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Your search keyword '"Vromman, Amélie"' showing total 15 results
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15 results on '"Vromman, Amélie"'

2. Loss-of-function mutations in Dnmt3a and Tet2 lead to accelerated atherosclerosis and concordant macrophage phenotypes

Author

Rauch, Philipp J., Gopakumar, Jayakrishnan, Silver, Alexander J., Nachun, Daniel, Ahmad, Herra, McConkey, Marie, Nakao, Tetsushi, Bosse, Marc, Rentz, Thiago, Vivanco Gonzalez, Nora, Greenwald, Noah F., McCaffrey, Erin F., Khair, Zumana, Gopakumar, Manu, Rodrigues, Kameron B., Lin, Amy E., Sinha, Eti, Fefer, Maia, Cohen, Drew N., Vromman, Amélie, Shvartz, Eugenia, Sukhova, Galina, Bendall, Sean, Angelo, Michael, Libby, Peter, Ebert, Benjamin L., and Jaiswal, Siddhartha

Published
2023
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3. Multiomics of Tissue Extracellular Vesicles Identifies Unique Modulators of Atherosclerosis and Calcific Aortic Valve Stenosis

Author

Blaser, Mark C., Buffolo, Fabrizio, Halu, Arda, Turner, Mandy E., Schlotter, Florian, Higashi, Hideyuki, Pantano, Lorena, Clift, Cassandra L., Saddic, Louis A., Atkins, Samantha K., Rogers, Maximillian A., Pham, Tan, Vromman, Amélie, Shvartz, Eugenia, Sukhova, Galina K., Monticone, Silvia, Camussi, Giovanni, Robson, Simon C., Body, Simon C., Muehlschlegel, Jochen D., Singh, Sasha A., Aikawa, Masanori, and Aikawa, Elena

Published
2023
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4. The clonal hematopoiesis mutation Jak2 aggravates endothelial injury and thrombosis in arteries with erosion-like intimas

Author

Molinaro, R, Sellar, R, Vromman, A, Sausen, G, Folco, E, Sukhova, G, Mcconke, M, Corbo, C, Ebert, B, Libby, P, Molinaro, Roberto, Sellar, Rob S., Vromman, Amélie, Sausen, Grasiele, Folco, Eduardo, Sukhova, Galina K., McConke, Marie E., Corbo, Claudia, Ebert, Benjamin L., Libby, Peter, Molinaro, R, Sellar, R, Vromman, A, Sausen, G, Folco, E, Sukhova, G, Mcconke, M, Corbo, C, Ebert, B, Libby, P, Molinaro, Roberto, Sellar, Rob S., Vromman, Amélie, Sausen, Grasiele, Folco, Eduardo, Sukhova, Galina K., McConke, Marie E., Corbo, Claudia, Ebert, Benjamin L., and Libby, Peter

Abstract

Background: Superficial plaque erosion causes many acute coronary syndromes. However, mechanisms of plaque erosion remain poorly understood, and we lack directed therapeutics for thrombotic complication. Human eroded plaques can harbor neutrophil extracellular traps (NETs) that propagate endothelial damage at experimental arterial lesions that recapitulate superficial erosion. Clonal Hematopoiesis of Indeterminate Potential (CHIP) denotes age-related clonal expansion of bone marrow-derived cells harboring somatic mutations in the absence of overt hematological disease. CHIP heightens the risk of cardiovascular disease, with the greatest increase seen in individuals with JAK2V617F. Neutrophils from mice and humans with JAK2V617F undergo NETosis more readily than Jak2WT (wild-type) cells. We hypothesized that JAK2V617F, by increasing propensity to NETosis, exacerbates aspects of superficial erosion. Methods and results: We generated Jak2V617F and Jak2WT mice with heterozygous Jak2V617F in myeloid cells. We induced areas of denuded endothelium that recapitulate features of superficial erosion and assessed endothelial integrity, cellular composition of the erosion, thrombosis rates, and response to ruxolitinib, a clinically available JAK1/2 inhibitor, in relation to genotype. Following experimental erosion, Jak2V617F mice have greater impairment of endothelial barrier function and increased rates of arterial thrombosis. Neointimas in Jak2V617F mice exhibit increased apoptosis, NETosis, and platelet recruitment. Jak2V617F mice treated with ruxolitinib show increased endothelial continuity and reduced apoptosis in the neointima comparable to levels in Jak2WT. Conclusions: These observations provide new mechanistic insight into the pathophysiology of superficial erosion, the heightened risk for myocardial infarction in JAK2V617F CHIP, and point the way to personalized therapeutics based on CHIP status.

Published
2024

7. Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) Promotes Macrophage Activation via LDL Receptor-Independent Mechanisms

Author

Katsuki, Shunsuke, primary, K. Jha, Prabhash, additional, Lupieri, Adrien, additional, Nakano, Toshiaki, additional, Passos, Livia S.A., additional, Rogers, Maximillian A., additional, Becker-Greene, Dakota, additional, Le, Thanh-Dat, additional, Decano, Julius L., additional, Ho Lee, Lang, additional, Guimaraes, Gabriel C., additional, Abdelhamid, Ilyes, additional, Halu, Arda, additional, Muscoloni, Alessandro, additional, V. Cannistraci, Carlo, additional, Higashi, Hideyuki, additional, Zhang, Hengmin, additional, Vromman, Amélie, additional, Libby, Peter, additional, Keith Ozaki, C., additional, Sharma, Amitabh, additional, Singh, Sasha A., additional, Aikawa, Elena, additional, and Aikawa, Masanori, additional

Published
2022
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8. Mechanisms and Therapeutic Strategies to Reverse TET2 Mutant Clonal Hematopoiesis and the Risk of MDS, AML, and Atherosclerotic Cardiovascular Disease

Author

Prutsch, Nicole, Vromman, Amélie, Leeper, Brittaney, Chen, Mengyu, He, Shuning, Ren, Siyang, Walker, Christopher J., Zimmerman, Mark W., Janini Gomes, Mariana, Folco, Eduardo J., Rauch, Philipp J., Gokhale, Prafulla C., Abraham, Brian J., Neuberg, Donna S., Ebert, Benjamin L., Libby, Peter, and Look, A. Thomas

Published
2023
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11. Stage-dependent differential effects of interleukin-1 isoforms on experimental atherosclerosis

Author

Vromman, Amélie, primary, Ruvkun, Victoria, additional, Shvartz, Eugenia, additional, Wojtkiewicz, Gregory, additional, Santos Masson, Gustavo, additional, Tesmenitsky, Yevgenia, additional, Folco, Eduardo, additional, Gram, Hermann, additional, Nahrendorf, Matthias, additional, Swirski, Filip K, additional, Sukhova, Galina K, additional, and Libby, Peter, additional

Published
2019
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15. Human Plasma Proteomic Profile of Clonal Hematopoiesis.

Author

Yu Z, Vromman A, Nguyen NQH, Schuermans A, Rentz T, Vellarikkal SK, Uddin MM, Niroula A, Griffin G, Honigberg MC, Lin AE, Gibson CJ, Katz DH, Tahir U, Fang S, Haidermota S, Ganesh S, Antoine T, Weinstock J, Austin TR, Ramachandran VS, Peloso GM, Hornsby W, Ganz P, Manson JE, Haring B, Kooperberg CL, Reiner AP, Bis JC, Psaty BM, Min YI, Correa A, Lange LA, Post WS, Rotter JI, Rich SS, Wilson JG, Ebert BL, Yu B, Ballantyne CM, Coresh J, Sankaran VG, Bick AG, Jaiswal S, Gerszten RE, Libby P, Gupta RM, and Natarajan P

Abstract

Plasma proteomic profiles associated with subclinical somatic mutations in blood cells may offer novel insights into downstream clinical consequences. Here, we explore such patterns in clonal hematopoiesis of indeterminate potential (CHIP), which is linked to several cancer and non-cancer outcomes, including coronary artery disease (CAD). Among 61,833 ancestrally diverse participants (3,881 with CHIP) from NHLBI TOPMed and UK Biobank with blood-based DNA sequencing and proteomic measurements (1,148 proteins by SomaScan in TOPMed and 2,917 proteins by Olink in UK Biobank), we identified 32 and 345 unique proteins from TOPMed and UK Biobank, respectively, associated with the most prevalent driver genes ( DNMT3A , TET2 , and ASXL1 ). These associations showed substantial heterogeneity by driver genes, sex, and race, and were enriched for immune response and inflammation pathways. Mendelian randomization in humans, coupled with ELISA in hematopoietic Tet2 -/- vs wild-type mice validation, disentangled causal proteomic perturbations from TET2 CHIP. Lastly, we identified plasma proteins shared between CHIP and CAD.

Published
2024
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