JVS-vascular science最新文献

{"title":"Venous thromboembolism swine model with reflux-induced venous hypertension","authors":"Mengjun Wang MD ,&nbsp;Xiao Lu PhD ,&nbsp;Ling Han BS ,&nbsp;José A. Diaz MD ,&nbsp;Seshadri Raju MD ,&nbsp;Ghassan S. Kassab PhD","doi":"10.1016/j.jvssci.2024.100200","DOIUrl":"10.1016/j.jvssci.2024.100200","url":null,"abstract":"<div><h3>Objective</h3><p>This study describes a novel swine model of venous thromboembolism (VTE) with reflux-induced venous hypertension.</p></div><div><h3>Methods</h3><p>Six pigs underwent disruption of the tricuspid chordae tendineae to create reflux and venous hypertension in the femoral vein. The vein was traumatized 2 to 3 weeks later by repeated withdrawal of a slightly overinflated occlusion balloon across the lumen, followed by balloon occlusion of the outflow. A small amount of thrombin was injected into the traumatized vein segment immediately after outflow occlusion. Thrombosis of the traumatized vein evolved into an organized thrombus seven weeks later. The histological features of the harvested post-thrombotic femoral vein were studied with hematoxylin and eosin and Trichrome stains.</p></div><div><h3>Results</h3><p>In all six pigs, initial disruption of the chordae tendineae was successfully performed to create tricuspid reflux and venous hypertension. After two-stage sequential procedures, a thrombus formed in the target femoral vein segment. Histology of the harvested thrombotic vein showed features of an organizing thrombus with collagen formation and fibrosis.</p></div><div><h3>Conclusions</h3><p>The novel swine VTE model may serve as a platform for developing and testing human-sized therapeutic procedures and devices in translational venous research.</p></div><div><h3>Clinical Relevance</h3><p>This study describes a swine model of VTE created by incorporating all three elements of Virchow’s triad. The model uniquely incorporates reflux-induced venous hypertension, which may be used in studying venous insufficiency and VTE in those with systemic venous hypertension. Likewise, this model may serve as a platform for development and evaluation of diagnostic imaging or therapeutic procedures and devices in subjects with systemic venous hypertension.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100200"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000117/pdfft?md5=e4da82e55e93a6015beb2e6e9d227379&pid=1-s2.0-S2666350324000117-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140273276","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}

{"title":"Hyperoxia impairs induced pluripotent stem cell-derived endothelial cells and drives an atherosclerosis-like transcriptional phenotype","authors":"Sean M. Carr PhD ,&nbsp;Katherine Owsiany MD, PhD ,&nbsp;Ottis Scrivner PhD ,&nbsp;Dylan McLaughlin MD ,&nbsp;Hanjoong Jo PhD ,&nbsp;Luke P. Brewster ,&nbsp;Katherine E. Hekman MD, PhD","doi":"10.1016/j.jvssci.2024.100193","DOIUrl":"10.1016/j.jvssci.2024.100193","url":null,"abstract":"<div><h3>Background</h3><p>Induced pluripotent stem cells (iPSCs) directed to endothelial identity (iPSC-ECs) are emerging as a potent tool for regenerative medicine in vascular disease. However, iPSC-ECs lose expression of key identity markers under standard in vitro conditions, limiting their clinical applications.</p></div><div><h3>Methods</h3><p>To model physiological in vivo conditions, we examined the bioenergetics, presence of key cell markers, and proliferative and angiogenic capacity in iPSC-ECs at late and early passage under hyperoxic (21%) and physiological (4%) oxygen concentrations.</p></div><div><h3>Results</h3><p>Physoxia resulted in relative preservation of mitochondrial bioenergetic activity, as well as CD144 expression in late passage iPSC-ECs, but not proliferative capacity or tube formation. Single cell RNA sequencing (scRNA-seq) revealed that late passage hyperoxic iPSC-ECs develop an endothelial-to-mesenchymal phenotype. Comparing scRNA-seq data from iPSC-ECs and from atherosclerotic ECs revealed overlap of their transcriptional phenotypes.</p></div><div><h3>Conclusions</h3><p>Taken together, our studies demonstrate that physiological 4% oxygen culture conditions were sufficient to improve mitochondrial function in high passage cells, but alone was insufficient to preserve angiogenic capacity. Furthermore, late passage cells under typical conditions take on an endothelial-to-mesenchymal phenotype with similarities to ECs found in atherosclerosis.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100193"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266635032400004X/pdfft?md5=8e5c3056fafd9f25b14200fbd26c3111&pid=1-s2.0-S266635032400004X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140279855","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}

{"title":"Hypercholesterolemia impairs collateral artery enlargement by ten-eleven translocation 1-dependent hematopoietic stem cell autonomous mechanism in a murine model of limb ischemia","authors":"Jinglian Yan PhD,&nbsp;Guodong Tie PhD,&nbsp;Amanda Tutto MS,&nbsp;Louis M. Messina MD","doi":"10.1016/j.jvssci.2024.100203","DOIUrl":"10.1016/j.jvssci.2024.100203","url":null,"abstract":"<div><h3>Objective</h3><p>The extent of collateral artery enlargement determines the risk of limb loss due to peripheral arterial disease. Hypercholesterolemia impairs collateral artery enlargement, but the underlying mechanism remains poorly characterized. This study tests the hypothesis that hypercholesterolemia impairs collateral artery enlargement through a ten-eleven translocation 1 (Tet1)-dependent hematopoietic stem cell (HSC)-autonomous mechanism that increases their differentiation into proinflammatory Ly6C^hi monocytes and restricts their conversion into proangiogenic Ly6C^low monocytes.</p></div><div><h3>Methods</h3><p>To test our hypothesis, we induced limb ischemia and generated chimeric mouse models by transplanting HSCs from either wild-type (WT) mice or hypercholesterolemic mice into lethally irradiated WT recipient mice.</p></div><div><h3>Results</h3><p>We found that the lethally irradiated WT recipient mice reconstituted with HSCs from hypercholesterolemic mice displayed lower blood flow recovery and collateral artery enlargement that was nearly identical to that observed in hypercholesterolemic mice, despite the absence of hypercholesterolemia and consistent with an HSC-autonomous mechanism. We showed that hypercholesterolemia impairs collateral artery enlargement by a Tet1-dependent mechanism that increases HSC differentiation toward proinflammatory Ly6C^hi monocytes and restricts the conversion of Ly6C^hi monocytes into proangiogenic Ly6C^low monocytes. Moreover, Tet1 epigenetically reprograms monocyte gene expression within the HSCs. Restoration of Tet1 expression in HSCs of hypercholesterolemic mice restores WT collateral artery enlargement and blood flow recovery after induction of hindlimb ischemia.</p></div><div><h3>Conclusions</h3><p>These results show that hypercholesterolemia impairs collateral artery enlargement by a novel Tet1-dependent HSC-autonomous mechanism that epigenetically reprograms monocyte gene expression within the HSCs.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100203"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000142/pdfft?md5=49f36588f10b5565ecc9178f0c001b46&pid=1-s2.0-S2666350324000142-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140797169","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}

{"title":"Characterization of a phenol-based model for denervation of the abdominal aorta and its implications for aortic remodeling","authors":"Calvin Chao MD ,&nbsp;Caitlyn Dang BS ,&nbsp;Nidhi Reddy BA ,&nbsp;Sara Alharbi MS ,&nbsp;Jimmy Doan ,&nbsp;Akashraj Karthikeyan ,&nbsp;Brandon Applewhite PhD ,&nbsp;Bin Jiang PhD","doi":"10.1016/j.jvssci.2024.100202","DOIUrl":"10.1016/j.jvssci.2024.100202","url":null,"abstract":"<div><h3>Objective</h3><p>Sympathetic innervation plays a pivotal role in regulating cardiovascular health, and its dysregulation is implicated in a wide spectrum of cardiovascular diseases. This study seeks to evaluate the impact of denervation of the abdominal aorta on its morphology and wall homeostasis.</p></div><div><h3>Methods</h3><p>Male and female Sprague-Dawley rats (N = 12), aged 3 months, underwent midline laparotomy for infrarenal aorta exposure. Chemical denervation was induced via a one-time topical application of 10% phenol (n = 6), whereas sham controls received phosphate-buffered saline (n = 6). Animals were allowed to recover and subsequently were sacrificed after 6 months for analysis encompassing morphology, histology, and immunohistochemistry.</p></div><div><h3>Results</h3><p>At 6 months post-treatment, abdominal aortas subjected to phenol denervation still exhibited a significant reduction in nerve fiber density compared with sham controls. Denervated aortas demonstrated reduced intima-media thickness, increased elastin fragmentation, decreased expression of vascular smooth muscle proteins (α-SMA and MYH11), and elevated adventitial vascular density. Sex-stratified analyses revealed additional dimorphic responses, particularly in aortic collagen and medial cellular density in female animals.</p></div><div><h3>Conclusions</h3><p>Single-timepoint phenol-based chemical denervation induces alterations in abdominal aortic morphology and vascular remodeling over a 6-month period. These findings underscore the potential of the sympathetic nervous system as a therapeutic target for aortic pathologies.</p></div><div><h3>Clinical Relevance</h3><p>Aortic remodeling remains an important consideration in the pathogenesis of aortic disease, including occlusive, aneurysmal, and dissection disease states. The paucity of medical therapies for the treatment of aortic disease has driven considerable interest in elucidating the pathogenesis of these conditions; new therapeutic targets are critically needed. Here, we show significant remodeling after phenol-induced denervation with morphologic, histologic, and immunohistochemical features. Future investigations should integrate sympathetic dysfunction as a potential driver of pathologic aortic wall changes with additional consideration of the sympathetic nervous system as a therapeutic target.</p></div>","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100202"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666350324000130/pdfft?md5=a268668ec326d9c73541b8e91aa1791d&pid=1-s2.0-S2666350324000130-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140401435","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}

{"title":"Tenascin-C in Arteriovenous Fistula Failure: Unraveling Venous Remodeling Dynamics","authors":"Luis Gonzalez,&nbsp;Weichang Zhang,&nbsp;Yuichi Ohashi,&nbsp;Roberto Vazquez-Padron,&nbsp;Alan Dardik","doi":"10.1016/j.jvssci.2024.100254","DOIUrl":"10.1016/j.jvssci.2024.100254","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100254"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143151474","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}

{"title":"Associations of Genetic and Lifestyle Risk Factors With Incident Peripheral Artery Disease: A Prospective Cohort Study","authors":"Shuai Yuan,&nbsp;Yuhao Sun,&nbsp;Jie Chen,&nbsp;Pranav Sharma,&nbsp;Michael G. Levin,&nbsp;Susanna Larsson,&nbsp;Scott M. Damrauer","doi":"10.1016/j.jvssci.2024.100258","DOIUrl":"10.1016/j.jvssci.2024.100258","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100258"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143151962","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}

{"title":"Loss of the ETS Transcription Factor ERG Disrupts Fate-defining Programs in the Aortic Endothelium and Promotes Expansion of Endothelial Lineage Cells in Atherosclerotic Plaque","authors":"Steven R. Botts,&nbsp;Kristen Schulz,&nbsp;Corey A. Scipione,&nbsp;Sneha Raju,&nbsp;Leandro C. Breda,&nbsp;Kamalben Prajapati,&nbsp;Kai Yu,&nbsp;Aniqa Khan,&nbsp;Chanele K. Polenz,&nbsp;Sharon J. Hyduk,&nbsp;Joshua D. Wythe,&nbsp;Clint S. Robbins,&nbsp;Myron I. Cybulsky,&nbsp;Jason E. Fish,&nbsp;Kathryn L. Howe","doi":"10.1016/j.jvssci.2024.100239","DOIUrl":"10.1016/j.jvssci.2024.100239","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100239"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143153071","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}

{"title":"Indoleamine 2,3-dioxygenase-Mediated Tryptophan Catabolism Limits Experimental Abdominal Aortic Aneurysms","authors":"Baohui Xu,&nbsp;Gang Li,&nbsp;Hongping Deng,&nbsp;Yankui Li,&nbsp;Fanru Shen,&nbsp;Makoto Samura,&nbsp;Philip S. Tsao,&nbsp;Ronald L. Dalman","doi":"10.1016/j.jvssci.2024.100248","DOIUrl":"10.1016/j.jvssci.2024.100248","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100248"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143135143","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}

{"title":"Harnessing Limb Revascularization With Synthetic Probiotics","authors":"John Vlahos,&nbsp;Molly Ratner,&nbsp;Tetsuhiro Harimoto,&nbsp;Ariadne Zias,&nbsp;Cristobal Rivera,&nbsp;Yogi Pratama,&nbsp;Karan Garg,&nbsp;Tal Danido,&nbsp;Bhama Ramkhelawon","doi":"10.1016/j.jvssci.2024.100231","DOIUrl":"10.1016/j.jvssci.2024.100231","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100231"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143139822","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}

{"title":"Development of a Bio-Hybrid Endovascular Stent-Graft That Enables Immunosuppression Free Islet Cell Transplantation","authors":"Brandon T. Gaston,&nbsp;Varun Singh,&nbsp;Anil Kharga,&nbsp;Kevin Deng,&nbsp;Kang Mi Lee,&nbsp;Marc Succi,&nbsp;Anahita Dua,&nbsp;James F. Markmann","doi":"10.1016/j.jvssci.2024.100264","DOIUrl":"10.1016/j.jvssci.2024.100264","url":null,"abstract":"","PeriodicalId":74035,"journal":{"name":"JVS-vascular science","volume":"5 ","pages":"Article 100264"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143133491","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}