Dataset Information

Single Cell Analysis in Vascular Biology.

ABSTRACT: The ability to quantify DNA, RNA, and protein variations at the single cell level has revolutionized our understanding of cellular heterogeneity within tissues. Via such analyses, individual cells within populations previously thought to be homogeneous can now be delineated into specific subpopulations expressing unique sets of genes, enabling specialized functions. In vascular biology, studies using single cell RNA sequencing have revealed extensive heterogeneity among endothelial and mural cells even within the same vessel, key intermediate cell types that arise during blood and lymphatic vessel development, and cell-type specific responses to disease. Thus, emerging new single cell analysis techniques are enabling vascular biologists to elucidate mechanisms of vascular development, homeostasis, and disease that were previously not possible. In this review, we will provide an overview of single cell analysis methods and highlight recent advances in vascular biology made possible through single cell RNA sequencing.

SUBMITTER: Chavkin NW

PROVIDER: S-EPMC7137757 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Single Cell Analysis in Vascular Biology.

Chavkin Nicholas W NW Hirschi Karen K KK

Frontiers in cardiovascular medicine 20200331

The ability to quantify DNA, RNA, and protein variations at the single cell level has revolutionized our understanding of cellular heterogeneity within tissues. Via such analyses, individual cells within populations previously thought to be homogeneous can now be delineated into specific subpopulations expressing unique sets of genes, enabling specialized functions. In vascular biology, studies using single cell RNA sequencing have revealed extensive heterogeneity among endothelial and mural cel ...[more]

PMID: 32296715

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Project description:BackgroundTransradial catheterization is associated with radial artery injury and vasomotor dysfunction and represents an accessible model of acute vascular injury in humans. We characterized vascular injury and functional recovery to understand the role of circulating endothelial progenitor cells in vascular repair.Methods and resultsIn 50 patients (aged 64±10 years, 70% male) undergoing transradial cardiac catheterization, radial artery injury was assessed by optical coherence tomography and examination of explanted vascular sheaths. Flow- and nitrate-mediated dilatation of the radial artery was assessed in both arms at baseline, at 24 hours, and at 1, 4, and 12 weeks. Circulating endothelial progenitor cell populations were quantified using flow cytometry. Late endothelial outgrowth colonies were isolated and examined in vitro. Optical coherence tomography identified macroscopic injury in 12 of 50 patients (24%), but endothelial cells (1.9±1.2×104 cells) were isolated from all arterial sheaths examined. Compared with the noncatheterized radial artery, flow-mediated vasodilatation was impaired in the catheterized artery at 24 hours (9.9±4.6% versus 4.1±3.1%, P<0.0001) and recovered by 12 weeks (8.1±4.9% versus 10.1±4.9%, P=0.09). Although the number of CD133+ cells increased 24 hours after catheterization (P=0.02), the numbers of CD34+ cells and endothelial outgrowth colonies were unchanged. Migration of endothelial cells derived from endothelial outgrowth colonies correlated with arterial function before catheterization but was not related to recovery of function following injury.ConclusionsTransradial cardiac catheterization causes endothelial denudation, vascular injury, and vasomotor dysfunction that recover over 12 weeks. Recovery of vascular function does not appear to be dependent on the mobilization or function of endothelial progenitor cells.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT02147119.

Project description:This review discusses recent research on the genetic, molecular, cellular, and developmental mechanisms underlying the etiology of vascular malformations of the brain (VMBs), including cerebral cavernous malformation, sporadic brain arteriovenous malformation, and the arteriovenous malformations of hereditary hemorrhagic telangiectasia. Summary of Review- The identification of gene mutations and genetic risk factors associated with cerebral cavernous malformation, hereditary hemorrhagic telangiectasia, and sporadic arteriovenous malformation has enabled the development of animal models for these diseases and provided new insights into their etiology. All of the genes associated with VMBs to date have known or plausible roles in angiogenesis and vascular remodeling. Recent work suggests that the angiogenic process most severely disrupted by VMB gene mutation is that of vascular stabilization, the process whereby vascular endothelial cells form capillary tubes, strengthen their intercellular junctions, and recruit smooth muscle cells to the vessel wall. In addition, there is now good evidence that in some cases, cerebral cavernous malformation lesion formation involves a genetic 2-hit mechanism in which a germline mutation in one copy of a cerebral cavernous malformation gene is followed by a somatic mutation in the other copy. There is also increasing evidence that environmental second hits can produce lesions when there is a mutation to a single allele of a VMB gene.Recent findings begin to explain how mutations in VMB genes render vessels vulnerable to rupture when challenged with other inauspicious genetic or environmental factors and have suggested candidate therapeutics. Understanding of the cellular mechanisms of VMB formation and progression in humans has lagged behind that in animal models. New knowledge of lesion biology will spur new translational work. Several well-established clinical and genetic database efforts are already in place, and further progress will be facilitated by collaborative expansion and standardization of these.

Dataset Information

Single Cell Analysis in Vascular Biology.

Publications

Single Cell Analysis in Vascular Biology.

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