Journal of Vascular Research最新文献_第10页

Front & Back Matter 正面和背面

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-03-01 DOI: 10.1159/000515792

B. Fisslthaler, C. Garland, A. Heagerty

引用次数: 0

Endothelium-Specific GTP Cyclohydrolase I Overexpression Restores Endothelial Function in Aged Mice. 过表达内皮特异性 GTP 环化酶 I 可恢复老年小鼠的内皮功能

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-02-08 DOI: 10.1159/000513464

Lang Yan, Ji-Qian-Zhu Zhang, Xiao-Yu Dai, Jin-Feng Li, Fang-Yuan Gao, Xiao-Fang Zhang, Yi-Jun Tian, Wen-Jing Shi, Jiang-Bo Zhu, Ji-Kuai Chen

引用次数: 0

Pyridoxamine and Caloric Restriction Improve Metabolic and Microcirculatory Abnormalities in Rats with Non-Alcoholic Fatty Liver Disease. 吡多胺和热量限制改善非酒精性脂肪肝大鼠的代谢和微循环异常

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-02-03 DOI: 10.1159/000512832

Evelyn Nunes Goulart da Silva Pereira, Raquel Rangel Silvares, Karine Lino Rodrigues, Edgar Eduardo Ilaquita Flores, Anissa Daliry

{"title":"Pyridoxamine and Caloric Restriction Improve Metabolic and Microcirculatory Abnormalities in Rats with Non-Alcoholic Fatty Liver Disease.","authors":"Evelyn Nunes Goulart da Silva Pereira, Raquel Rangel Silvares, Karine Lino Rodrigues, Edgar Eduardo Ilaquita Flores, Anissa Daliry","doi":"10.1159/000512832","DOIUrl":"10.1159/000512832","url":null,"abstract":"Introduction: This study aims to examine the effect of a diet intervention and pyridoxamine (PM) supplementation on hepatic microcirculatory and metabolic dysfunction in nonalcoholic fatty liver disease (NAFLD).Methods: NAFLD in Wistar rats was induced with a high-fat diet for 20 weeks (NAFLD 20 weeks), and control animals were fed with a standard diet. The NAFLD diet intervention group received the control diet between weeks 12 and 20 (NAFLD 12 weeks), while the NAFLD 12 weeks + PM group also received PM. Fasting blood glucose (FBG) levels, body weight (BW), visceral adipose tissue (VAT), and hepatic microvascular blood flow (HMBF) were evaluated at the end of the protocol.Results: The NAFLD group exhibited a significant increase in BW and VAT, which was prevented by the diet intervention, irrespective of PM treatment. The FBG was elevated in the NAFLD group, and caloric restriction improved this parameter, although additional improvement was achieved by PM. The NAFLD group displayed a 31% decrease in HMBF, which was partially prevented by caloric restriction and completely prevented when PM was added. HMBF was negatively correlated to BW, FBG, and VAT content.Conclusion: PM supplementation in association with lifestyle modifications could be an effective intervention for metabolic and hepatic vascular complications.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.7,"publicationDate":"2021-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25327120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reciprocal Antagonism between MicroRNA-138 and SIRT1 and Its Implications for the Angiogenesis of Endothelial Cells. MicroRNA-138 与 SIRT1 之间的相互拮抗作用及其对内皮细胞血管生成的影响

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-02-03 DOI: 10.1159/000511786

Shangyu Wang, Zengwu Shao, Xin Tang, Kaijie Wang, Jinping Zhao, Zhe Dong

{"title":"Reciprocal Antagonism between MicroRNA-138 and SIRT1 and Its Implications for the Angiogenesis of Endothelial Cells.","authors":"Shangyu Wang, Zengwu Shao, Xin Tang, Kaijie Wang, Jinping Zhao, Zhe Dong","doi":"10.1159/000511786","DOIUrl":"10.1159/000511786","url":null,"abstract":"MicroRNAs and sirtuins are important epigenetic regulators of gene expression and both contribute significantly to postnatal vascular development. However, the crosstalk between miRNAs and sirtuins in the modulation of angiogenesis has rarely been discussed. Here, we investigated the interactions between miR-138 and sirtuins in the process of angiogenesis. We found that overexpression of miR-138 markedly suppressed the proliferation, migration, and tube-forming capacities of the endothelial cells. And, miR-138 inhibitor-treated endothelial cells showed a reversed phenotype. Furthermore, miR-138 plays a negative role in vascular development in vivo. Western blot and qPCR assays demonstrated that SIRT1 was silenced by miR-138, and a luciferase reporter assay showed that miR-138 bound to the 3'-UTR of SIRT1. The re-expression of SIRT1 alleviated miR-138-mediated suppression of angiogenesis. Furthermore, silencing SIRT1 could boost the level of miR-138. And, upon miR-138 inhibitor treatment, SIRT1 silencing no longer reduced the angiogenic ability of endothelial cells significantly. These results demonstrated that the circuitry involving miR-138 and SIRT1 may participate in vascular homeostasis and also offered the possibility of identifying a new approach in the treatment of angiogenic diseases.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1-16"},"PeriodicalIF":1.7,"publicationDate":"2021-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25327125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Elevated Angiopoietin-2 inhibits thrombomodulin-mediated anticoagulation in critically ill COVID-19 patients 血管生成素-2升高抑制COVID-19危重症患者血栓调节素介导的抗凝

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-15 DOI: 10.1101/2021.01.13.21249429

M. Hultstrom, K. Fromell, A. Larsson, S. Quaggin, C. Betsholtz, R. Frithiof, M. Lipcsey, M. Jeansson

{"title":"Elevated Angiopoietin-2 inhibits thrombomodulin-mediated anticoagulation in critically ill COVID-19 patients","authors":"M. Hultstrom, K. Fromell, A. Larsson, S. Quaggin, C. Betsholtz, R. Frithiof, M. Lipcsey, M. Jeansson","doi":"10.1101/2021.01.13.21249429","DOIUrl":"https://doi.org/10.1101/2021.01.13.21249429","url":null,"abstract":"Several studies suggest that hypercoagulation and endothelial dysfunction play central roles in severe forms of COVID-19. Here, we hypothesized that the high levels of the inflammatory cytokine Angiopoietin-2 (ANGPT2) reported in hospitalized COVID-19 patients might promote hypercoagulation through ANGPT2 binding to thrombomodulin with resulting inhibition of thrombin/thrombomodulin-mediated physiological anticoagulation. We therefore investigated plasma samples taken at two timepoints from 20 critically ill COVID-19 patients in intensive care regarding ANGPT2 levels and coagulation markers in comparison with 20 healthy blood donors. We found that ANGPT2 levels were increased in the COVID-19 patients in correlation with disease severity, hypercoagulation, and mortality. To test causality, we administered ANGPT2 to wildtype mice and found that it shortened bleeding time in a tail injury model. In further support of a role for ANGPT2 in physiological coagulation, bleeding time was increased in endothelial-specific Angpt2 knockout mice. Using in vitro assays, we found that ANGPT2 inhibited thrombomodulin-mediated anticoagulation and protein C activation in human donor plasma. Our data reveal a novel mechanism for ANGPT2 in hypercoagulation and suggest that Angiopoietin-2 inhibition may be tested in the treatment of hypercoagulation in severe COVID-19, as well as in certain other conditions, including sepsis.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"9 1","pages":""},"PeriodicalIF":1.7,"publicationDate":"2021-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88989626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Polarized Proteins in Endothelium and Their Contribution to Function. 内皮细胞中的极化蛋白及其对功能的贡献。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-01 Epub Date: 2021-01-27 DOI: 10.1159/000512618

Abigail G Wolpe, Claire A Ruddiman, Phillip J Hall, Brant E Isakson

{"title":"Polarized Proteins in Endothelium and Their Contribution to Function.","authors":"Abigail G Wolpe, Claire A Ruddiman, Phillip J Hall, Brant E Isakson","doi":"10.1159/000512618","DOIUrl":"https://doi.org/10.1159/000512618","url":null,"abstract":"Protein localization in endothelial cells is tightly regulated to create distinct signaling domains within their tight spatial restrictions including luminal membranes, abluminal membranes, and interendothelial junctions, as well as caveolae and calcium signaling domains. Protein localization in endothelial cells is also determined in part by the vascular bed, with differences between arteries and veins and between large and small arteries. Specific protein polarity and localization is essential for endothelial cells in responding to various extracellular stimuli. In this review, we examine protein localization in the endothelium of resistance arteries, with occasional references to other vessels for contrast, and how that polarization contributes to endothelial function and ultimately whole organism physiology. We highlight the protein localization on the luminal surface, discussing important physiological receptors and the glycocalyx. The protein polarization to the abluminal membrane is especially unique in small resistance arteries with the presence of the myoendothelial junction, a signaling microdomain that regulates vasodilation, feedback to smooth muscle cells, and ultimately total peripheral resistance. We also discuss the interendothelial junction, where tight junctions, adherens junctions, and gap junctions all convene and regulate endothelial function. Finally, we address planar cell polarity, or axial polarity, and how this is regulated by mechanosensory signals like blood flow.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"58 2","pages":"65-91"},"PeriodicalIF":1.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000512618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38872121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Possible Mechanism of Human Recombinant Leptin-Induced VEGF A Synthesis via PI3K/Akt/mTOR/S6 Kinase Signaling Pathway while Inducing Angiogenesis: An Analysis Using Chicken Chorioallantoic Membrane Model. 重组瘦素通过PI3K/Akt/mTOR/S6激酶信号通路诱导血管生成诱导VEGF A合成的可能机制:基于鸡绒毛膜尿囊膜模型的分析

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-01 Epub Date: 2021-06-24 DOI: 10.1159/000516498

Reji Manjunathan, Nalini Devarajan, Malathi Ragunathan

{"title":"Possible Mechanism of Human Recombinant Leptin-Induced VEGF A Synthesis via PI3K/Akt/mTOR/S6 Kinase Signaling Pathway while Inducing Angiogenesis: An Analysis Using Chicken Chorioallantoic Membrane Model.","authors":"Reji Manjunathan, Nalini Devarajan, Malathi Ragunathan","doi":"10.1159/000516498","DOIUrl":"https://doi.org/10.1159/000516498","url":null,"abstract":"Introduction: The present study aimed to realize human recombinant leptin 's ability to synthesize VEGF A while inducing neovascularization through PI3K/Akt/mTOR/S6 kinase involved signaling pathway.Methods: To examine the PI3K/Akt/mTOR/S6 kinase pathway involvement in leptin-induced VEGF A synthesis, the chick chorioallantoic membrane (CAM) was incubated with human recombinant leptin and specific inhibitors of the proposed signaling molecules (rapamycin and wortmannin). We analyzed the role of specified signaling molecules in human recombinant leptin-induced physiological angiogenesis via VEGF A synthesis in detail with the support of various methodologies.Results: Human recombinant leptin's ability to synthesize VEGF A is diminished significantly in the presence of inhibitors. This observation supported the role of PI3K/Akt/mTOR/S6 kinase signaling molecules in human recombinant leptin-mediated VEGF A synthesis while inducing angiogenesis in CAM.Conclusion: Synthesis of VEGF A, followed by the growth of new blood vessels, by human recombinant leptin via the activation of the PI3K/Akt/mTOR/S6 kinase signaling pathway reflects mechanistic therapeutic application of human recombinant leptin. The data also signify the role of mTOR and S6 kinase molecules in angiogenesis under a physiological environment.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"58 6","pages":"343-360"},"PeriodicalIF":1.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000516498","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39102636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Association of Circulating Extracellular Matrix Components with Central Hemodynamics and Arterial Distensibility of Peripheral Arteries. 循环细胞外基质成分与中央血流动力学和外周动脉扩张的关系。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-01 Epub Date: 2021-07-12 DOI: 10.1159/000516841

Vladimir N Melnikov, Lena B Kim, Anna N Putyatina, Sergey G Krivoschekov

{"title":"Association of Circulating Extracellular Matrix Components with Central Hemodynamics and Arterial Distensibility of Peripheral Arteries.","authors":"Vladimir N Melnikov, Lena B Kim, Anna N Putyatina, Sergey G Krivoschekov","doi":"10.1159/000516841","DOIUrl":"https://doi.org/10.1159/000516841","url":null,"abstract":"Background: In addition to neuronal and endothelial regulators of vascular tone, the passive mechanical properties of arteries, determined by the molecular structure of extracellular matrices, are the principle modulators of vascular distensibility. Specifically, the association between collagen type IV (Col IV), a constituent of basement membrane, and arterial compliance remains unclear.Methods: In 31 healthy adult men, radial applanation tonometry and pulse wave analysis were used to assess aortic augmentation index (AIx), aortic-to-radial pulse pressure amplification (PPAmpl), and time to reflection wave.Results: Plasma Col IV and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) concentrations were correlated with AIx (r = 0.51, p = 0.021 and r = -0.45, p = 0.042, respectively) after adjustment for age and heart rate (HR). Greater matrix metalloproteinase-9 (MMP-9) and TIMP-1 levels were associated with high PPAmpl (r = 0.45 and r = 0.64, respectively) and hence with compliant arteries. Multiple regression analyses revealed that 99% of the variation in PPAmpl was attributable to age, HR, Col IV, TIMP-1, and Col × TIMP-1 interaction (p < 0.001). No relations between tonometric variables and levels of MMP-1, -2, and -3; TIMP-2 and -4; fibronectin; glycosaminoglycans; and hydroxyproline were found.Conclusion: High circulating Col IV level indexes were associated with stiffer peripheral arteries whereas increased MMP-9 and TIMP-1 concentrations were associated with more compliant ones.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"58 6","pages":"370-378"},"PeriodicalIF":1.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000516841","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39178713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Plasmalemmal Vesicle-Associated Protein Is Associated with Endothelial Cells Sprouting from the Peribiliary Capillary Plexus in Human Cirrhotic Liver. 血浆小泡相关蛋白与肝硬化患者胆管周围毛细血管丛内皮细胞萌发有关。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-01 Epub Date: 2021-07-19 DOI: 10.1159/000516923

Hiroaki Yokomori, Wataru Ando, Masaya Oda

{"title":"Plasmalemmal Vesicle-Associated Protein Is Associated with Endothelial Cells Sprouting from the Peribiliary Capillary Plexus in Human Cirrhotic Liver.","authors":"Hiroaki Yokomori, Wataru Ando, Masaya Oda","doi":"10.1159/000516923","DOIUrl":"https://doi.org/10.1159/000516923","url":null,"abstract":"Introduction: Plasmalemmal vesicle-associated protein (PLVAP) is an endothelial-specific integral membrane glycoprotein that localizes to caveolae and fenestrae in animal models; however, little is known about PLVAP in endothelial cells (ECs) in hepatic sinusoids during liver cirrhosis (LC). Here, we aimed to elucidate PLVAP localization and expression in the human liver during LC progression.Methods: PLVAP protein expression was detected in specimens from normal control livers and hepatitis C-related cirrhotic livers using immunohistochemistry, Western blotting, and immunoelectron microscopy.Results: PLVAP mainly localized to the peribiliary capillary plexus (PCP) and was rarely observed in hepatic artery branches and portal venules in control tissue, but was aberrantly expressed in capillarized sinusoids and proliferated capillaries in fibrotic septa within cirrhotic liver tissue. Ultrastructural analysis indicated that PLVAP localized to thin ECs in some caveolae, whereas PLVAP localized primarily to caveolae-like structures and proliferative sinusoid capillary EC vesicles in cirrhotic liver tissue. Western blot analysis confirmed that PLVAP was overexpressed at the protein level in advanced cirrhotic liver tissue.Conclusion: PLVAP was strongly expressed in the caveolae of proliferated capillaries directly connected with sinusoids linked with the PCP, suggesting that it plays a role in angiogenesis and sinusoidal remodeling in LC.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"58 6","pages":"361-369"},"PeriodicalIF":1.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000516923","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39199685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Opioids Cause Sex-Specific Vascular Changes via Cofilin-Extracellular Signal-Regulated Kinase Signaling: Female Mice Present Higher Risk of Developing Morphine-Induced Vascular Dysfunction than Male Mice. 阿片类药物通过Cofilin-细胞外信号调节激酶信号传导导致血管发生性别特异性变化：与雄性小鼠相比，雌性小鼠出现吗啡诱导的血管功能障碍的风险更高。

IF 1.7 4区医学

Journal of Vascular Research Pub Date : 2021-01-01 Epub Date: 2021-09-14 DOI: 10.1159/000517555

Soyoung Cheon, Jeremy C Tomcho, Jonnelle M Edwards, Nicole R Bearss, Emily Waigi, Bina Joe, Cameron G McCarthy, Camilla F Wenceslau

{"title":"Opioids Cause Sex-Specific Vascular Changes via Cofilin-Extracellular Signal-Regulated Kinase Signaling: Female Mice Present Higher Risk of Developing Morphine-Induced Vascular Dysfunction than Male Mice.","authors":"Soyoung Cheon, Jeremy C Tomcho, Jonnelle M Edwards, Nicole R Bearss, Emily Waigi, Bina Joe, Cameron G McCarthy, Camilla F Wenceslau","doi":"10.1159/000517555","DOIUrl":"10.1159/000517555","url":null,"abstract":"Recent studies have shown that chronic use of prescription or illicit opioids leads to an increased risk of cardiovascular events and pulmonary arterial hypertension. Indices of vascular age and arterial stiffness are also shown to be increased in opioid-dependent patients, with the effects being more marked in women. There are currently no studies investigating sex-specific vascular dysfunction in opioid use, and the mechanisms leading to opioid-induced vascular damage remain unknown. We hypothesized that exposure to exogenous opioids causes sex-specific vascular remodeling that will be more pronounced in female. Acknowledging the emerging roles of cofilins and extracellular signal-regulated kinases (ERKs) in mediating actin dynamics, we investigated the effects of morphine on these molecules. Twenty-four hour exposure to morphine increased inactivated cofilin and activated ERKs in resistance arteries from female mice, which may promote stress fiber over-assembly. We also performed continuous intraluminal infusion of morphine in pressurized resistance arteries from male and female mice using culture pressure myographs. We observed that morphine reduced the vascular diameter in resistance arteries from female, but not male mice. These results have significant implications for the previously unexplored role of exogenous opioids as a modifiable cardiovascular risk factor, especially in women.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"58 6","pages":"392-402"},"PeriodicalIF":1.7,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8612963/pdf/nihms-1716520.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39415430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0