT RQ = 0.10 ± 0.03 vs. NT RQ = 0.22 ± 0.04; p<0.05), while β-myosin expression was not different (HT RQ = 0.22 ± 0.17 vs. NT RQ = 0.20 ± 0.16; p=0.83). Thus, spontaneous HT in outbred vervets induces LVH in response to factors other than cardiac fibrosis. Myosin gene expression may shift from α-myosin to other contractile protein isoforms, characteristic of human heart failure. In this nonhuman primate model, HT does not induce significant aortic fibrosis that may occur in aged animals. Future studies will further characterize contractile and pro-inflammatory proteins in LVH of spontaneous HT vervets.

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