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3. Clonally expanding smooth muscle cells promote atherosclerosis by escaping efferocytosis and activating the complement cascade

Author

Wang, Ying, Nanda, Vivek, Direnzo, Daniel, Ye, Jianqin, Xiao, Sophia, Kojima, Yoko, Howe, Kathryn L., Jarr, Kai-Uwe, Flores, Alyssa M., Tsantilas, Pavlos, Tsao, Noah, Rao, Abhiram, Newmane, Alexandra A. C., Eberhard, Anne V., Priest, James R., Ruusalepp, Arno, Pasterkamp, Gerard, Maegdefessel, Lars, Miller, Clint L., Lind, Lars, Koplev, Simon, Björkegren, Johan L. M., Owense, Gary K., Ingelsson, Erik, Weissmanr, Irving L., and Leeper, Nicholas J.

Published
2020

15. International Union of Angiology consensus document on vascular compression syndromes.

Author

D'ORIA, Mario, ZLATANOVIC, Petar, ANTHONY, Anthony, DUA, Anahita, FLORES, Alyssa M., TANIOUS, Adam, RODRÍGUEZ MORATA, Alejandro, SCERRATI, Alba, BACCELLIERI, Domenico, BISCETTI, Federico, BALDAZZI, Giulia, MANTOVANI, Giorgio, SEN, Indrani, PEINADO CEBRIAN, Javier, ROCHA-NEVES, Joao, SOUSA, Joel, DAVIDOVIC, Lazar, JUSZYNSKI, Michal, MARKOVIC, Miroslav, and OLLER GRAU, Mar

Published
2023
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21. Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability

Author

Tsantilas, Pavlos, Lao, Shen, Wu, Zhiyuan, Eberhard, Anne, Winski, Greg, Vaerst, Monika, Nanda, Vivek, Wang, Ying, Kojima, Yoko, Ye, Jianqin, Flores, Alyssa, Jarr, Kai-Uwe, Pelisek, Jaroslav, Eckstein, Hans-Henning, Matic, Ljubica, Hedin, Ulf, Tsao, Philip S, Paloschi, Valentina, Maegdefessel, Lars, Leeper, Nicholas J, and University of Zurich

Subjects
11548 Clinic for Vascular Surgery, 610 Medicine & health
Published
2021

22. Impact of Defense of the Ancients to the Male Players ages 16-18 on Their Academic Performance as Students of San Pedro College in the Senior High School Department: School Year 2016-2017

Author

Orillaneda, Kenneth Neil O., primary, Del Campo, Ikn Dzaia Erika A., additional, Flores, Alyssa Kyla T., additional, Malda, Lorelie M., additional, Morales, Coleen Eve B., additional, Caracal, Emmanuel S., additional, Reniedo, Chloe Jane D., additional, and Cadavas, Alexis, additional

Published
2022
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28. Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability

Author

Tsantilas, Pavlos, primary, Lao, Shen, additional, Wu, Zhiyuan, additional, Eberhard, Anne, additional, Winski, Greg, additional, Vaerst, Monika, additional, Nanda, Vivek, additional, Wang, Ying, additional, Kojima, Yoko, additional, Ye, Jianqin, additional, Flores, Alyssa, additional, Jarr, Kai-Uwe, additional, Pelisek, Jaroslav, additional, Eckstein, Hans-Henning, additional, Matic, Ljubica, additional, Hedin, Ulf, additional, Tsao, Philip S, additional, Paloschi, Valentina, additional, Maegdefessel, Lars, additional, and Leeper, Nicholas J, additional

Published
2021
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29. (18)F-FDG-PET imaging detects response to therapeutic intervention and plaque vulnerability in a murine model of advanced atherosclerotic disease

Author

Jarr, Kai-Uwe, Ye, Jianqin, Kojima, Yoko, Nanda, Vivek, Flores, Alyssa M., Tsantilas, Pavlos, Wang, Ying, Hosseini-Nassab, Niloufar, Eberhard, Anne V., Lotfi, Mozhgan, Käller, Max, Smith, Bryan R., Maegdefessel, Lars, and Leeper, Nicholas J.

Subjects
Article
Abstract

OBJECTIVE: This study sought to determine whether (18)F-fluorodeoxyglucose-positron emission tomography/computed tomography ((18)F-FDG-PET/CT) could be applied to a murine model of advanced atherosclerotic plaque vulnerability to detect response to therapeutic intervention and changes in lesion stability. APPROACH AND RESULTS: To analyze plaques susceptible to rupture, we fed ApoE(−/−) mice a high-fat diet and induced vulnerable lesions by cast placement over the carotid artery. After 9 weeks of treatment with orthogonal therapeutic agents (including lipid-lowering and pro-efferocytic therapies), we assessed vascular inflammation and several features of plaque vulnerability by (18)F-FDG-PET/CT and histopathology, respectively. We observed that (18)F-FDG-PET/CT had the capacity to resolve histopathologically-proven changes in plaque stability after treatment. Moreover, mean target-to-background ratios (TBRmean) correlated with multiple characteristics of lesion instability, including the corrected vulnerability index. CONCLUSIONS: These results suggest that the application of noninvasive (18)F-FDG-PET/CT to a murine model can allow for the identification of vulnerable atherosclerotic plaques and their response to therapeutic intervention. This approach may prove useful as a drug discovery and prioritization method.

Published
2020

30. Clonally expanding smooth muscle cells promote atherosclerosis by escaping efferocytosis and activating the complement cascade

Author

Electrofysiologie, CDL Onderzoek Pasterkamp, Circulatory Health, Wang, Ying, Nanda, Vivek, Direnzo, Daniel, Ye, Jianqin, Xiao, Sophia, Kojima, Yoko, Howe, Kathryn L., Jarr, Kai Uwe, Flores, Alyssa M., Tsantilas, Pavlos, Tsao, Noah, Rao, Abhiram, Newman, Alexandra A.C., Eberhard, Anne V., Priest, James R., Ruusalepp, Arno, Pasterkamp, Gerard, Maegdefessel, Lars, Miller, Clint L., Lind, Lars, Koplev, Simon, Björkegren, Johan L.M., Owens, Gary K., Ingelsson, Erik, Weissman, Irving L., Leeper, Nicholas J., Electrofysiologie, CDL Onderzoek Pasterkamp, Circulatory Health, Wang, Ying, Nanda, Vivek, Direnzo, Daniel, Ye, Jianqin, Xiao, Sophia, Kojima, Yoko, Howe, Kathryn L., Jarr, Kai Uwe, Flores, Alyssa M., Tsantilas, Pavlos, Tsao, Noah, Rao, Abhiram, Newman, Alexandra A.C., Eberhard, Anne V., Priest, James R., Ruusalepp, Arno, Pasterkamp, Gerard, Maegdefessel, Lars, Miller, Clint L., Lind, Lars, Koplev, Simon, Björkegren, Johan L.M., Owens, Gary K., Ingelsson, Erik, Weissman, Irving L., and Leeper, Nicholas J.

Published
2020

31. 18 F-Fluorodeoxyglucose-Positron Emission Tomography Imaging Detects Response to Therapeutic Intervention and Plaque Vulnerability in a Murine Model of Advanced Atherosclerotic Disease—Brief Report

Author

Jarr, Kai-Uwe, primary, Ye, Jianqin, additional, Kojima, Yoko, additional, Nanda, Vivek, additional, Flores, Alyssa M., additional, Tsantilas, Pavlos, additional, Wang, Ying, additional, Hosseini-Nassab, Niloufar, additional, Eberhard, Anne V., additional, Lotfi, Mozhgan, additional, Käller, Max, additional, Smith, Bryan R., additional, Maegdefessel, Lars, additional, and Leeper, Nicholas J., additional

Published
2020
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33. Knockout of the Murine Ortholog to the Human 9p21 Coronary Artery Disease Locus Leads to SMC Proliferation, Vascular Calcification, and Advanced Atherosclerosis

Author

Kojima, Yoko, primary, Ye, Jianqin, additional, Nanda, Vivek, additional, Wang, Ying, additional, Flores, Alyssa M., additional, Jarr, Kai-Uwe, additional, Tsantilas, Pavlos, additional, Guo, Liang, additional, Finn, Aloke V., additional, Virmani, Renu, additional, and Leeper, Nicholas, additional

Published
2020
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34. Chitinase-3-Like Protein 1 is an Inhibitor of Vascular Smooth Muscle Cell Dedifferentiation in Advanced Atherosclerosis

Author

Tsantilas, Pavlos, primary, Lao, Shen, additional, Vaerst, Monika, additional, Li, Yuhuang, additional, Nanda, Vivek, additional, Wang, Ying, additional, Kojima, Yoko, additional, Ye, Jianqin, additional, Flores, Alyssa, additional, Jarr, Kai-Uwe, additional, Pelisek, Jaroslav, additional, Eckstein, Hans-Henning, additional, Maegdefessel, Lars, additional, and Leeper, Nicholas, additional

Published
2019
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35. Clinical and Genetic Determinants of Varicose Veins Prospective, Community-Based Study of approximate to 500 000 Individuals

Author

Fukaya, Eri, Flores, Alyssa M., Lindholm, Daniel P, Gustafsson, Stefan, Zanetti, Daniela, Ingelsson, Erik, Leeper, Nicholas J., Fukaya, Eri, Flores, Alyssa M., Lindholm, Daniel P, Gustafsson, Stefan, Zanetti, Daniela, Ingelsson, Erik, and Leeper, Nicholas J.

Abstract

BACKGROUND: Varicose veins are a common problem with no approved medical therapies. Although it is believed that varicose vein pathogenesis is multifactorial, there is limited understanding of the genetic and environmental factors that contribute to their formation. Large-scale studies of risk factors for varicose veins may highlight important aspects of pathophysiology and identify groups at increased risk for disease. METHODS: We applied machine learning to agnostically search for risk factors of varicose veins in 493 519 individuals in the UK Biobank. Predictors were further studied with univariable and multivariable Cox regression analyses (2441 incident events). A genome-wide association study of varicose veins was also performed among 337 536 unrelated individuals (9577 cases) of white British descent, followed by expression quantitative loci and pathway analyses. Because height emerged as a new candidate risk factor, we performed mendelian randomization analyses to assess a potential causal role for height in varicose vein development. RESULTS: Machine learning confirmed several known (age, sex, obesity, pregnancy, history of deep vein thrombosis) and identified several new risk factors for varicose vein disease, including height. After adjustment for traditional risk factors in Cox regression, greater height remained independently associated with varicose veins (hazard ratio for upper versus lower quartile, 1.74; 95% Cl, 1.51-2.01; P<0.0001). A genomewide association study identified 30 new genome-wide significant loci, identifying pathways involved in vascular development and skeletal/ limb biology. Mendelian randomization analysis provided evidence that increased height is causally related to varicose veins (inverse -variance weighted: odds ratio, 1.26; P=2.07x10(-16)). CONCLUSIONS: Using data from nearly a half -million individuals, we present a comprehensive genetic and epidemiological study of varicose veins. We identified novel clinical and genetic

Published
2018
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37. Clonally expanding smooth muscle cells promote atherosclerosis by escaping efferocytosis and activating the complement cascade.

Author

Ying Wang, Nanda, Vivek, Direnzo, Daniel, Jianqin Ye, Sophia Xiao, Yoko Kojima, Howe, Kathryn L., Jarr, Kai-Uwe, Flores, Alyssa M., Tsantilas, Pavlos, Noah Tsao, Rao, Abhiram, Newman, Alexandra A. C., Eberhard, Anne V., Priest, James R., Ruusalepp, Arno, Pasterkamp, Gerard, Maegdefessel, Lars, Miller, Clint L., and Lind, Lars

Subjects
MUSCLE cells, SMOOTH muscle, VASCULAR smooth muscle, ATHEROSCLEROSIS, ATHEROSCLEROTIC plaque
Abstract

Atherosclerosis is the process underlying heart attack and stroke. Despite decades of research, its pathogenesis remains unclear. Dogma suggests that atherosclerotic plaques expand primarily via the accumulation of cholesterol and inflammatory cells. However, recent evidence suggests that a substantial portion of the plaque may arise from a subset of “dedifferentiated” vascular smooth muscle cells (SMCs) which proliferate in a clonal fashion. Herein we use multicolor lineage-tracing models to confirm that the matureSMCcangive riseto a hyperproliferativecellwhich appearsto promote inflammation via elaboration of complement-dependent anaphylatoxins. Despite being extensively opsonized with prophagocytic complement fragments, we find that this cell also escapes immune surveillance by neighboring macrophages, thereby exacerbating its relative survival advantage. Mechanistic studies indicate this phenomenon results from a generalized opsoninsensing defect acquired by macrophages during polarization. This defect coincides with the noncanonical up-regulation of so-called don’t eat me molecules on inflamed phagocytes, which reduces their capacity for programmed cell removal (PrCR). Knockdown or knockout of the key antiphagocytic molecule CD47 restores the ability of macrophages to sense and clear opsonized targets in vitro, allowing for potent and targeted suppression of clonal SMC expansion in the plaque in vivo. Because integrated clinical and genomic analyses indicate that similar pathways are active in humans with cardiovascular disease, these studies suggest that the clonally expanding SMC may represent a translational target for treating atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2020
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45. Using the Evaluating Devices Using Claims and RegisTry Data (EDUCATe) Plan within the Vascular Implant Surveillance and Interventional Outcomes Network (VISION) to Analyze the Long-Term Outcomes following Endovascular Aortic Aneurysm Repair

Author

Suckow, Bjoern D., Mao, Jialin, Williams, Scott, Saunders, Alan, Flores, Alyssa Monica T., Eid, Mark T., Moore, Kayla, Hoel, Andrew, Eldrup-Jorgensen, Jens, Sedrakyan, Art, and Goodney, Philip P.

Abstract

Implanted devices undergo clinical trials to assess their safety and effectiveness. However, pivotal device trials are limited in their follow-up while postmarket surveillance may incompletely capture late failure. Linking clinical trials to Medicare claims can address these limitations. This study matched patients from investigational device exemption (IDE) clinical trials for endovascular aortic aneurysm repair (EVAR) to Medicare claims-based registry data to compare long-term device outcomes between the 2 sources.

Published
2022
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46. Abstract 14663: Clonally-Expanding Smooth Muscle Cells Promote Atherosclerosis by Escaping From Efferocytosis and Activating the Complement Cascade

Author

Wang, Ying, Direnzo, Dan, Nanda, Vivek, Ye, Jianqin, Xiao, Sophia, Kojima, Yoko, Howe, Kathryn L, Jarr, Kai-Uwe, Flores, Alyssa M, Tsantilas, Pavlos, Tsao, Noah, Wirka, Robert C, Rao, Abhiram, Newman, Alexandra, Priest, James, Ruusalepp, Arno, Pasterkamp, Gerard, Maegdefessel, Lars, Miller, Clint, Weissman, Irving, Lind, Lars, Koplev, Simon, Bj?rkegren, Johan L, Owens, Gary K, Ingelsson, Erik, and Leeper, Nicholas J

Abstract

Atherosclerosis is the process underlying heart attack and stroke. Dogma suggests that atherosclerotic plaques expand primarily via the accumulation of cholesterol and inflammatory cells. However, recent evidence suggests that a substantial portion of the plaque may arise from a subset of de-differentiated vascular smooth muscle cells (SMCs) which proliferate in a clonal fashion. Herein we use multi-color lineage tracing models to confirm that the mature SMC can give rise to a ?stem-like? cell that is not only hyperproliferative, but also proinflammatory given its ability to produce complement-dependent anaphylatoxins. Despite being extensively opsonized with pro-phagocytic complement fragments, we find that this cell also escapes immune surveillance, thereby exacerbating its relative survival advantage. Mechanistic studies indicate this phenomenon results from a generalized opsonin-sensing defect acquired by macrophages during polarization. This defect occurs due to the non-canonical upregulation and redistribution of so-called ?don?t eat-me? molecules on inflamed phagocytes, which impairs the functionality of their complement receptors and reduces their capacity for programmed cell removal (PrCR). Knockdown or knockout of the responsible anti-phagocytic molecule, CD47, restores the ability of macrophages to sense and clear opsonized targets in vitro, allowing for potent and targeted suppression of clonal SMC expansion in the plaque in vivo. Because integrated clinical and genomic analyses indicate that similar pathways are active in humans with cardiovascular disease, these studies suggest that the ?atherosclerotic stem cell? may represent a new translational target, similar to current oncology efforts directed against the cancer stem cell.

Published
2019
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47. Small-molecule CFTR activators increase tear secretion and prevent experimental dry eye disease.

Author

Flores AM, Casey SD, Felix CM, Phuan PW, Verkman AS, and Levin MH

Subjects
Animals, Cells, Cultured, Female, Humans, Mice, Mice, Inbred BALB C, Molecular Structure, Mutation, Rats, Rats, Inbred F344, Cystic Fibrosis Transmembrane Conductance Regulator agonists, Dry Eye Syndromes prevention & control, Gene Expression Regulation drug effects, Tears metabolism
Abstract

Dry eye disorders, including Sjögren's syndrome, constitute a common problem in the aging population, with limited effective therapeutic options available. The cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR) is a major prosecretory channel at the ocular surface. We investigated whether compounds that target CFTR can correct the abnormal tear film in dry eye. Small-molecule activators of human wild-type CFTR identified by high-throughput screening were evaluated in cell culture and in vivo assays, to select compounds that stimulate Cl(-)-driven fluid secretion across the ocular surface in mice. An aminophenyl-1,3,5-triazine, CFTRact-K089, fully activated CFTR in cell cultures with EC50 ∼250 nM and produced an ∼8.5 mV hyperpolarization in ocular surface potential difference. When delivered topically, CFTRact-K089 doubled basal tear volume for 4 h and had no effect in CF mice. CFTRact-K089 showed sustained tear film bioavailability without detectable systemic absorption. In a mouse model of aqueous-deficient dry eye produced by lacrimal ablation, topical administration of 0.1 nmol CFTRact-K089 3 times daily restored tear volume to basal levels, preventing corneal epithelial disruption when initiated at the time of surgery and reversing it when started after development of dry eye. Our results support the potential utility of CFTR-targeted activators as a novel prosecretory treatment for dry eye.-Flores, A. M., Casey, S. D., Felix, C. M., Phuan, P. W., Verkman, A. S., Levin, M. H. Small-molecule CFTR activators increase tear secretion and prevent experimental dry eye disease., (© FASEB.)

Published
2016
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