scholarly journals The emerging role of cell senescence in atherosclerosis

2021 ◽  
Vol 59 (1) ◽  
pp. 27-38 ◽  
Author(s):  
Chang-Meng Wu ◽  
Lei Zheng ◽  
Qian Wang ◽  
Yan-Wei Hu
Keyword(s):  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Cell Senescence ◽  
Vascular Endothelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Plaque Instability ◽  
Inflammatory Molecules ◽  
Progression Of Atherosclerosis

AbstractCell senescence is a fundamental mechanism of aging and appears to play vital roles in the onset and prognosis of cardiovascular disease, fibrotic pulmonary disease, liver disease and tumor. Moreover, an increasing body of evidence shows that cell senescence plays an indispensable role in the formation and development of atherosclerosis. Multiple senescent cell types are associated with atherosclerosis, senescent human vascular endothelial cells participated in atherosclerosis via regulating the level of endothelin-1 (ET-1), nitric oxide (NO), angiotensin II and monocyte chemoattractant protein-1 (MCP-1), senescent human vascular smooth muscle cells-mediated plaque instability and vascular calcification via regulating the expression level of BMP-2, OPN, Runx-2 and inflammatory molecules, and senescent macrophages impaired cholesterol efflux and promoted the development of senescent-related cardiovascular diseases. This review summarizes the characteristics of cell senescence and updates the molecular mechanisms underlying cell senescence. Moreover, we also discuss the recent advances on the molecular mechanisms that can potentially regulate the development and progression of atherosclerosis.

scholarly journals First blood: the endothelial origins of hematopoietic progenitors

Angiogenesis ◽  
2021 ◽  
Author(s):  
Giovanni Canu ◽  
Christiana Ruhrberg
Keyword(s):  
Stem Cells ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Fetal Liver ◽  
Cell Types ◽  
Yolk Sac ◽  
Vascular Endothelial ◽  
Hematopoietic Stem ◽  
Close Proximity ◽  
Clinical Interest

AbstractHematopoiesis in vertebrate embryos occurs in temporally and spatially overlapping waves in close proximity to blood vascular endothelial cells. Initially, yolk sac hematopoiesis produces primitive erythrocytes, megakaryocytes, and macrophages. Thereafter, sequential waves of definitive hematopoiesis arise from yolk sac and intraembryonic hemogenic endothelia through an endothelial-to-hematopoietic transition (EHT). During EHT, the endothelial and hematopoietic transcriptional programs are tightly co-regulated to orchestrate a shift in cell identity. In the yolk sac, EHT generates erythro-myeloid progenitors, which upon migration to the liver differentiate into fetal blood cells, including erythrocytes and tissue-resident macrophages. In the dorsal aorta, EHT produces hematopoietic stem cells, which engraft the fetal liver and then the bone marrow to sustain adult hematopoiesis. Recent studies have defined the relationship between the developing vascular and hematopoietic systems in animal models, including molecular mechanisms that drive the hemato-endothelial transcription program for EHT. Moreover, human pluripotent stem cells have enabled modeling of fetal human hematopoiesis and have begun to generate cell types of clinical interest for regenerative medicine.

scholarly journals The Role of Angiogenesis and Pro-Angiogenic Exosomes in Regenerative Dentistry

2019 ◽  
Vol 20 (2) ◽  
pp. 406 ◽  
Author(s):  
Alina-Andreea Zimta ◽  
Oana Baru ◽  
Mandra Badea ◽  
Smaranda Buduru ◽  
Ioana Berindan-Neagoe
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Toxic Waste ◽  
Vascular Endothelial ◽  
Regenerative Dentistry ◽  
Oral Tissue ◽  
Cellular Components ◽  
Stimulation Of

Dental surgeries can result in traumatic wounds that provoke major discomfort and have a high risk of infection. In recent years, density research has taken a keen interest in finding answers to this problem by looking at the latest results made in regenerative medicine and adapting them to the specificities of oral tissue. One of the undertaken directions is the study of angiogenesis as an integrative part of oral tissue regeneration. The stimulation of this process is intended to enhance the local availability of stem cells, oxygen levels, nutrient supply, and evacuation of toxic waste. For a successful stimulation of local angiogenesis, two major cellular components must be considered: the stem cells and the vascular endothelial cells. The exosomes are extracellular vesicles, which mediate the communication between two cell types. In regenerative dentistry, the analysis of exosome miRNA content taps into the extended communication between these cell types with the purpose of improving the regenerative potential of oral tissue. This review analyzes the stem cells available for the dentistry, the molecular cargo of their exosomes, and the possible implications these may have for a future therapeutic induction of angiogenesis in the oral wounds.

scholarly journals The Role of Monocytes Cellular and Molecular Mechanisms in the Development of Systemic Immune Inflammation. Part 1

Psychiatry ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 76-85
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Cognitive Disorders ◽  
Research Data ◽  
Vascular Endothelial ◽  
Platelet Aggregates ◽  
Immune Inflammation ◽  
The Brain

Introduction: the important role of monocytes /macrophages, as well as cytokines produced by them was determined in the pathogenesis of mental disorders, as a macrophage-T-lymphocyte theory of bipolar disorder, schizophrenia and depression. According to this theory, there is an increase in the number of active circulating monocytes, macrophages and T-cells in patients with mental disorders. These cells migrate to the CNS as a result of the blood-brain barrier breach, destabilize the brain and lead to worsening of mental disorders.The aim of work: to review research data on the role of proinflammator monocytes in the development of immune inflammation in the pathogenesis of a number of systemic diseases and to examine the molecular mechanisms mediating the interaction of proinflammatory monocytes with other cells involved in immune inflammation.Material and methods: keywords “proinflammatory monocyte CD16+”, “cytokines”, “molecules of cell adhesion”, “monocyte-platelet aggregates”, “microglia”, “psychiatriс disorders”, are used to search for data published over the past 20 years in domestic and foreign studies in PubMed and e-Library.Conclusion: in the first part of the review, the research data concerning the studies of the functional characteristics of a monocytes subpopulation that express on their surface an increased level of CD16 receptors when activated were analyzed. Most of researchers associate the proinflammatory functions of monocytes with this subpopulation. Molecular mechanisms of monocytes activation, which include increased secretion of CD16 receptors, cytokines, chemokines and receptors for them involved in their interaction with vascular endothelial cells, with neurons in the CNS and also with platelets in the development of systemic inflammation, are considered. Analysis of these mechanisms allows us to better understand the immune aspects of inflammation in the brain mediated by the interaction of CD16+ monocytes with neuronal cells, which results in cognitive disorders in patients with mental disorders, as well as to identify related new approaches to the treatment of cognitive decline in these patients. Studies of the monocyte unit of immunity in patients with mental disorders will be covered in the second part of the review.

scholarly journals The Role of GPR15 Function in Blood and Vasculature

2021 ◽  
Vol 22 (19) ◽  
pp. 10824
Author(s):  
Mario Bauer
Keyword(s):  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Cytoprotective Effect ◽  
New Findings ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
G Protein Coupled

Since the first prominent description of the orphan G protein-coupled receptor 15 (GPR15) on lymphocytes as a co-receptor for the human immunodeficiency virus (HIV) type 1 and 2 and the first report about the GPR15-triggered cytoprotective effect on vascular endothelial cells by recombinant human thrombomodulin, several decades passed before the GPR15 has been recently deorphanized. Because of new findings on GPR15, this review will summarize the consequences of GPR15 signaling considering the variety of GPR15-expressing cell types and of GPR15 ligands, with a focus on blood and vasculature.

scholarly journals Molecular Dambusters: What Is Behind Hyperpermeability in Bradykinin-Mediated Angioedema?

2021 ◽  
Author(s):  
Márta L. Debreczeni ◽  
Zsuzsanna Németh ◽  
Erika Kajdácsi ◽  
Henriette Farkas ◽  
László Cervenak
Keyword(s):  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Edema Formation ◽  
Endothelial Cell Function ◽  
Number Of Factors ◽  
Complex Scenario

AbstractIn the last few decades, a substantial body of evidence underlined the pivotal role of bradykinin in certain types of angioedema. The formation and breakdown of bradykinin has been studied thoroughly; however, numerous questions remained open regarding the triggering, course, and termination of angioedema attacks. Recently, it became clear that vascular endothelial cells have an integrative role in the regulation of vessel permeability. Apart from bradykinin, a great number of factors of different origin, structure, and mechanism of action are capable of modifying the integrity of vascular endothelium, and thus, may participate in the regulation of angioedema formation. Our aim in this review is to describe the most important permeability factors and the molecular mechanisms how they act on endothelial cells. Based on endothelial cell function, we also attempt to explain some of the challenging findings regarding bradykinin-mediated angioedema, where the function of bradykinin itself cannot account for the pathophysiology. By deciphering the complex scenario of vascular permeability regulation and edema formation, we may gain better scientific tools to be able to predict and treat not only bradykinin-mediated but other types of angioedema as well.

scholarly journals VEGF involvement in psoriasis

2015 ◽  
Vol 88 (3) ◽  
pp. 247-252 ◽  
Author(s):  
Mihaela Elena Marina ◽  
Iulia Ioana Roman ◽  
Anne-Marie Constantin ◽  
Carmen Mihaela Mihu ◽  
Alexandru Dumitru Tătaru
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Hematopoietic Stem ◽  
Promising Target ◽  
Vegf Pathway ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a key growth factor, regulating the neovascularization, during embryogenesis, skeletal growth, reproductive functions and pathological processes. The VEGF receptors (VEGFR) are present in endothelial cells and other cell types, such as vascular smooth muscle cells, hematopoietic stem cells, monocytes, neurons, macrophages, and platelets.Angiogenesis is initiated by the activation of vascular endothelial cells through several factors. The excess dermal vascularity and VEGF production are markers of psoriasis.The pathological role of VEGF/VEGFR signaling during the psoriasis onset and evolution makes it a promising target for the treatment of psoriasis. Antibodies and other types of molecules targeting the VEGF pathway are currently evaluated in arresting the evolution of psoriasis.

Multifunctional RNase MCPIP1 and its Role in Cardiovascular Diseases

2020 ◽  
Vol 27 ◽  
Author(s):  
Binjie Yan ◽  
Yanan Guo ◽  
Yu Gui ◽  
Zhi-sheng Jian ◽  
Xi-Long Zheng
Keyword(s):  
Cardiovascular Diseases ◽  
Vascular Endothelial Cells ◽  
Ischemia Reperfusion ◽  
Vascular Diseases ◽  
Cell Types ◽  
Deubiquitinating Enzyme ◽  
Vascular Endothelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cardiac Functions ◽  
Cytokine Mrnas

: Monocyte chemoattractant protein-1 induced protein 1 (MCPIP1), one of the MCPIP family members, is characterized by the presence of both C-x8-C-x5-C-x3-H (CCCH)-type zinc finger and PilT-N-terminal domains. As a potent regulator of innate immunity, MCPIP1 exerts anti-inflammatory effects through its ribonuclease (RNase) and deubiquitinating enzyme activities to degrade cytokine mRNAs and inhibit nuclear factor-kappa B (NF-κB), respectively. MCPIP1 is expressed not only in immune cells but also in many other cell types, including cardiomyocytes, vascular endothelial cells (ECs) and smooth muscle cells (SMCs). Increasing evidence indicates that MCPIP1 plays a role in the regulation of cardiac functions and is involved in the processes of vascular diseases, such as ischemia-reperfusion (I/R) and atherosclerosis. To better understand the emerging roles of MCPIP1 in the cardiovascular system, we reviewed the current literature with respect to MCPIP1 functions and discussed its association with the pathogenesis of cardiovascular diseases and the implication as a therapeutic target.

scholarly journals Dual Role of Jam3b in Early Hematopoietic and Vascular Development

2019 ◽  
Author(s):  
Isao Kobayashi ◽  
Jingjing Kobayashi-Sun ◽  
Yuto Hirakawa ◽  
Madoka Ouchi ◽  
Koyuki Yasuda ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Fate ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Vascular Development ◽  
Signaling Cascade ◽  
Vascular Endothelial ◽  
Lateral Plate ◽  
Hematopoietic Stem

AbstractIn order to efficiently derive hematopoietic stem cells (HSCs) from pluripotent precursors, it is crucial to understand how mesodermal cells acquire hematopoietic or endothelial identity due to their close developmental connection. Although Npas4 has been recently identified as a conserved master regulator of hemato-vascular development, the molecular mechanisms underlying the cell fate divergence between hematopoietic and vascular endothelial cells are still unclear. Here, we show in zebrafish that the divergence of hematopoietic and vascular endothelial cells in mesodermal cells is regulated by Junctional adhesion molecule 3b (Jam3b) via two independent signaling pathways. Mutation of jam3b led to the reduction of npas4l expression in the posterior lateral plate mesoderm and defect of both hematopoietic and vascular development. Mechanistically, we uncover that Jam3b promotes endothelial specification by regulating npas4l expression through the repression of the Rap1a-Erk signaling cascade. Jam3b subsequently promotes hematopoietic development including HSCs by regulating lrrc15 expression in endothelial precursors through the activation of an integrin-dependent signaling cascade. Our data provide insight into the divergent mechanisms for instructing hematopoietic or vascular fates from mesodermal cells.

Effect of Neuroinflammation on ABC Transporters: Possible Contribution to Refractory Epilepsy

2018 ◽  
Vol 17 (10) ◽  
pp. 728-735 ◽  
Author(s):  
Xiaolin Deng ◽  
Yangmei Xie ◽  
Yinghui Chen
Keyword(s):  
Antiepileptic Drugs ◽  
Abc Transporters ◽  
Refractory Epilepsy ◽  
Vascular Endothelial Cells ◽  
Efflux Transporters ◽  
Vascular Endothelial ◽  
Intracellular Signalling Pathways ◽  
The Brain ◽  
Transporter Expression

Background & Objective: Epilepsy is a common and serious chronic neurological disorder that is mainly treated with antiepileptic drugs. Although current antiepileptic drugs used in clinical practice have advanced to the third generation, approximately one-third of patients are refractory to these treatments. More efficacious treatments for refractory epilepsy are therefore needed. A better understanding of the mechanism underlying refractory epilepsy is likely to facilitate the development of a more effective therapy. The abnormal expression and/or dysfunction of efflux transporters, particularly ABC transporters, might contribute to certain cases of refractory epilepsy. Inflammation in the brain has recently been shown to regulate the expression and/or function of ABC transporters in the cerebral vascular endothelial cells and glia of the blood-brain barrier by activating intracellular signalling pathways. Conclusion: Therefore, in this review, we will briefly summarize recent research advances regarding the possible role of neuroinflammation in regulating ABC transporter expression in epilepsy.

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