Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice
Open accessAbstract
Rationale: The mechanisms driving atherothrombotic risk in individuals with JAK2 V617F ( Jak2 VF ) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood. Objective: The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2 VF expression. Methods and Results: Irradiated low-density lipoprotein receptor knockout ( Ldlr −/− ) mice were transplanted with bone marrow from wild-type or Jak2 VF mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2 VF mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2 VF lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2 VF erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a “don’t-eat-me” signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2 VF macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis. Conclusions: Hematopoietic Jak2 VF expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2 VF caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability.
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There is evidence that Jak2 mutations enhance atherosclerosis in mouse models by altering macrophage function.
“There is also evidence that Jak2 mutations enhance atherosclerosis in mouse models by altering macrophage function 89.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [89]
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- Authors
- Wang, W., Liu, W., Fidler, T., Wang, Y., Tang, Y., Woods, B., Welch, C., Cai, B., Silvestre-Roig, C., Ai, D., Yang, Y.-G., Hidalgo, A., Soehnlein, O., Tabas, I., Levine, R. L., Tall, A. R., & Wang, N.
- Affiliations
- Columbia University Irving Medical Center (US)
- Memorial Sloan Kettering Cancer Center (US)
- Ludwig-Maximilians-Universität München (DE)
- Tianjin Medical University (CN)
- Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (C.S.-R., A.H., O.S.)
- Karolinska Institutet (SE)
- Corresponding author
- Wang, Wei
- Liu, Wenli
- ORCID
- Venue
- Circulation Research
- Published
- 2018-11-09
- Volume
- 123
- Issue
- 11
- Pages
- e35-e47
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC6309796
- OpenAlex
- W2891613655
- Cited by
- 262
- References
- 58
- Citations by year
- 2026: 23 · 2025: 39 · 2024: 34 · 2023: 43 · 2022: 41 · 2021: 35 · 2020: 26 · 2019: 19 · 2018: 1
- FWCI
- 8.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion)
- Funders
- Ministerio de Ciencia, Innovación y Universidades (SEV-2015-0505)
- Centro Nacional de Investigaciones Cardiovasculares (SEV‐2015‐0505)
- National Institutes of Health (1s10od020056-01, 1k99dk115778-01a1, TL1TR001875)
- National Heart, Lung, and Blood Institute (R01HL118567, R01HL107653)
- NIH Office of the Director (S10OD020056, S10RR027050)
- National Cancer Institute (P30CA008748)
- National Institute of Diabetes and Digestive and Kidney Diseases (K99-DK115778, P30DK063608)
- National Center for Research Resources (S10RR027050)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- JAK2 V617F mutation, clonal hematopoiesis, myeloproliferative neoplasms, atherosclerosis, erythrophagocytosis, efferocytosis, macrophage inflammation, CD47, MERTK, neutrophil infiltration, iron accumulation, necrotic core, inflammasome, p38 MAPK signaling, plaque vulnerability, hypercholesterolemia, Western diet, Ldlr knockout mice, hematopoietic stem cell transplantation
- MeSH terms
- c-Mer Tyrosine Kinase, Adult, Aged, Animals, Erythrocytes, Female, Hematopoiesis, Humans, Iron, Macrophages, Male, Mice, Inbred C57BL, Middle Aged, Neutrophils, Phagocytosis, Cytokines, p38 Mitogen-Activated Protein Kinases, Atherosclerosis, Mice, CD47 Antigen, Janus Kinase 2
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