Vascular biology (Bristol, England)最新文献_第5页

Vascular biology (Bristol, England) Pub Date : 2022-08-18 Print Date: 2022-08-01 DOI: 10.1530/VB-22-0019

Paul Quax, Marie-José Goumans

引用次数: 13

SARS-CoV-2, platelets, and endothelium: coexistence in space and time, or a pernicious ménage à trois? 严重急性呼吸系统综合征冠状病毒2型、血小板和内皮细胞：空间和时间共存，还是有害的三驾马车？

Vascular biology (Bristol, England) Pub Date : 2022-06-08 eCollection Date: 2022-02-01 DOI: 10.1530/VB-22-0004

Vladimir Y Bogdanov, Vladimir N Khirmanov

引用次数: 4

Omics of endothelial cell dysfunction in sepsis. 败血症内皮细胞功能障碍的奥密克戎

Vascular biology (Bristol, England) Pub Date : 2022-04-07 eCollection Date: 2022-02-01 DOI: 10.1530/VB-22-0003

Jordan C Langston, Michael T Rossi, Qingliang Yang, William Ohley, Edwin Perez, Laurie E Kilpatrick, Balabhaskar Prabhakarpandian, Mohammad F Kiani

{"title":"Omics of endothelial cell dysfunction in sepsis.","authors":"Jordan C Langston, Michael T Rossi, Qingliang Yang, William Ohley, Edwin Perez, Laurie E Kilpatrick, Balabhaskar Prabhakarpandian, Mohammad F Kiani","doi":"10.1530/VB-22-0003","DOIUrl":"10.1530/VB-22-0003","url":null,"abstract":"During sepsis, defined as life-threatening organ dysfunction due to dysregulated host response to infection, systemic inflammation activates endothelial cells and initiates a multifaceted cascade of pro-inflammatory signaling events, resulting in increased permeability and excessive recruitment of leukocytes. Vascular endothelial cells share many common properties but have organ-specific phenotypes with unique structure and function. Thus, therapies directed against endothelial cell phenotypes are needed to address organ-specific endothelial cell dysfunction. Omics allow for the study of expressed genes, proteins and/or metabolites in biological systems and provide insight on temporal and spatial evolution of signals during normal and diseased conditions. Proteomics quantifies protein expression, identifies protein-protein interactions and can reveal mechanistic changes in endothelial cells that would not be possible to study via reductionist methods alone. In this review, we provide an overview of how sepsis pathophysiology impacts omics with a focus on proteomic analysis of mouse endothelial cells during sepsis/inflammation and its relationship with the more clinically relevant omics of human endothelial cells. We discuss how omics has been used to define septic endotype signatures in different populations with a focus on proteomic analysis in organ-specific microvascular endothelial cells during sepsis or septic-like inflammation. We believe that studies defining septic endotypes based on proteomic expression in endothelial cell phenotypes are urgently needed to complement omic profiling of whole blood and better define sepsis subphenotypes. Lastly, we provide a discussion of how in silico modeling can be used to leverage the large volume of omics data to map response pathways in sepsis.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"4 1","pages":"R15-R34"},"PeriodicalIF":0.0,"publicationDate":"2022-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9066943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45272959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

srGAP2 deactivates RhoA to control the duration of thrombin-mediated endothelial permeability. srGAP2使RhoA失活以控制凝血酶介导的内皮通透性的持续时间

Vascular biology (Bristol, England) Pub Date : 2022-02-28 eCollection Date: 2022-02-01 DOI: 10.1530/VB-21-0012

Alba Lopez Rioja, Ashton Faulkner, Harry Mellor

{"title":"srGAP2 deactivates RhoA to control the duration of thrombin-mediated endothelial permeability.","authors":"Alba Lopez Rioja, Ashton Faulkner, Harry Mellor","doi":"10.1530/VB-21-0012","DOIUrl":"10.1530/VB-21-0012","url":null,"abstract":"The endothelial barrier is a tightly regulated gateway in the transport of material between circulation and the tissues. Inflammatory mediators such as thrombin are able to open paracellular spaces in the endothelial monolayer to allow the extravasation of plasma proteins and leukocytes. Here we show that the protein SLIT-ROBO Rho GTPase-activating protein 2 (srGAP2) plays a critical role in regulating the extent of thrombin-mediated opening. We show that srGAP2 is not required for normal barrier function in resting endothelial cells, but that depletion of srGAP2 significantly increases the magnitude and duration of junctional opening in response to thrombin. We show that srGAP2 acts to switch off RhoA signaling after the contraction phase of thrombin-induced permeability, allowing respreading of cells and reformation of the barrier. srGAP2 is also required for effective restoration of the barrier after treatment with two other vasoactive agents that active RhoA - TNFα and angiotensin II. Taken together, we show that srGAP2 has a general function in controlling RhoA signaling in endothelial permeability, acting to limit the degree and duration of opening, by triggering the switch from endothelial cell contraction to respreading.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"4 1","pages":"K1-K10"},"PeriodicalIF":0.0,"publicationDate":"2022-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9012936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41709242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Progerin mislocalizes myocardin-related transcription factor in Hutchinson-Guilford Progeria syndrome. 在Hutchinson-Guilford早衰综合征中，Progerin错定位心肌蛋白相关转录因子。

Vascular biology (Bristol, England) Pub Date : 2022-02-15 eCollection Date: 2022-02-01 DOI: 10.1530/VB-21-0018

Ryan von Kleeck, Paola Castagnino, Richard K Assoian

{"title":"Progerin mislocalizes myocardin-related transcription factor in Hutchinson-Guilford Progeria syndrome.","authors":"Ryan von Kleeck, Paola Castagnino, Richard K Assoian","doi":"10.1530/VB-21-0018","DOIUrl":"10.1530/VB-21-0018","url":null,"abstract":"Hutchinson-Guilford Progeria syndrome (HGPS) is a rare genetic disease of premature aging and early death due to cardiovascular disease. The arteries of HGPS children and mice are pathologically stiff, and HGPS mice also display reduced arterial contractility. We recently showed that reduced contractility is an early event in HGPS and linked to an aberrantly low expression of smooth muscle myosin heavy chain (smMHC). Here, we have explored the basis for reduced smMHC abundance and asked whether it is a direct effect of progerin expression or a longer-term adaptive response. Myh11, the gene encoding for smMHC, is regulated by myocardin-related transcription factors (MRTFs), and we show that HGPS aortas have a reduced MRTF signature. Additionally, smooth muscle cells (SMCs) isolated from HGPS mice display reduced MRTF nuclear localization. Acute progerin expression in WT SMCs phenocopied both the decrease in MRTF nuclear localization and expression of Myh11 seen in HGPS. Interestingly, RNA-mediated depletion of MRTF-A in WT SMCs reproduced the preferential inhibitory effect of progerin on Myh11 mRNA relative to Acta2 mRNA. Our results show that progerin expression acutely disrupts MRTF localization to the nucleus and suggest that the consequent decrease in nuclear coactivator activity can help to explain the reduction in smMHC abundance and SMC contractility seen in HGPS.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"4 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2022-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/db/a3/VB-21-0018.PMC9012937.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9106395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Rethinking growth factors: the case of BMP9 during vessel maturation. 重新思考生长因子:血管成熟过程中BMP9的情况

Vascular biology (Bristol, England) Pub Date : 2022-02-07 eCollection Date: 2022-02-01 DOI: 10.1530/VB-21-0019

Ferran Medina-Jover, Antoni Riera-Mestre, Francesc Viñals

{"title":"Rethinking growth factors: the case of BMP9 during vessel maturation.","authors":"Ferran Medina-Jover, Antoni Riera-Mestre, Francesc Viñals","doi":"10.1530/VB-21-0019","DOIUrl":"10.1530/VB-21-0019","url":null,"abstract":"Angiogenesis is an essential process for correct development and physiology. This mechanism is tightly regulated by many signals that activate several pathways, which are constantly interacting with each other. There is mounting evidence that BMP9/ALK1 pathway is essential for a correct vessel maturation. Alterations in this pathway lead to the development of hereditary haemorrhagic telangiectasias. However, little was known about the BMP9 signalling cascade until the last years. Recent reports have shown that while BMP9 arrests cell cycle, it promotes the activation of anabolic pathways to enhance endothelial maturation. In light of this evidence, a new criterion for the classification of cytokines is proposed here, based on the physiological objective of the activation of anabolic routes. Whether this activation by a growth factor is needed to sustain mitosis or to promote a specific function such as matrix formation is a critical characteristic that needs to be considered to classify growth factors. Hence, the state-of-the-art of BMP9/ALK1 signalling is reviewed here, as well as its implications in normal and pathogenic angiogenesis.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"4 1","pages":"R1-R14"},"PeriodicalIF":0.0,"publicationDate":"2022-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8942324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47607955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Interleukin role in the regulation of endothelial cell pathological activation. 白细胞介素在内皮细胞病理活化调控中的作用。

Vascular biology (Bristol, England) Pub Date : 2021-10-18 eCollection Date: 2021-01-01 DOI: 10.1530/VB-21-0010

Maria Luigia Carbone, Cristina Maria Failla

{"title":"Interleukin role in the regulation of endothelial cell pathological activation.","authors":"Maria Luigia Carbone, Cristina Maria Failla","doi":"10.1530/VB-21-0010","DOIUrl":"https://doi.org/10.1530/VB-21-0010","url":null,"abstract":"Interleukins (ILs) are the group of cytokines firstly identified as expressed by leukocytes and playing different immunomodulatory functions. With increasing evidence of a constant crosstalk between leukocytes and endothelial cells in the regulation of immune cell differentiation and activation, a role of ILs also in endothelial cell stimulation and vascular inflammation has been shown. ILs act on endothelial cells both in an autocrine and a paracrine manner. In fact, a cross regulation is present among ILs expressed by different cell types, leading to amplification or blocking of the initial inflammatory signal with the secretion of additional ILs or involvement of other adjacent cells and tissues. Based on selective structural features, ILs can be divided into four major groups, a fifth group comprises ILs that do not fit into any of the other four. Most of the ILs playing a role in endothelial cell activation belong to the IL1-like cytokine group, but the number of ILs involved in vascular inflammation is constantly growing, and a special contribution of IL6, IL8, and IL17 has been underlined. This review aims at presenting current knowledge and at underling missing information about the role of IL in activating endothelial cells in selected pathological settings such as tumours, psoriasis, systemic sclerosis, and viral infection.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"3 1","pages":"R96-R105"},"PeriodicalIF":0.0,"publicationDate":"2021-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e2/07/VB-21-0010.PMC8630758.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39697273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Breast cancer chemotherapy vascular toxicity: a review of mediating mechanisms and exercise as a potential therapeutic. 乳腺癌化疗的血管毒性：介导机制和运动作为潜在疗法的综述。

Vascular biology (Bristol, England) Pub Date : 2021-10-18 eCollection Date: 2021-01-01 DOI: 10.1530/VB-21-0013

Marie Mclaughlin, Geraint Florida-James, Mark Ross

{"title":"Breast cancer chemotherapy vascular toxicity: a review of mediating mechanisms and exercise as a potential therapeutic.","authors":"Marie Mclaughlin, Geraint Florida-James, Mark Ross","doi":"10.1530/VB-21-0013","DOIUrl":"10.1530/VB-21-0013","url":null,"abstract":"Breast cancer chemotherapy, although very potent against tumour tissue, results in significant cardiovascular toxicity. The focus of research in this area has been predominantly towards cardiotoxicity. There is limited evidence detailing the impact of such treatment on the vasculature despite its central importance within the cardiovascular system and resultant detrimental effects of damage and dysfunction. This review highlights the impact of chemotherapy for breast cancer on the vascular endothelium. We consider the most likely mechanisms of endothelial toxicity to be through direct damage and dysfunction of the endothelium. There are sharp consequences of these detrimental effects as they can lead to cardiovascular disease. However, there is potential for exercise to alleviate some of the vascular toxicity of chemotherapy, and the evidence for this is provided. The potential role of exercise in protecting against vascular toxicity is explained, highlighting the recent in-human and animal model exercise interventions. Lastly, the mediating mechanisms of exercise protection of endothelial health is discussed, focusing on the importance of exercise for endothelial health, function, repair, inflammation and hyperlipidaemia, angiogenesis, and vascular remodelling. These are all important counteracting measures against chemotherapy-induced toxicity and are discussed in detail.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"3 1","pages":"R106-R120"},"PeriodicalIF":0.0,"publicationDate":"2021-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a3/99/VB-21-0013.PMC8630759.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39697274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rho GTPase signalling networks in cancer cell transendothelial migration. Rho GTPase信号网络在癌细胞跨内皮迁移中的作用。

Vascular biology (Bristol, England) Pub Date : 2021-09-14 eCollection Date: 2021-01-01 DOI: 10.1530/VB-21-0008

Wessel S Rodenburg, Jaap D van Buul

{"title":"Rho GTPase signalling networks in cancer cell transendothelial migration.","authors":"Wessel S Rodenburg, Jaap D van Buul","doi":"10.1530/VB-21-0008","DOIUrl":"https://doi.org/10.1530/VB-21-0008","url":null,"abstract":"Rho GTPases are small signalling G-proteins that are central regulators of cytoskeleton dynamics, and thereby regulate many cellular processes, including the shape, adhesion and migration of cells. As such, Rho GTPases are also essential for the invasive behaviour of cancer cells, and thus involved in several steps of the metastatic cascade, including the extravasation of cancer cells. Extravasation, the process by which cancer cells leave the circulation by transmigrating through the endothelium that lines capillary walls, is an essential step for metastasis towards distant organs. During extravasation, Rho GTPase signalling networks not only regulate the transmigration of cancer cells but also regulate the interactions between cancer and endothelial cells and are involved in the disruption of the endothelial barrier function, ultimately allowing cancer cells to extravasate into the underlying tissue and potentially form metastases. Thus, targeting Rho GTPase signalling networks in cancer may be an effective approach to inhibit extravasation and metastasis. In this review, the complex process of cancer cell extravasation will be discussed in detail. Additionally, the roles and regulation of Rho GTPase signalling networks during cancer cell extravasation will be discussed, both from a cancer cell and endothelial cell point of view.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"3 1","pages":"R77-R95"},"PeriodicalIF":0.0,"publicationDate":"2021-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8d/4c/VB-21-0008.PMC8558887.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39591936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

The effect of absent blood flow on the zebrafish cerebral and trunk vasculature. 无血流对斑马鱼大脑和躯干血管系统的影响。

Vascular biology (Bristol, England) Pub Date : 2021-07-29 eCollection Date: 2021-01-01 DOI: 10.1530/VB-21-0009

Elisabeth Kugler, Ryan Snodgrass, George Bowley, Karen Plant, Jovana Serbanovic-Canic, Noémie Hamilton, Paul C Evans, Timothy Chico, Paul Armitage

{"title":"The effect of absent blood flow on the zebrafish cerebral and trunk vasculature.","authors":"Elisabeth Kugler, Ryan Snodgrass, George Bowley, Karen Plant, Jovana Serbanovic-Canic, Noémie Hamilton, Paul C Evans, Timothy Chico, Paul Armitage","doi":"10.1530/VB-21-0009","DOIUrl":"10.1530/VB-21-0009","url":null,"abstract":"The role of blood flow in vascular development is complex and context-dependent. In this study, we quantify the effect of the lack of blood flow on embryonic vascular development on two vascular beds, namely the cerebral and trunk vasculature in zebrafish. We perform this by analysing vascular topology, endothelial cell (EC) number, EC distribution, apoptosis, and inflammatory response in animals with normal blood flow or absent blood flow. We find that absent blood flow reduced vascular area and EC number significantly in both examined vascular beds, but the effect is more severe in the cerebral vasculature, and severity increases over time. Absent blood flow leads to an increase in non-EC-specific apoptosis without increasing tissue inflammation, as quantified by cerebral immune cell numbers and nitric oxide. Similarly, while stereotypic vascular patterning in the trunk is maintained, intra-cerebral vessels show altered patterning, which is likely to be due to vessels failing to initiate effective fusion and anastomosis rather than sprouting or path-seeking. In conclusion, blood flow is essential for cellular survival in both the trunk and cerebral vasculature, but particularly intra-cerebral vessels are affected by the lack of blood flow, suggesting that responses to blood flow differ between these two vascular beds.","PeriodicalId":75294,"journal":{"name":"Vascular biology (Bristol, England)","volume":"3 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2021-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/93/VB-21-0009.PMC8428019.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39417190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0