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1. Human atherosclerotic plaque transcriptomics reveals endothelial beta-2 spectrin as a potential regulator a leaky plaque microvasculature phenotype

Author

Rademakers, Timo, Manca, Marco, Jin, Han, Orban, Tanguy, Perisic, Ljubica Matic, Frissen, Hubertus J. M., Rühle, Frank, Hautvast, Petra, van Rijssel, Jos, van Kuijk, Kim, Mees, Barend M. E., Peutz-Kootstra, Carine J., Heeneman, Sylvia, Daemen, Mat J. A. P., Pasterkamp, Gerard, Stoll, Monika, van Zandvoort, Marc A. M. J., Hedin, Ulf, Dequiedt, Franck, van Buul, Jaap D., Sluimer, Judith C., and Biessen, Erik A. L.

Published
2024
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2. PIEZO1 targeting in macrophages boosts phagocytic activity and foam cell apoptosis in atherosclerosis

Author

Pourteymour, Shirin, Fan, Jingxue, Majhi, Rakesh Kumar, Guo, Shuyuan, Sun, Xin, Huang, Zhen, Liu, Ying, Winter, Hanna, Bäcklund, Alexandra, Skenteris, Nikolaos-Taxiarchis, Chernogubova, Ekaterina, Werngren, Olivera, Li, Zhaolong, Skogsberg, Josefin, Li, Yuhuang, Matic, Ljubica, Hedin, Ulf, Maegdefessel, Lars, Ehrenborg, Ewa, Tian, Ye, and Jin, Hong

Published
2024
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4. Lipoproteins and lipoprotein lipid composition are associated with stages of dysglycemia and subclinical coronary atherosclerosis

Author

Gigante, Bruna, Chen, Qiaosen, Björkbacka, Harry, Björnson, Elias, Brinck, Jonas, Chorell, Elin, Djekic, Demir, Edsfeldt, Andreas, Engström, Gunnar, Eriksson, Jan W., Gottsäter, Anders, Gummesson, Anders, Hagström, Emil, Hedin, Ulf, Jernberg, Tomas, Johnston, Nina, Nilsson, Lennart, Nyström, Fredrik, Otten, Julia, Rosengren, Annika, Söderberg, Stefan, Haglöw, Jenny Theorell, and Östgren, Carl Johan

Published
2025
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12. Atheroma transcriptomics identifies ARNTL as a smooth muscle cell regulator and with clinical and genetic data improves risk stratification.

Author

Narayanan, Sampath, Vuckovic, Sofija, Bergman, Otto, Wirka, Robert, Mosquera, Jose Verdezoto, Chen, Qiao Sen, Baldassarre, Damiano, Tremoli, Elena, Veglia, Fabrizio, Lengquist, Mariette, Aherahrrou, Redouane, Razuvaev, Anton, Gigante, Bruna, Björck, Hanna M, Miller, Clint L, Quertermous, Thomas, Hedin, Ulf, and Matic, Ljubica

Subjects
LOCUS (Genetics), MEDICAL genetics, VASCULAR smooth muscle, GENE expression, SINGLE nucleotide polymorphisms
Abstract

Background and Aims The role of vascular smooth muscle cells (SMCs) in atherosclerosis has evolved to indicate causal genetic links with the disease. Single cell RNA sequencing (scRNAseq) studies have identified multiple cell populations of mesenchymal origin within atherosclerotic lesions, including various SMC sub-phenotypes, but it is unknown how they relate to patient clinical parameters and genetics. Here, mesenchymal cell populations in atherosclerotic plaques were correlated with major coronary artery disease (CAD) genetic variants and functional analyses performed to identify SMC markers involved in the disease. Methods Bioinformatic deconvolution was done on bulk microarrays from carotid plaques in the Biobank of Karolinska Endarterectomies (BiKE, n = 125) using public plaque scRNAseq data and associated with patient clinical data and follow-up information. BiKE patients were clustered based on the deconvoluted cell fractions. Quantitative trait loci (QTLs) analyses were performed to predict the effect of CAD associated genetic variants on mesenchymal cell fractions (cfQTLs) and gene expression (eQTLs) in plaques. Results Lesions from symptomatic patients had higher fractions of Type 1 macrophages and pericytes, but lower fractions of classical and modulated SMCs compared with asymptomatic ones, particularly females. Presence of diabetes or statin treatment did not affect the cell fraction distribution. Clustering based on plaque cell fractions, revealed three patient groups, with relative differences in their stability profiles and associations to stroke, even during long-term follow-up. Several single nucleotide polymorphisms associated with plaque mesenchymal cell fractions, upstream of the circadian rhythm gene ARNTL were identified. In vitro silencing of ARNTL in human carotid SMCs increased the expression of contractile markers and attenuated cell proliferation. Conclusions This study shows the potential of combining scRNAseq data with vertically integrated clinical, genetic, and transcriptomic data from a large biobank of human plaques, for refinement of patient vulnerability and risk prediction stratification. The study revealed novel CAD-associated variants that may be functionally linked to SMCs in atherosclerotic plaques. Specifically, variants in the ARNTL gene may influence SMC ratios and function, and its role as a regulator of SMC proliferation should be further investigated. [ABSTRACT FROM AUTHOR]

Published
2025
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16. Clinical impact of the Kidney Failure Risk Equation for vascular access planning.

Author

Lundström, Ulrika Hahn, Ramspek, Chava L, Dekker, Friedo W, Diepen, Merel van, Carrero, Juan Jesus, Hedin, Ulf, and Evans, Marie

Subjects
CENTRAL venous catheters, RENAL replacement therapy, UNNECESSARY surgery, CHRONIC kidney failure, KIDNEY failure
Abstract

Background Risk-based thresholds for arteriovenous (AV) access creation has been proposed to aid vascular access planning. We aimed to assess the clinical impact of implementing the Kidney Failure Risk Equation (KFRE) for vascular access referral. Methods A total of 16 102 nephrology-referred chronic kidney disease (CKD) patients from the Swedish Renal Registry 2008–18 were included. The KFRE was calculated repeatedly, and the timing was identified for when the KFRE risk exceeded several pre-defined thresholds and/or the estimated glomerular filtration rate was <15 mL/min/1.73 m2 (eGFR15). To assess the utility of the KFRE/eGFR thresholds, cumulative incidence curves of kidney replacement therapy (KRT) or death, and decision-curve analyses were computed at 6 and 12 months, and 2 years. The potential impact of using the different thresholds was illustrated by an example from the Swedish access registry. Results The 12-month specificity for KRT initiation was highest for KFRE >50% {94.5 [95% confidence interval (CI) 94.3–94.7]} followed by KFRE >40% [90.0 (95% CI 89.7–90.3)], while sensitivity was highest for KFRE >30% [79.3 (95% CI 78.2–80.3)] and eGFR <15 mL/min/1.73 m2 [81.2 (95% CI 80.2–82.2)]. The 2-year positive predictive value was 71.5 (95% CI 70.2–72.8), 61.7 (95% CI 60.4–63.0) and 47.2 (95% CI 46.1–48.3) for KFRE >50%, KFRE >40% and eGFR <15, respectively. Decision curve analyses suggested the largest net benefit for KFRE >40% over 2 years and KFRE >50% over 12 months when it is important to avoid the harm of possibly unnecessary surgery. In Sweden, 54% of nephrology-referred patients started hemodialysis in a central venous catheter (CVC), of whom only 5% had AV access surgery >6 months before initiation. Sixty percent of the CVC patients exceeded KFRE >40% a median of 0.8 years (interquartile range 0.4–1.5) before KRT initiation. Conclusions The utility of using KFRE >40% and KFRE >50% is higher compared with the more traditionally used eGFR threshold <15 mL/min/1.73 m2 for vascular access planning. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Red blood cells from patients with ST-elevation myocardial infarction and elevated C-reactive protein levels induce endothelial dysfunction.

Author

Tengbom, John, Humoud, Rawan, Kontidou, Eftychia, Jiao, Tong, Yang, Jiangning, Hedin, Ulf, Zhou, Zhichao, Jurga, Juliane, Collado, Aida, Mahdi, Ali, and Pernow, John

Subjects
ST elevation myocardial infarction, MYOCARDIAL infarction, ENDOTHELIUM diseases, ERYTHROCYTES, CORONARY disease
Abstract

Endothelial dysfunction is an early consequence of vascular inflammation and a driver of coronary atherosclerotic disease leading to myocardial infarction. The red blood cells (RBCs) mediate endothelial dysfunction in patients at cardiovascular risk, but their role in patients with acute myocardial infarction is unknown. This study aimed to investigate if RBCs from patients with ST-elevation myocardial infarction (STEMI) induced endothelial dysfunction and the role of systemic inflammation in this effect. RBCs from patients with STEMI and aged-matched healthy controls were coincubated with rat aortic segments for 18 h followed by evaluation of endothelium-dependent (EDR) and endothelium-independent relaxation (EIDR). RBCs and aortic segments were also analyzed for arginase and oxidative stress. The patients were divided into groups depending on C-reactive protein (CRP) levels at admission. RBCs from patients with STEMI and CRP levels ≥2 mg/L induced impairment of EDR, but not EIDR, compared with RBCs from STEMI and CRP <2 mg/L and healthy controls. Aortic expression of arginase 1 was increased following incubation with RBCs from patients with STEMI and CRP ≥2, and arginase inhibition prevented the RBC-induced endothelial dysfunction. RBCs from patients with STEMI and CRP ≥2 had increased reactive oxygen species compared with RBCs from patients with CRP <2 and healthy controls. Vascular inhibition of NADPH oxidases and increased dismutation of superoxide improved EDR. RBCs from patients with STEMI and low-grade inflammation induce endothelial dysfunction through a mechanism involving arginase 1 as well as increased RBC and vascular superoxide by NADPH oxidases. NEW & NOTEWORTHY: Red blood cells from patients with STEMI and systemic inflammation induce endothelial dysfunction ex vivo. The RBC-induced endothelial dysfunction is mediated through increased arginase 1 and a shift in the redox balance toward oxidative stress. Inhibition of arginase or free radicals attenuates the impairment of endothelial function. The study suggests that red blood cells deserve attention as a key player in systemic inflammation and STEMI. [ABSTRACT FROM AUTHOR]

Published
2024
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18. A neutralizing antibody against DKK1 does not reduce plaque formation in classical murine models of atherosclerosis: Is the therapeutic potential lost in translation?

Author

Rakipovski, Günaj, Rolin, Bidda, Barascuk, Natasha, Lund, Heidi Engslev, Bjørn Bonde, Mathilde Frederikke, Djordjevic, Djordje, Wulff-Larsen, Pernille Gry, Petersen, Maj, Kirk, Rikke Kaae, Hultman, Karin, Manfe, Valentina, Blume, Niels, Zahn, Stefan, Lengquist, Mariette, Maegdefessel, Lars, Hovingh, G. Kees, Conde-Knape, Karin, Hedin, Ulf, Matic, Ljubica, and Nyberg, Michael

Published
2020
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20. Transcriptomic profiling of experimental arterial injury reveals new mechanisms and temporal dynamics in vascular healing response

Author

Röhl, Samuel, Rykaczewska, Urszula, Seime, Till, Suur, Bianca E., Diez, Maria Gonzalez, Gådin, Jesper R., Gainullina, Anastasiia, Sergushichev, Alexey A., Wirka, Robert, Lengquist, Mariette, Kronqvist, Malin, Bergman, Otto, Odeberg, Jacob, Lindeman, Jan H.N., Quertermous, Thomas, Hamsten, Anders, Eriksson, Per, Hedin, Ulf, Razuvaev, Anton, and Matic, Ljubica Perisic

Published
2020
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22. CDKN2B Regulates TGFβ Signaling and Smooth Muscle Cell Investment of Hypoxic Neovessels.

Author

Nanda, Vivek, Downing, Kelly P, Ye, Jianqin, Xiao, Sophia, Kojima, Yoko, Spin, Joshua M, DiRenzo, Daniel, Nead, Kevin T, Connolly, Andrew J, Dandona, Sonny, Perisic, Ljubica, Hedin, Ulf, Maegdefessel, Lars, Dalman, Jessie, Guo, Liang, Zhao, XiaoQing, Kolodgie, Frank D, Virmani, Renu, Davis, Harry R, and Leeper, Nicholas J

Subjects
Muscle, Skeletal, Muscle, Smooth, Vascular, Carotid Arteries, Coronary Vessels, Cells, Cultured, Chromosomes, Human, Pair 9, Myocytes, Smooth Muscle, Hindlimb, Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Disease Models, Animal, Genetic Predisposition to Disease, Neovascularization, Pathologic, Transfection, Signal Transduction, Cell Hypoxia, RNA Interference, Neovascularization, Physiologic, Phenotype, Time Factors, Female, Male, Atherosclerosis, Cyclin-Dependent Kinase Inhibitor p15, Smad7 Protein, Transforming Growth Factor beta1, atherosclerosis, cyclin-dependent kinase inhibitor p15, genetic variation, pathologic angiogenesis, peripheral artery disease, smooth muscle cells, Cardiovascular, Aging, Genetics, 2.1 Biological and endogenous factors, Aetiology, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

RationaleGenetic variation at the chromosome 9p21 cardiovascular risk locus has been associated with peripheral artery disease, but its mechanism remains unknown.ObjectiveTo determine whether this association is secondary to an increase in atherosclerosis, or it is the result of a separate angiogenesis-related mechanism.Methods and resultsQuantitative evaluation of human vascular samples revealed that carriers of the 9p21 risk allele possess a significantly higher burden of immature intraplaque microvessels than carriers of the ancestral allele, irrespective of lesion size or patient comorbidity. To determine whether aberrant angiogenesis also occurs under nonatherosclerotic conditions, we performed femoral artery ligation surgery in mice lacking the 9p21 candidate gene, Cdkn2b. These animals developed advanced hindlimb ischemia and digital autoamputation, secondary to a defect in the capacity of the Cdkn2b-deficient smooth muscle cell to support the developing neovessel. Microarray studies identified impaired transforming growth factor β (TGFβ) signaling in cultured cyclin-dependent kinase inhibitor 2B (CDKN2B)-deficient cells, as well as TGFβ1 upregulation in the vasculature of 9p21 risk allele carriers. Molecular signaling studies indicated that loss of CDKN2B impairs the expression of the inhibitory factor, SMAD-7, which promotes downstream TGFβ activation. Ultimately, this manifests in the upregulation of a poorly studied effector molecule, TGFβ1-induced-1, which is a TGFβ-rheostat known to have antagonistic effects on the endothelial cell and smooth muscle cell. Dual knockdown studies confirmed the reversibility of the proposed mechanism, in vitro.ConclusionsThese results suggest that loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFβ signaling and hypoxic neovessel maturation.

Published
2016

23. Human atherosclerotic plaque transcriptomics reveals endothelial beta-2 spectrin as a potential regulator a leaky plaque microvasculature phenotype

Author

Centraal Diagnostisch Laboratorium, Circulatory Health, Rademakers, Timo, Manca, Marco, Jin, Han, Orban, Tanguy, Perisic, Ljubica Matic, Frissen, Hubertus J.M., Rühle, Frank, Hautvast, Petra, van Rijssel, Jos, van Kuijk, Kim, Mees, Barend M.E., Peutz-Kootstra, Carine J., Heeneman, Sylvia, Daemen, Mat J.A.P., Pasterkamp, Gerard, Stoll, Monika, van Zandvoort, Marc A.M.J., Hedin, Ulf, Dequiedt, Franck, van Buul, Jaap D., Sluimer, Judith C., Biessen, Erik A.L., Centraal Diagnostisch Laboratorium, Circulatory Health, Rademakers, Timo, Manca, Marco, Jin, Han, Orban, Tanguy, Perisic, Ljubica Matic, Frissen, Hubertus J.M., Rühle, Frank, Hautvast, Petra, van Rijssel, Jos, van Kuijk, Kim, Mees, Barend M.E., Peutz-Kootstra, Carine J., Heeneman, Sylvia, Daemen, Mat J.A.P., Pasterkamp, Gerard, Stoll, Monika, van Zandvoort, Marc A.M.J., Hedin, Ulf, Dequiedt, Franck, van Buul, Jaap D., Sluimer, Judith C., and Biessen, Erik A.L.

Published
2024

24. Long Non-coding RNA MIAT Controls Advanced Atherosclerotic Lesion Formation and Plaque Destabilization

Author

Fasolo, Francesca, Jin, Hong, Winski, Greg, Chernogubova, Ekaterina, Pauli, Jessica, Winter, Hanna, Li, Daniel Y., Glukha, Nadiya, Bauer, Sabine, Metschl, Susanne, Wu, Zhiyuan, Koschinsky, Marlys L., Reilly, Muredach, Pelisek, Jaroslav, Kempf, Wolfgang, Eckstein, Hans-Henning, Soehnlein, Oliver, Matic, Ljubica, Hedin, Ulf, Bäcklund, Alexandra, Bergmark, Claes, Paloschi, Valentina, and Maegdefessel, Lars

Published
2021
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30. Contributors

Author

Akyildiz, Ali C., primary, Antoniadis, Antonios P., additional, Athanasiou, Lambros S., additional, Barrett, Hilary E., additional, Billiar, Kristen, additional, Canet Soulas, Emmanuelle, additional, Cardoso, Luis, additional, Cawthon, Claire, additional, Chatzizisis, Yiannis S., additional, Chiastra, Claudio, additional, Cilla, Myriam, additional, Cloutier, Guy, additional, Coppel, Ricardo, additional, Demos, Catherine, additional, Dérimay, François, additional, Dubini, Gabriele, additional, Edelman, Elazer R., additional, Ehman, Richard L., additional, Finet, Gérard, additional, Fok, Pak-Wing, additional, Gasser, T. Christian, additional, Giddens, Don P., additional, Gijsen, Frank J.H., additional, Goerlich, Erin, additional, Gómez, Armida, additional, Goudot, Guillaume, additional, Guo, Xiaoya, additional, Hays, Allison G., additional, Hedin, Ulf, additional, Holzapfel, Gerhard A., additional, Jia, Haibo, additional, Jo, Hanjoong, additional, Kamm, Roger D., additional, Kassab, Ghassan S., additional, Kolipaka, Arunark, additional, Konofagou, Elisa E., additional, Lagache, Manuel, additional, Latorre, Álvaro T., additional, Le Floc'h, Simon, additional, Lehoux, Stephanie, additional, Ma, Genshan, additional, Maehara, Akiko, additional, Malvè, Mauro, additional, Martiel, Jean-Louis, additional, Martínez, Miguel A., additional, Matsumoto, Takeo, additional, Matsumura, Mitsuaki, additional, Migliavacca, Francesco, additional, Mintz, Gary S., additional, Mohammad Mirzaei, Navid, additional, Molony, David, additional, Nezami, Farhad Rikhtegar, additional, Ohayon, Jacques, additional, Oshinski, John N., additional, Peña, Estefanía, additional, Pernot, Mathieu, additional, Pettigrew, Roderic I., additional, Pomeroy, William L., additional, Rioufol, Gilles, additional, Roy, Joy, additional, Samady, Habib, additional, Shelton, Sarah E., additional, Stuber, Matthias, additional, Tacheau, Antoine, additional, Tamargo, Ian, additional, Tang, Dalin, additional, Timmins, Lucas H., additional, Turner, Emily A., additional, Wang, Liang, additional, Weinbaum, Sheldon, additional, Weiss, Robert G., additional, White, Richard D., additional, Yang, Chun, additional, Yazdani, Saami K., additional, Zheng, Jie, additional, and Zhu, Jian, additional

Published
2021
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31. Long Noncoding RNA MIAT Controls Advanced Atherosclerotic Lesion Formation and Plaque Destabilization

Author

Fasolo, Francesca, Jin, Hong, Winski, Greg, Chernogubova, Ekaterina, Pauli, Jessica, Winter, Hanna, Li, Daniel Y., Glukha, Nadiya, Bauer, Sabine, Metschl, Susanne, Wu, Zhiyuan, Koschinsky, Marlys L., Reilly, Muredach, Pelisek, Jaroslav, Kempf, Wolfgang, Eckstein, Hans-Henning, Soehnlein, Oliver, Matic, Ljubica, Hedin, Ulf, Bäcklund, Alexandra, Bergmark, Claes, Paloschi, Valentina, and Maegdefessel, Lars

Published
2021
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32. Integrated Human Evaluation of the Lysophosphatidic Acid Pathway as a Novel Therapeutic Target in Atherosclerosis

Author

Aldi, Silvia, Matic, Ljubica Perisic, Hamm, Gregory, van Keulen, Daniëlle, Tempel, Dennie, Holmstrøm, Kim, Szwajda, Agnieszka, Nielsen, Boye Schnack, Emilsson, Valur, Ait-Belkacem, Rima, Lengquist, Mariette, Paulsson-Berne, Gabrielle, Eriksson, Per, Lindeman, Jan H.N., Gool, Alain J., Stauber, Jonathan, Hedin, Ulf, and Hurt-Camejo, Eva

Published
2018
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33. Novel Multiomics Profiling of Human Carotid Atherosclerotic Plaques and Plasma Reveals Biliverdin Reductase B as a Marker of Intraplaque Hemorrhage

Author

Matic, Ljubica Perisic, Jesus Iglesias, Maria, Vesterlund, Mattias, Lengquist, Mariette, Hong, Mun-Gwan, Saieed, Shanga, Sanchez-Rivera, Laura, Berg, Martin, Razuvaev, Anton, Kronqvist, Malin, Lund, Kent, Caidahl, Kenneth, Gillgren, Peter, Pontén, Fredrik, Uhlén, Mathias, Schwenk, Jochen M., Hansson, Göran K., Paulsson-Berne, Gabrielle, Fagman, Erika, Roy, Joy, Hultgren, Rebecka, Bergström, Göran, Lehtiö, Janne, Odeberg, Jacob, and Hedin, Ulf

Published
2018
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34. Editor's Choice – Vascular Access: 2018 Clinical Practice Guidelines of the European Society for Vascular Surgery (ESVS)

Author

Schmidli, Jürg, Widmer, Matthias K., Basile, Carlo, de Donato, Gianmarco, Gallieni, Maurizio, Gibbons, Christopher P., Haage, Patrick, Hamilton, George, Hedin, Ulf, Kamper, Lars, Lazarides, Miltos K., Lindsey, Ben, Mestres, Gaspar, Pegoraro, Marisa, Roy, Joy, Setacci, Carlo, Shemesh, David, Tordoir, Jan H.M., van Loon, Magda, ESVS Guidelines Committee, Kolh, Philippe, de Borst, Gert J., Chakfe, Nabil, Debus, Sebastian, Hinchliffe, Rob, Kakkos, Stavros, Koncar, Igor, Lindholt, Jes, Naylor, Ross, Vega de Ceniga, Melina, Vermassen, Frank, Verzini, Fabio, ESVS Guidelines Reviewers, Mohaupt, Markus, Ricco, Jean-Baptiste, and Roca-Tey, Ramon

Published
2018
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35. Local Delivery of miR-21 Stabilizes Fibrous Caps in Vulnerable Atherosclerotic Lesions

Author

Jin, Hong, Li, Daniel Y., Chernogubova, Ekaterina, Sun, Changyan, Busch, Albert, Eken, Suzanne M., Saliba-Gustafsson, Peter, Winter, Hanna, Winski, Greg, Raaz, Uwe, Schellinger, Isabel N., Simon, Nancy, Hegenloh, Renate, Matic, Ljubica Perisic, Jagodic, Maja, Ehrenborg, Ewa, Pelisek, Jaroslav, Eckstein, Hans-Henning, Hedin, Ulf, Backlund, Alexandra, and Maegdefessel, Lars

Published
2018
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36. Reactive Oxygen-Forming Nox5 Links Vascular Smooth Muscle Cell Phenotypic Switching and Extracellular Vesicle-Mediated Vascular Calcification

Author

Furmanik, Malgorzata, Chatrou, Martijn, van Gorp, Rick, Akbulut, Asim, Willems, Brecht, Schmidt, Harald, van Eys, Guillaume, Bochaton-Piallat, Marie-Luce, Proudfoot, Diane, Biessen, Erik, Hedin, Ulf, Matic, Ljubica Perisic, Mees, Barend, Shanahan, Catherine, Reutelingsperger, Chris, and Schurgers, Leon

Published
2020
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40. The long noncoding RNA CHROME regulates cholesterol homeostasis in primates

Author

Hennessy, Elizabeth J., van Solingen, Coen, Scacalossi, Kaitlyn R., Ouimet, Mireille, Afonso, Milessa S., Prins, Jurrien, Koelwyn, Graeme J., Sharma, Monika, Ramkhelawon, Bhama, Carpenter, Susan, Busch, Albert, Chernogubova, Ekaterina, Matic, Ljubica Perisic, Hedin, Ulf, Maegdefessel, Lars, Caffrey, Brian E., Hussein, Maryem A., Ricci, Emiliano P., Temel, Ryan E., Garabedian, Michael J., Berger, Jeffrey S., Vickers, Kasey C., Kanke, Matthew, Sethupathy, Praveen, Teupser, Daniel, Holdt, Lesca M., and Moore, Kathryn J.

Published
2019
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43. PCSK6 Is a Key Protease in the Control of Smooth Muscle Cell Function in Vascular Remodeling

Author

Rykaczewska, Urszula, Suur, Bianca E., Röhl, Samuel, Razuvaev, Anton, Lengquist, Mariette, Sabater-Lleal, Maria, van der Laan, Sander W., Miller, Clint L., Wirka, Robert C., Kronqvist, Malin, Gonzalez Diez, Maria, Vesterlund, Mattias, Gillgren, Peter, Odeberg, Jacob, Lindeman, Jan H., Veglia, Fabrizio, Humphries, Steve E., de Faire, Ulf, Baldassarre, Damiano, Tremoli, Elena, Lehtiö, Janne, Hansson, Göran K., Paulsson-Berne, Gabrielle, Pasterkamp, Gerard, Quertermous, Thomas, Hamsten, Anders, Eriksson, Per, Hedin, Ulf, and Matic, Ljubica

Published
2020
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45. Biliverdin Reductase B Is a Plasma Biomarker for Intraplaque Hemorrhage and a Predictor of Ischemic Stroke in Patients with Symptomatic Carotid Atherosclerosis

Author

Chemaly, Melody, Marlevi, David, Iglesias, Maria Jesus, Lengquist, Mariette, Kronqvist, Malin, Bos, Daniel, van Dam-Nolen, Dianne H. K., van der Kolk, Anja, Hendrikse, Jeroen, Kassem, Mohamed, Matic, Ljubica, Odeberg, Jacob, de Vries, Margreet R., Kooi, M. Eline, Hedin, Ulf, Chemaly, Melody, Marlevi, David, Iglesias, Maria Jesus, Lengquist, Mariette, Kronqvist, Malin, Bos, Daniel, van Dam-Nolen, Dianne H. K., van der Kolk, Anja, Hendrikse, Jeroen, Kassem, Mohamed, Matic, Ljubica, Odeberg, Jacob, de Vries, Margreet R., Kooi, M. Eline, and Hedin, Ulf

Abstract

Background: Intraplaque hemorrhage (IPH) is a hallmark of atherosclerotic plaque instability. Biliverdin reductase B (BLVRB) is enriched in plasma and plaques from patients with symptomatic carotid atherosclerosis and functionally associated with IPH. Objective: We explored the biomarker potential of plasma BLVRB through (1) its correlation with IPH in carotid plaques assessed by magnetic resonance imaging (MRI), and with recurrent ischemic stroke, and (2) its use for monitoring pharmacotherapy targeting IPH in a preclinical setting. Methods: Plasma BLVRB levels were measured in patients with symptomatic carotid atherosclerosis from the PARISK study (n = 177, 5 year follow-up) with and without IPH as indicated by MRI. Plasma BLVRB levels were also measured in a mouse vein graft model of IPH at baseline and following antiangiogenic therapy targeting vascular endothelial growth factor receptor 2 (VEGFR-2). Results: Plasma BLVRB levels were significantly higher in patients with IPH (737.32 & PLUSMN; 693.21 vs. 520.94 & PLUSMN; 499.43 mean fluorescent intensity (MFI), p = 0.033), but had no association with baseline clinical and biological parameters. Plasma BLVRB levels were also significantly higher in patients who developed recurrent ischemic stroke (1099.34 & PLUSMN; 928.49 vs. 582.07 & PLUSMN; 545.34 MFI, HR = 1.600, CI [1.092-2.344]; p = 0.016). Plasma BLVRB levels were significantly reduced following prevention of IPH by anti-VEGFR-2 therapy in mouse vein grafts (1189 & PLUSMN; 258.73 vs. 1752 & PLUSMN; 366.84 MFI; p = 0.004). Conclusions: Plasma BLVRB was associated with IPH and increased risk of recurrent ischemic stroke in patients with symptomatic low- to moderate-grade carotid stenosis, indicating the capacity to monitor the efficacy of IPH-preventive pharmacotherapy in an animal model. Together, these results suggest the utility of plasma BLVRB as a biomarker for atherosclerotic plaque instability., QC 20230714

Published
2023
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46. Biliverdin Reductase B Is a Plasma Biomarker for Intraplaque Hemorrhage and a Predictor of Ischemic Stroke in Patients with Symptomatic Carotid Atherosclerosis

Author

Researchgr. Hart-brein as., Computational Imaging, Brain, Cancer, Divisie Beeld, Chemaly, Melody, Marlevi, David, Iglesias, Maria-Jesus, Lengquist, Mariette, Kronqvist, Malin, Bos, Daniel, van Dam-Nolen, Dianne H K, van der Kolk, Anja, Hendrikse, Jeroen, Kassem, Mohamed, Matic, Ljubica, Odeberg, Jacob, de Vries, Margreet R, Kooi, M Eline, Hedin, Ulf, Researchgr. Hart-brein as., Computational Imaging, Brain, Cancer, Divisie Beeld, Chemaly, Melody, Marlevi, David, Iglesias, Maria-Jesus, Lengquist, Mariette, Kronqvist, Malin, Bos, Daniel, van Dam-Nolen, Dianne H K, van der Kolk, Anja, Hendrikse, Jeroen, Kassem, Mohamed, Matic, Ljubica, Odeberg, Jacob, de Vries, Margreet R, Kooi, M Eline, and Hedin, Ulf

Published
2023

47. Biliverdin Reductase B Is a Plasma Biomarker for Intraplaque Hemorrhage and a Predictor of Ischemic Stroke in Patients with Symptomatic Carotid Atherosclerosis

Author

Chemaly, Melody, primary, Marlevi, David, additional, Iglesias, Maria-Jesus, additional, Lengquist, Mariette, additional, Kronqvist, Malin, additional, Bos, Daniel, additional, van Dam-Nolen, Dianne H. K., additional, van der Kolk, Anja, additional, Hendrikse, Jeroen, additional, Kassem, Mohamed, additional, Matic, Ljubica, additional, Odeberg, Jacob, additional, de Vries, Margreet R., additional, Kooi, M. Eline, additional, and Hedin, Ulf, additional

Published
2023
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48. Abstract 112: Pcsk6 Ablation In Vascular Smooth Muscle Cells Promotes Abdominal Aortic Aneurysm Development And Rupture

Author

Jin, Hong, primary, Lindquist Liljeqvist, Moritz, additional, Wu, Zhiyuan, additional, Micali, Linda, additional, Suur, Bianca E, additional, Lengquist, Mariette, additional, Zhang, Xiang, additional, Kronqvist, Malin, additional, Pauli, Jessica, additional, Hedin, Ulf, additional, Roy, Joy, additional, and Matic, Ljubica, additional

Published
2023
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49. Abstract 451: Biliverdin Reductase B Is A Plasma Biomarker For Intraplaque Hemorrhage And A Predictor Of Ischemic Stroke In Symptomatic Carotid Stenosis

Author

Chemaly, Melody, primary, Marlevi, David, additional, Iglesias Mareque, Maria Jesus, additional, Lengquist, Mariette, additional, Kronqvist, Malin, additional, Bos, Daniel, additional, van Dam - Nolen, Dianne H.K, additional, van der Kolk, Anja, additional, Hendrikse, Jeroen, additional, Kassem, Mohamed, additional, Matic, Ljubica, additional, Odeberg, Jacob, additional, De Vries, Margreet R, additional, Kooi, M E, additional, and Hedin, Ulf, additional

Published
2023
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50. FHL5 Controls Vascular Disease–Associated Gene Programs in Smooth Muscle Cells

Author

Wong, Doris, primary, Auguste, Gaëlle, additional, Lino Cardenas, Christian L., additional, Turner, Adam W., additional, Chen, Yixuan, additional, Song, Yipei, additional, Ma, Lijiang, additional, Perry, R. Noah, additional, Aherrahrou, Redouane, additional, Kuppusamy, Maniselvan, additional, Yang, Chaojie, additional, Mosquera, Jose Verdezoto, additional, Dube, Collin J., additional, Khan, Mohammad Daud, additional, Palmore, Meredith, additional, Kalra, Jaspreet K., additional, Kavousi, Maryam, additional, Peyser, Patricia A., additional, Matic, Ljubica, additional, Hedin, Ulf, additional, Manichaikul, Ani, additional, Sonkusare, Swapnil K., additional, Civelek, Mete, additional, Kovaci, Jason C., additional, Björkegren, Johan L.M., additional, Malhotra, Rajeev, additional, and Miller, Clint L., additional

Published
2023
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