Journal of Vascular Research最新文献

{"title":"Receptor-Interacting Protein Kinase 3 Augments Neuroinflammation by Facilitating Neutrophil Infiltration during an Ischemic Stroke.","authors":"Baiyu Li, Zexia Ling, Yanyan Wang, Yinhua Xing","doi":"10.1159/000542571","DOIUrl":"10.1159/000542571","url":null,"abstract":"<p><strong>Introduction: </strong>Neutrophil infiltration is responsible for the neuroinflammation during an ischemic stroke. Here, we explored the role of receptor-interacting protein kinase 3 (RIP3) in neutrophil infiltration during an ischemic stroke.</p><p><strong>Methods: </strong>The rat middle cerebral artery occlusion (MCAO) model was utilized to identify pivotal proteins involved in neutrophil infiltration during an ischemic stroke. Neutrophils were isolated from the peripheral blood of mice, and a co-immunoprecipitation (co-IP) assay was performed to identify the proteins that interact with RIP3.</p><p><strong>Results: </strong>The rat MCAO model was successfully established. Myeloperoxidase (MPO) was significantly upregulated in the MCAO group, indicating the presence of neutrophil infiltration. RIP3 protein level exhibited a similar trend to MPO protein level, suggesting that neuroinflammation might be partly activated by RIP3 through the promotion of neutrophil infiltration. Co-IP and mass spectrometry analyses suggested that RIP3 facilitated neutrophil infiltration partly by affecting protein kinases (Rock1 and Prkaca) downstream of RIP3, and the interaction between RIP3 and Rock1 or Prkaca was validated by IF and co-IP assays.</p><p><strong>Conclusion: </strong>In this study, it was observed that RIP3 affects neutrophil infiltration, a critical phenomenon associated with neuronal injury during ischemic stroke, partly by the modulation of downstream proteins such as Rock1 and Prkaca.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"51-62"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686954","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}

{"title":"Sympathetic Nerve Activity following Acute Type B Aortic Dissection: A Pilot Study.","authors":"Eric T A Lim, David Jardine, Christopher Frampton, Christopher J Pemberton, Richard Troughton, Justin Roake, Adib Khanafer","doi":"10.1159/000543340","DOIUrl":"10.1159/000543340","url":null,"abstract":"<p><strong>Introduction: </strong>Control of blood pressure following acute type B aortic dissection usually requires sympatholytic antihypertensive medication. Although sympathetic nerve activity is central to blood pressure control, its role in the hypertensive response to acute aortic dissection has not been assessed.</p><p><strong>Methods: </strong>A prospective pilot study was performed over an 18-month period. Patients presenting with acute type B aortic dissection confirmed on computed tomographic angiography were recruited. We measured blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), and plasma catecholamine levels in patients following acute type B dissection and controls. Comparisons between groups were made 1 week (acute phase) and 3 months after dissection (recovery phase).</p><p><strong>Results: </strong>Five patients and four controls were recruited in the study. MSNA was higher in patients than controls during the acute phase of aortic dissection: 62 (60-62) versus 46 (29-60) bursts/min (effect size 0.88) and 88 (54-96) versus 71 (44-101) bursts/100 beats (effect size 0.60). Plasma normetanephrines were also increased acutely: 821.0 (489.0-884.0) versus 417.0 (348.5-561.5) pmol/L (effect size 0.85).</p><p><strong>Conclusion: </strong>Sympathetic nerve activity is increased acutely during the first week after type B aortic dissection, resolving towards control values after 3 months. Immediate sympatholytic drug treatment is likely to be crucial in order to prevent the acute and chronic complications of this response. This may confer benefits over and above simply lowering the blood pressure to protect the aorta in the acute phase.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"88-95"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903302","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}

{"title":"Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study.","authors":"Fernanda Bocanegra-Zamora,Fernanda Espinosa-Bautista,Gian M Jiménez-Rodríguez,Felipe Masso,Araceli Paez,Hector Gonzalez-Pacheco,Mariana Patlán,Guering Eid-Lidt,Luis M Amezcua-Guerra","doi":"10.1159/000541069","DOIUrl":"https://doi.org/10.1159/000541069","url":null,"abstract":"INTRODUCTIONIn ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear.METHODSWe examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls.RESULTSOur findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar.CONCLUSIONCD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"9 1","pages":"1-7"},"PeriodicalIF":1.7,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142253533","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}

{"title":"In Memoriam: A Tribute to Eva Aralikatti.","authors":"Pooneh Bagher","doi":"10.1159/000540829","DOIUrl":"https://doi.org/10.1159/000540829","url":null,"abstract":"","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"1"},"PeriodicalIF":1.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108792","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}

{"title":"RNA Sequencing Screens the Key Genes and Pathways in a Mouse Model of HFpEF.","authors":"Yuxi Sun, Jiaxin Li, Xinxin Zhang, Ning Wang, Ying Liu","doi":"10.1159/000539305","DOIUrl":"10.1159/000539305","url":null,"abstract":"<p><strong>Introduction: </strong>Heart failure with preserved ejection fraction (HFpEF) is a common syndrome with high morbidity and mortality but without available evidence-based therapies. It is essential to investigate changes in gene expression profiles in preclinical HFpEF animal models, with the aim of searching for novel therapeutic targets.</p><p><strong>Methods: </strong>Wild-type male C57BL/6J mice were administrated with a combination of high-fat diet (HFD) and inhibition of constitutive nitric oxide synthase using N-nitro-<sc>l</sc>-arginine methyl ester (<sc>l</sc>-NAME) for 5 and 7 weeks. RNA sequencing was conducted to detect gene expression profiles, and bioinformatic analysis was performed to identify the core genes, pathways, and biological processes involved.</p><p><strong>Results: </strong>A total of 1,347 genes were differentially expressed in the heart at week 5 and 7 post-intervention. Gene Ontology enrichment analysis indicated that these greatly changed genes were involved mainly in cell adhesion, neutrophil chemotaxis, cell communication, and other functions. Using hierarchical cluster analysis, these differentially expressed genes were classified into 16 profiles. Of these, three significant profiles were ultimately identified. Gene co-expression network analysis suggested troponin T type 1 (Tnnt1) directly regulated 31 neighboring genes and was considered to be at the core of the associated gene network.</p><p><strong>Conclusion: </strong>The combined application of RNA sequencing, hierarchical cluster analysis, and gene network analysis identified Tnnt1 as the most important gene in the development of HFpEF.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"166-178"},"PeriodicalIF":1.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331296","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}

{"title":"The Effect of High-Salt Diet on Oxidative Stress Production and Vascular Function in Tff3-/-/C57BL/6N Knockout and Wild Type (C57BL/6N) Mice.","authors":"Nataša Kozina, Ivana Jukić, Zrinka Mihaljević, Anita Matić, Marina Dobrivojević Radmilović, Anja Barić, Ines Drenjančević","doi":"10.1159/000539614","DOIUrl":"10.1159/000539614","url":null,"abstract":"<p><strong>Introduction: </strong>It is well documented that high-salt (HS) diet increases systemic and vascular oxidative stress in various animal models and in humans, leading to impairment of vascular reactivity. The present study examined the interaction of genotype and HS diet intake and the potential effects of oxidative stress - antioxidative system balance on the flow-induced dilation (FID) in pressurized carotid arteries of normotensive Tff3-/-/C57BL/6N knockout mice and their wild-type (WT) controls.</p><p><strong>Methods: </strong>Male, ten-week-old transgenic Tff3-/-/C57BL/6N (Tff3-/-) knockout mice and WT/C57BL/6N (WT) (parental strain) healthy mice were divided in LS (0.4% NaCl in rodent chow) and HS (4% NaCl in rodent chow fed for 1 week) groups. Additionally, LS and HS groups were treated with 1 mmol/L 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL) dissolved in the drinking water. After anesthesia with ketamine chloride (100 mg/kg) and midazolam (5 mg/kg), blood pressure was measured, carotid arteries and aortas were isolated, and blood samples were collected.</p><p><strong>Results: </strong>FID was decreased in WT_HS mice and restored by superoxide scavenger TEMPOL in vivo. On the other hand, attenuated FID of Tff3-/- mice was not further affected by HS diet or TEMPOL in vivo treatment. Vascular superoxide/reactive oxygen species levels were increased with HS diet in both strains and restored by TEMPOL. HS upregulated glutathione peroxidase 1 (GPx1) gene expression in WT_HS and Tff3-/-_HS mice, while GPx activity was significantly decreased only in WT_HS group. Systemic (serum) markers of oxidative stress (oxLDL and AOPP) and arterial blood pressure were similar among groups.</p><p><strong>Conclusion: </strong>HS diet increases vascular oxidative stress and impairs vasodilation in WT mice. Tff3 gene deficiency attenuates vasodilation per se, without further effects of HS intake. This can be attributed to vascular upregulation of antioxidative enzyme GPx1 in Tff3-/-/C57BL/6N mice conferring protection from oxidative stress.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"214-224"},"PeriodicalIF":1.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792735","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}

{"title":"14th International Symposium on Resistance Arteries, Helsingør, Denmark, 2nd to 5th December 2024: Abstracts.","authors":"","doi":"10.1159/000544092","DOIUrl":"10.1159/000544092","url":null,"abstract":"<p><p>The 14th edition of this conference was held back in Denmark, the country where it all began in 1984. It is hard to overstate the importance to the vascular network and, in particular, the resistance arteries when it comes to ensuring the appropriate regulation of blood flow to each organ of the body and the arterial pressure. Ultimately, healthy resistance arteries are essential to a healthy life. Compromised arterial health is at the center of diseases, including hypertension, stroke, heart failure, coronary artery disease, diabetes, vascular dementia and even Alzheimer's disease. However, understanding the role of resistance arteries in the development and progression of these diseases is difficult given the complex mix of endothelial cells, smooth muscle cells, elastic and connective tissue, fibroblasts, inflammatory cells, perivascular adipose tissue and perivascular nerves that make up the arterial wall. Combining knowledge and expertise on vascular health across groups studying different cell types and diseases is a challenge. This conference united basic and clinical scientists from around the world, and industry leaders that are focused on cardiometabolic diseases involving dysregulated resistance arteries.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"61 Suppl 1","pages":"1-75"},"PeriodicalIF":1.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586206","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}

{"title":"Expression of Concern.","authors":"","doi":"10.1159/000535557","DOIUrl":"10.1159/000535557","url":null,"abstract":"","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"50"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138805882","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}

{"title":"Plasma Volume Oscillations during Fluid Therapy in Humans.","authors":"Robert G Hahn","doi":"10.1159/000535376","DOIUrl":"10.1159/000535376","url":null,"abstract":"<p><strong>Introduction: </strong>Oscillations are frequently observed on plasma dilution curves during intravenous fluid therapy. This study aimed to examine how common these oscillations are and what they represent.</p><p><strong>Methods: </strong>Fourier transforms were used to analyze the residuals obtained during fitting of a volume kinetic model to 269 plasma dilution curves. Oscillating patterns were identified in two-thirds of the fluid infusion experiments.</p><p><strong>Results: </strong>The wave frequency usually had a dominating frequency of 1 h or multiples thereof. The wave amplitudes varied between 1% and 4% of the plasma volume. The \"peak-to-peak\" amplitudes were then twice as large, which corresponded to blood volume changes of 60-240 mL. A population kinetic analysis of the distribution of infused fluid between body fluid compartments was then applied to search for clues that could explain the oscillations. This analysis showed that amplitudes &gt;1.5% were associated with doubled turnover of fluid in a fast-exchange interstitial fluid compartment and, together with data on plasma albumin, suggested that oscillations might represent bursts of efferent lymph.</p><p><strong>Conclusions: </strong>Oscillations with very low frequency were often observed on plasma dilution-time curves obtained during fluid therapy. They were associated with fast turnover of interstitial fluid and can possibly have resulted from accelerated lymphatic flow.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"16-25"},"PeriodicalIF":1.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10836926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138805884","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}

{"title":"Toll-Like Receptor 2 Attenuates the Formation and Progression of Angiotensin II-Induced Abdominal Aortic Aneurysm in ApoE-/- Mice.","authors":"Yali Zhang, Jessamyn Bagley, Ho-Jin Park, Xuehong Cao, Elena Maganto-Garcia, Andrew Lichtman, Debbie Beasley, Jonas B Galper","doi":"10.1159/000541651","DOIUrl":"10.1159/000541651","url":null,"abstract":"<p><strong>Introduction: </strong>We demonstrated Toll-like receptor (TLR) 4 in the pathogenesis of angiotensin II (AngII)-mediated abdominal aortic aneurysm (AAA) formation. Here, we study TLR2 in the AAA formation.</p><p><strong>Methods: </strong>Male ApoE-/- and ApoE-/-TLR2-/- mice were treated with AngII. Mice were injected with the TLR2 agonist Pam3CSK4. The incidence and severity of AAA were determined. MCP-1, MCP-5, RANTES, CXCL10, CCR5, and CXCR3 were analyzed. M1 and M2 macrophages in the aorta were detected by flow cytometry.</p><p><strong>Results: </strong>These studies demonstrated an increase in AAA formation in TLR2-/- mice and a decrease by Pam3CSK4. Pam3CSK4 decreased the ratio of M1/M2 and the levels of RANTES, CXCL10, CCR5, and CXCR3. Furthermore, Pam3CSK4 treatment 1 week following AngII retarded the progression of AAA.</p><p><strong>Conclusion: </strong>These data demonstrated a protective effect of TLR2 signaling on AAA in association with a decrease in the ratio of M1 to M2 macrophages and the expression of chemokines and their receptors. Furthermore, the treatment of Pam3CSK4 after AngII demonstrated a marked retardation of lesion progression. Given the fact that most AAA patients are detected late in the disease process, these findings suggest that TLR2 stimulation may play a therapeutic role in retarding disease progression.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"304-317"},"PeriodicalIF":1.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522250","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}