Coronary blood vessels from distinct origins converge to equivalent states during mouse and human development

2021 ◽  
Author(s):  
Yen Tran
Keyword(s):  
Human Development ◽  
Blood Vessels ◽  
Coronary Blood Vessels

scholarly journals Coronary blood vessels from distinct origins converge to equivalent states during mouse and human development

2021 ◽  
Author(s):  
Ragini S Phansalkar ◽  
Josephine Krieger ◽  
Mingming Zhao ◽  
Sai Saroja Kolluru ◽  
Robert C Jones ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Cell Fate ◽  
Adult Mouse ◽  
Coronary Vessels ◽  
Lineage Tracing ◽  
Specific Gene ◽  
Cell Type ◽  
Functional Differences ◽  
Coronary Blood Vessels ◽  
Two Populations

Most cell fate trajectories during development follow a diverging, tree-like branching pattern, but the opposite can occur when distinct progenitors contribute to the same cell type. During this convergent differentiation, it is unknown if cells "remember" their origins transcriptionally or whether this influences cell behavior. Most coronary blood vessels of the heart develop from two different progenitor sources-the endocardium (Endo) and sinus venosus (SV)-but whether transcriptional or functional differences related to origin are retained is unknown. We addressed this by combining lineage tracing with single-cell RNA sequencing (scRNAseq) in embryonic and adult mouse hearts. Shortly after coronary development begins, capillary ECs transcriptionally segregated into two states that retained progenitor-specific gene expression. Later in development, when the coronary vasculature is well-established but still remodeling, capillary ECs again segregated into two populations, but transcriptional differences were related to tissue localization rather than lineage. Specifically, ECs in the heart septum expressed genes indicative of increased local hypoxia and decreased blood flow. Adult capillary ECs were more homogeneous and lacked indications of either lineage or location. In agreement, SV- and Endo-derived ECs in adult hearts displayed similar responses to injury. Finally, scRNAseq of developing human coronary vessels indicated that the human heart followed similar principles. Thus, over the course of development, transcriptional heterogeneity in coronary ECs is first influenced by lineage, then by location, until heterogeneity disappears in the homeostatic adult heart. These results highlight the plasticity of ECs during development, and the validity of the mouse as a model for human coronary development.

Abstract 237: PRMT1-p53-Slug Axis Regulates Epicardial EMT and Ventricular Development

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Olan Jackson-Weaver ◽  
Jian Wu ◽  
Yongchao Gou ◽  
Yibu Chen ◽  
Meng Li ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Heart Development ◽  
Cultured Cells ◽  
Migration And Invasion ◽  
P53 Expression ◽  
Epicardial Cells ◽  
Coronary Blood Vessels

Rationale: Epicardial epithelial-to-mesenchymal trasition (EMT) is a vital process in embryonic heart development. During EMT, epicardial cells acquire migratory and invasive properties, and differentiate into new cell types, including cardiac fibroblasts and coronary smooth muscle cells. Non-histone protein methylation is an emerging modulator of cell signaling. We have recently established a role for protein arginine methyltransferase-1 (PRMT1) in TGF-β-induced EMT in cultured cells. Objective: To determine the role of PRMT1 in epicardial EMT. Methods and Results: We investigated the role of PRMT1 in epicardial EMT in mouse epicardial cells. Embryonic day 9.5 (E9.5) tamoxifen administration of WT1-Cre ERT ;PRMT1 fl/fl ;ROSA-YFP fl/fl mouse embryos was used to delete PRMT1 in the epicardium. Epicardial PRMT1 deletion led to reduced epicardial migration into the myocardium, a thinner compact myocardial layer, and dilated coronary blood vessels at E15.5. Using the epicardial cell line MEC1, we found that PRMT1 siRNA prevented the increase in mesenchymal proteins Slug and Fibronectin and the decrease in epithelial protein E-Cadherin during TGF-β treatment-induced EMT. PRMT1 siRNA also reduced the migration and invasion of MEC1 cells. We further identified that PRMT1 siRNA also increased the expression of p53, a key regulator of the Slug degradation pathway. PRMT1 siRNA increases p53 expression by decreasing p53 degradation, and shifted p53 localization to the cytoplasm. In vitro methylation assays further demonstrated that PRMT1 methylates p53. Knockdown of p53 increased Slug levels and enhanced EMT, establishing p53 as a regulator of epicardial EMT through controlling Slug expression. Furthermore, RNAseq experiments in MEC1 cells demonstrated that 40% (545/1,351) of TGF-β-induced transcriptional changes were prevented by PRMT1 siRNA. Furthermore, when p53 and PRMT1 were simultaneously knocked down, TGF-β induced transcriptional control of 37% (201/545) of these PRMT1-dependent genes was restored. Conclusions: The PRMT1-p53-Slug pathway is necessary for epicardial EMT in cultured MEC1 cells as well as in the epicardium in vivo . Epicardial PRMT1 is required for the development of compact myocardium and coronary blood vessels.

Bio-Inspired Active Electrolocation Sensors for Inspection of Tube Systems

2012 ◽  
Vol 84 ◽  
pp. 45-50 ◽  
Author(s):  
Martin Gottwald ◽  
Gerhard von der Emde
Keyword(s):  
Blood Vessels ◽  
Electric Fields ◽  
Skin Surface ◽  
Ring Electrode ◽  
Weakly Electric Fish ◽  
Atherosclerotic Lesions ◽  
Electric Image ◽  
Coronary Blood Vessels ◽  
Weakly Electric ◽  
Gnathonemus Petersii

At night, weakly electric fish Gnathonemus petersii use active electrolocation to scan their environment with self generated electric fields. Nearby objects distort the electric fields and are recognized as electric images on the electroreceptive skin surface of the animal. By analyzing the electric image, G. petersii can sense an object’s distance, dimensions and electrical properties. The principles and algorithms of active electrolocation can be applied to catheter-based sensor systems for analysing wall changes in fluid filled tube systems, for example atherosclerotic plaques of the coronary blood vessels. We used a basic atherosclerosis model of synthetic blood vessels and plaques, which were scanned with a ring electrode catheter applying active electrolocation. Based on the electric images of the plaques and the evaluation of bio-inspired image parameters, the plaque’s fine-structure could be assessed. Our results show that imaging through active electrolocation principally has the potential to detect and characterize atherosclerotic lesions.

Combined Atherosclerotic Lesions of Cerebral and Coronary Blood Vessels: Risk Factors

2015 ◽  
Vol 6 (1) ◽  
pp. 105-114
Author(s):  
Robert Vladimirovich Bilyutin-Aslanyan ◽  
Andrei Glebovich Vasiliev ◽  
Pavel Vasil’yevich Rodichkin ◽  
Aleksandr Petrovich Trashkov ◽  
Nikolay Valentinovich Khaytsev
Keyword(s):  
Risk Factors ◽  
Blood Vessels ◽  
Significant Risk ◽  
Cerebral Blood Vessels ◽  
Atherosclerotic Lesions ◽  
Prophylactic Measures ◽  
Coronary Blood Vessels ◽  
Atherosclerotic Process ◽  
Working Out ◽  
Pathophysiologic Mechanisms

Data is presented specifying the extent of influence of traditional and novel (C-reactive protein (CRP), fibrinogen, intima-media complex (IMC)) risk-factors of atherosclerotic lesions upon cerebral blood vessels in case of isolated variant vs. combined lesions of coronary and cerebral blood vessels. The role of CRP and fibrinogen as atherosclerotic process development markers is discussed. The most significant risk factors of combined and isolated atherosclerotic lesions of coronary and cerebral blood vessels are discussed important for understanding of this pathology ethiology and pathogenesis. Pathogenetic interrelation of cerebral and cardiac pathology is specified manifesting itself by mutual aggravation in case of atherosclerotic process. Pathophysiologic mechanisms of cerebral and coronary blood vessels’ atherosclerotic lesions are common, hence the risk factors are also analogous, however their import is not identical in case of isolated and combined variants and this feature should be taken into account while working out the approach to this ailment treatment and prophylaxis. Atherosclerotic lesions of arteries from various vascular basins alongside with common pathophysiologic mechanisms also possess a score of peculiarities that predetermine different approaches to their treatment and prophylaxis. Separate risk factors determine predominant localization of pathologic process in certain vascular basins thus identification of isolated and combined coronary and cerebral principal blood vessels atherosclerotic lesions’ risk factors is a subject of profound studies. Thus working out new approaches to cerebrovascular ailments risk prognosis on the basis of cardiovascular ailments risk factors as well as existing prophylactic measures monitoring is actual for contemporary medicine.

scholarly journals THE OCCURRENCE OF LEUCOCYTE-PLATELET THROMBOSIS IN RHEUMATIC CARDITIS

1951 ◽  
Vol 94 (6) ◽  
pp. 493-500 ◽  
Author(s):  
Chandler A. Stetson
Keyword(s):  
Rheumatic Fever ◽  
Blood Vessels ◽  
Vascular Lesions ◽  
Rheumatic Carditis ◽  
Platelet Thrombi ◽  
Coronary Blood Vessels

Leucocyte-platelet thrombi, involving the smaller branches of the coronary blood vessels, have been found in the hearts of patients with active rheumatic fever and rheumatic carditis. A consistent correlation has been observed between the existence of these vascular lesions and the presence of typical Aschoff bodies. It is suggested that these cellular thrombi may play a role in the pathogenesis of rheumatic carditis.

Th-P15:178 Correlation between blood values of the lipoprotein (A) and degree of stenosis of the coronary blood vessels

2006 ◽  
Vol 7 (3) ◽  
pp. 532
Author(s):  
M. Noshpal ◽  
V. Arsova ◽  
J. Lovcanska ◽  
M. Otljanska ◽  
B. Sidovska ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Lipoprotein A ◽  
Coronary Blood Vessels

Control of myocardial oxygen consumption in transgenic mice overexpressing vascular eNOS

2004 ◽  
Vol 287 (5) ◽  
pp. H2115-H2121 ◽  
Author(s):  
E. K. Walsh ◽  
H. Huang ◽  
Z. Wang ◽  
J. Williams ◽  
R. de Crom ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Blood Vessels ◽  
Myocardial Oxygen Consumption ◽  
Cardiac Tissue ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Oxygen Electrode ◽  
Left Ventricular ◽  
Similar Degree ◽  
Coronary Blood Vessels

Our objective was to investigate the potential role of selective endothelial nitric oxide (NO) synthase (eNOS) overexpression in coronary blood vessels in the control of myocardial oxygen consumption (MVo2). Transgenic (Tg) eNOS-overexpressing mice (eNOS Tg) ( n = 22) and wild-type (WT) mice ( n = 24) were studied. Western blot analysis indicated greater than sixfold increase of eNOS in cardiac tissue. Echocardiography in awake mice indicated no difference in cardiac function between WT and eNOS Tg; however, systolic pressure in eNOS Tg mice decreased significantly (126 ± 2.3 to 109 ± 2.3 mmHg; P < 0.05), whereas heart rate (HR) was not different. Total peripheral resistance (TPR) was also decreased (9.8 ± 0.8 to 7.6 ± 0.4 4 mmHg·ml−1·min; P < 0.05) in eNOS Tg. Furthermore, female eNOS Tg mice showed even lower TPR (7.2 ± 0.4 mmHg·ml−1·min) compared with male eNOS mice (8.6 ± 0.5, mmHg·ml·min−1; P < 0.05). Left ventricular slices were isolated from WT and eNOS Tg mice. With the use of a Clark-type oxygen electrode in an airtight bath, MVo2 was determined as the percent decrease during increasing doses (10−10 to 10−4 mol/l) of bradykinin (BK), carbachol (CCh), forskolin (10−12 to 10−6 mol/l), or S-nitroso- N-acetyl penicillamine (SNAP; 10−7 to 10−4 mol/l). Baseline MVo2 was not different between WT (181 ± 13 nmol·g−1·min−1) and eNOS Tg (188 ± 14 nmol·g−1·min−1). BK decreased MVo2 (10−4 mol/l) in WT by 17% ± 1.1 and 33% ± 2.7 in eNOS Tg ( P < 0.05). CCh also decreased MVo2, 10−4 mol/l, in WT by 20% ± 1.7 and 31% ± 2.0 in eNOS Tg ( P < 0.05). Forskolin (10−6 mol/l) or SNAP (10−4 mol/l) also decreased MVo2 in WT by 24% ± 2.8 and 36% ± 1.8 versus eNOS 31% ± 1.8 and 37% ± 3.5, respectively. N-nitro-l-arginine methyl ester (10−3 mol/l) inhibited the MVo2 reduction to BK, CCh, and forskolin by a similar degree ( P < 0.05), but not to SNAP. Thus selective overexpression of eNOS in cardiac blood vessels in mice enhances the control of MVo2 by eNOS-derived NO.

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