scholarly journals Myocardial migration by fibroblast progenitor cells is blood pressure dependent in a model of angII myocardial fibrosis

2012 ◽  
Vol 35 (4) ◽  
pp. 449-456 ◽  
Author(s):  
Nicole L Rosin ◽  
Mryanda Sopel ◽  
Alec Falkenham ◽  
Tanya L Myers ◽  
Jean-Francois Légaré
Keyword(s):  
Blood Pressure ◽  
Progenitor Cells ◽  
Myocardial Fibrosis ◽  
Fibroblast Progenitor Cells

scholarly journals Fibroblast progenitor cells are recruited into the myocardium prior to the development of myocardial fibrosis

2012 ◽  
Vol 93 (2) ◽  
pp. 115-124 ◽  
Author(s):  
Mryanda Sopel ◽  
Alec Falkenham ◽  
Adam Oxner ◽  
Irene Ma ◽  
Timothy D.G. Lee ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Myocardial Fibrosis ◽  
Fibroblast Progenitor Cells

Fibroblast progenitor cells of the embryonic chick limb

Development ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 191-200
Author(s):  
Stuart A. Newman
Keyword(s):  
Progenitor Cells ◽  
Cell Types ◽  
Mesenchymal Cells ◽  
The Other ◽  
Embryonic Chick ◽  
Similar Morphology ◽  
Level Characteristic ◽  
Fibroblast Progenitor Cells ◽  
Wing Tip ◽  
Mesodermal Lineage

A population of mesenchymal cells derived from the stage-25 chick wing tip gives rise to progeny of a similar morphology and to authentic fibroblasts when grown in low densityculture. Mixed clones containing both cell types are often observed. As the more rapidly proliferating fibroblasts begin to predominate in these cultures, collagen biosynthesisrises from the basal mesenchymal level to a level characteristic of mature fibroblasts. Thefibroblast progenitor is discussed relative to the other cell types of the mesodermal lineage of the developing limb.

scholarly journals Angiotensin Type 2 and Mas Receptor Activation Prevents Myocardial Fibrosis and Hypertrophy through the Reduction of Inflammatory Cell Infiltration and Local Sympathetic Activity in Angiotensin II-Dependent Hypertension

2021 ◽  
Vol 22 (24) ◽  
pp. 13678
Author(s):  
Giovanna Castoldi ◽  
Raffaella Carletti ◽  
Silvia Ippolito ◽  
Andrea Stella ◽  
Gianpaolo Zerbini ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Myocardial Fibrosis ◽  
Inflammatory Cell ◽  
Renin Angiotensin System ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Ang Ii ◽  
Mas Receptor ◽  
Compound 21

Compound 21 (C21), an AT2 receptor agonist, and Angiotensin 1-7 (Ang 1-7), through Mas receptor, play an important role in the modulation of the protective arm of the renin-angiotensin system. The aim of this study was to investigate in an experimental model of angiotensin II-dependent hypertension whether the activation of the potentially protective arm of the renin-angiotensin system, through AT2 or Mas receptor stimulation, counteracts the onset of myocardial fibrosis and hypertrophy, and whether these effects are mediated by inflammatory mechanism and/or sympathetic activation. Sprague Dawley rats (n = 67) were treated for 1 (n = 25) and 4 (n = 42) weeks and divided in the following groups: (a) Angiotensin II (Ang II, 200 ng/kg/min, osmotic minipumps, sub cutis); (b) Ang II+Compound 21 (C21, 0.3 mg/kg/day, intraperitoneal); (c) Ang II+Ang 1-7 (576 µg/kg/day, intraperitoneal); (d) Ang II+Losartan (50 mg/kg/day, per os); (e) control group (physiological saline, sub cutis). Systolic blood pressure was measured by tail cuff method and, at the end of the experimental period, the rats were euthanized and the heart was excised to evaluate myocardial fibrosis, hypertrophy, inflammatory cell infiltration and tyrosine hydroxylase expression, used as marker of sympathetic activity. Ang II caused a significant increase of blood pressure, myocardial interstitial and perivascular fibrosis and myocardial hypertrophy, as compared to control groups. C21 or Ang 1-7 administration did not modify the increase in blood pressure in Ang II treated rats, but both prevented the development of myocardial fibrosis and hypertrophy. Treatment with losartan blocked the onset of hypertension and myocardial fibrosis and hypertrophy in Ang II treated rats. Activation of AT2 receptors or Mas receptors prevents the onset of myocardial fibrosis and hypertrophy in Ang II-dependent hypertension through the reduction of myocardial inflammatory cell infiltration and tyrosine hydroxylase expression. Unlike what happens in case of treatment with losartan, the antifibrotic and antihypertrophic effects that follow the activation of the AT2 or Mas receptors are independent on the modulation of blood pressure.

scholarly journals Acute impact of an endurance race on cardiac function and biomarkers of myocardial injury in triathletes with and without myocardial fibrosis

2019 ◽  
Vol 27 (1) ◽  
pp. 94-104 ◽  
Author(s):  
Enver Tahir ◽  
Benedikt Scherz ◽  
Jitka Starekova ◽  
Kai Muellerleile ◽  
Roland Fischer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Myocardial Fibrosis ◽  
Exercise Testing ◽  
Cardiac Dysfunction ◽  
Myocardial Injury ◽  
Troponin T ◽  
T2 Mapping ◽  
Creatine Kinase Mb

Aims The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis. Methods and results Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE–). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE– triathletes (192 ± 30 mmHg, P < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms ( P = 0.797) and 989 ± 21 ms versus 989 ± 28 ms ( P = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE– triathletes (53 ± 6% vs. 59 ± 6%, P < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE –  triathletes (121 ± 30 ml/s/m2) compared to LGE + triathletes (161 ± 34 ml/s/m2, P < 0.01). Post-race atrial peak filling rates increased in LGE– triathletes to 163 ± 46 ml/s/m2, P < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m2, P = 0.747). Conclusion Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.

Wine polyphenols improve cardiovascular remodeling and vascular function in NO-deficient hypertension

2002 ◽  
Vol 282 (3) ◽  
pp. H942-H948 ◽  
Author(s):  
Iveta Bernátová ◽  
Olga Pechánová ◽  
Pavel Babál ◽  
Sona Kyselá ◽  
Svetoslav Stvrtina ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Myocardial Fibrosis ◽  
Vascular Function ◽  
Spontaneous Recovery ◽  
Left Ventricular ◽  
No Synthase ◽  
Control Group ◽  
Cross Sectional ◽  
Wine Polyphenols ◽  
Group A

The effects of the red wine polyphenolic compounds (Provinol) on hypertension, left ventricular hypertrophy, myocardial fibrosis, and vascular remodeling were investigated after chronic inhibition of nitric oxide (NO) synthase by administration of N G-nitro-l-arginine methyl ester (l-NAME) to rats. Rats were divided into four groups: a control group, a group treated for 4 wk with l-NAME (40 mg · kg−1 · day−1), and two groups treated with l-NAME followed by 3 wk of either spontaneous recovery or recovery with Provinol treatment (40 mg · kg−1 · day−1). Administration of Provinol produced a greater readiness of the decrease in blood pressure than that in the spontaneous recovery group. Provinol significantly depressed myocardial fibrosis and expedited the decrease in aortic cross-sectional area, the increase in endothelium-dependent relaxation, and the decrease in contraction of the aorta. These effects of Provinol were associated with a greater increase of NO synthase activity in the left ventricle and the aorta. The present study provides evidence that Provinol accelerates the regression of blood pressure and improves structural and functional cardiovascular changes produced by chronic inhibition of NO synthesis.

scholarly journals Systemic microvascular rarefaction is correlated with dysfunction of late endothelial progenitor cells in mild hypertension: a substudy of EXCAVATION-CHN1

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Jianwen Liang ◽  
Yan Li ◽  
Long Chen ◽  
Wenhao Xia ◽  
Guifu Wu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Early Detection ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Capillary Density ◽  
Tube Formation ◽  
Endothelial Progenitor ◽  
Hypertensive Patients ◽  
Normotensive Subjects ◽  
Microvascular Rarefaction

Abstract Background Hypertension often presents with microvascular rarefaction (MVR), which is closely associated with impaired angiogenesis. Early detection of MVR is essential for systemic assessment in patient with hypertension. We aimed to determine the systemic MVR through both optical coherence tomography angiography (OCTA) and intravital capillaroscopy, and to investigate their respective efficacies and related mechanisms associated with late endothelial progenitor cells (LEPCs) dysfunction. Methods Seventy-one hypertensive and sixty-nine age-match normotensive subjects were included in this study. All subjects received intravital capillaroscopy for skin capillary density (SCD) and OCTA for retinal capillary density (RCD) and non-perfused areas (R-NPA). Subsequently, correlation of LEPCs activities and microvascular rarefaction were examined. Results Compared with normotensive subjects, hypertensive patients had significantly lower RCD [(52.9 ± 2.9)% vs. (57.8 ± 1.6)%, P < 0.01] and higher R-NPA [(0.12 ± 0.07) mm2 vs. (0.053 ± 0.020) mm2, P < 0.01]. SCD correlated positively with RCD but negatively with R-NPA [(RCD: OR = 0.40, 95% CI 0.25–0.67, P < 0.01); (R-NPA: OR = 0.39, 95% CI − 0.0029 to 0.0011, P < 0.01)]. The discriminative powers of RCD performed best (AUC 0.79 versus SCD AUC 0.59, P < 0.001) followed by R-NPA (AUC 0.73 versus SCD AUC 0.59, P < 0.001) for systolic blood pressure. Similar pattern is also found for diastolic blood pressure (RCD AUC 0.80 versus SCD AUC 0.54, P < 0.001; R-NPA AUC 0.77 versus SCD AUC 0.54, P < 0.001). Furthermore, LEPCs tube formation was impaired in hypertensive patients (36.8 ± 2.3 vs. 28 ± 3.7, P < 0.01). After multivariate adjustments, positive correlation existed between RCD or R-NPA with LEPCs tube formation (RCD: β = 0.64, 95% CI 0.34–0.91, P < 0.01; R-NPA: β = − 24.67, 95% CI − 43.14 to − 4.63, P < 0.05) but not with SCD (β = 0.082, 95% CI 0.01–0.18, P = 0.085). Conclusion Compared to intravital capillaroscopy, OCTA is a more precise technique for early detection of hypertensive microvascular rarefaction, which is associated with the fall in LEPC-mediated angiogenesis. Both of OCTA and LEPCs function can help identify hypertension-related capillary abnormality. Trail Registration The trial is a substudy of EXCAVATION-CHN1, registered at clinicaltrials.gov as NCT02817204 (June 26, 2016).

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