ArticleArteriosclerosis, thrombosis, and vascular biology2016
Monocyte Adhesion and Plaque Recruitment During Atherosclerosis Development Is Regulated by the Adapter Protein Chat-H/SHEP1.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Monocytes as a convergent nanoparticle therapeutic target for cardiovascular diseases.Advanced drug delivery reviews · 2022Pooled it
- Nanomaterials and exercise interventions: A synergistic approach for atherosclerosis therapy (Review).International journal of molecular medicine · 2026Review
- SHEP1 alleviates cardiac ischemia reperfusion injury via targeting G3BP1 to regulate macrophage infiltration and inflammation.Cell death & disease · 2024Article
- Vitexin Suppresses High-Glucose-upregulated Adhesion Molecule Expression in Endothelial Cells through Inhibiting NF-κB Signaling Pathway.ACS omega · 2024Article
- Lack of NPR1 Increases Vascular Endothelial Adhesion through Induction of Integrin Beta 4.International journal of molecular sciences · 2022Article
- Dirty Jobs: Macrophages at the Heart of Cardiovascular Disease.Biomedicines · 2022Review
- Vascular Protective Effects ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Modular 3D In Vitro Artery-Mimicking Multichannel System for Recapitulating Vascular Stenosis and Inflammation.Micromachines · 2021Article
- Hyperglycemia Induces Trained Immunity in Macrophages and Their Precursors and Promotes Atherosclerosis.Circulation · 2021Article
- Osteocalcin, Osteopontin and RUNX2 Expression in Patients' Leucocytes with Arteriosclerosis.Diseases (Basel, Switzerland) · 2021Article
- Effects of coal-fired PMBMC pharmacology & toxicology · 2020Article
- 7-Biomolecules · 2019Article
- Article
- Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Cardiovascular Immunotherapy and the Role of Imaging.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4.International journal of molecular medicine · 2017Article
- 15-oxoeicosatetraenoic acid mediates monocyte adhesion to endothelial cell.Lipids in health and disease · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe chronic inflammation associated with atherosclerosis is caused by lipid deposition followed by leukocyte recruitment to the arterial wall. We previously showed that the hematopoietic cell-specific adaptor protein Cas- and Hef1-associated signal transducer hematopoietic isoform (Chat-H)/SHEP1 regulated lymphocyte adhesion and migration. In this study, we analyzed the role of Chat-H in atherosclerosis development. APPROACH AND
resultsUsing Chat-H-deficient bone marrow transplantation in low-density lipoprotein receptor-deficient mice, we found that Chat-H regulated atherosclerotic plaque formation. Chat-H deficiency in hematopoietic cells associated with lower plaque complexity and fewer leukocytes in the lesions, whereas myeloid-specific deletion of Chat-H was sufficient for conferring atheroprotection. Chat-H deficiency resulted in reduced recruitment of classical Ly6c(high) and nonclassical Ly6c(low) monocytes to the plaques, which was accompanied by increased numbers of both monocyte subsets in the blood. This associated with defective adhesion of Chat-H-deficient Ly6c(high) and Ly6c(low) monocytes to vascular cell adhesion molecule-1 in vitro and impaired infiltration of fluorescent bead-loaded monocytes to atherosclerotic plaques. In contrast, Chat-H was dispensable for CX3CL1 and CCR1/CCR5-dependent migration of monocytes.
conclusionsOur findings highlight Chat-H as a key protein that regulates atherosclerosis development by controlling monocyte adhesion and recruitment to the plaques and identify a novel target that may be exploited for treating atherosclerosis.
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