ArticlePloS one2017
Chemokine Ligand 5 (CCL5) Derived from Endothelial Colony-Forming Cells (ECFCs) Mediates Recruitment of Smooth Muscle Progenitor Cells (SPCs) toward Critical Vascular Locations in Moyamoya Disease.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Modeling Moyamoya disease using patient-derived induced pluripotent stem cells and organoids.Molecular biology reports · 2026Review
- RNF213 in Panvascular Disease: A Molecular Hub Linking Genetic Susceptibility to Systemic Vasculopathy.Biomedicines · 2026Review
- Association between RNF213 p.R4810K and Progression of Cerebral Artery Negative Remodeling in Moyamoya Disease.Neurologia medico-chirurgica · 2025Article
- The role of the RING finger protein 213 gene in Moyamoya disease.Fluids and barriers of the CNS · 2025Review
- ExploringBiomedicines · 2024Review
- Molecular Biomarkers Affecting Moyamoya Disease.Advances and technical standards in neurosurgery · 2024Article
- RNF213 loss-of-function promotes pathological angiogenesis in moyamoya disease via the Hippo pathway.Brain : a journal of neurology · 2023Article
- Cyclin-Dependent Kinase Inhibitor 2A is a Key Regulator of Cell Cycle Arrest and Senescence in Endothelial Colony-Forming Cells in Moyamoya Disease.Journal of Korean Neurosurgical Society · 2023Article
- Physiological and pathophysiological mechanisms of the molecular and cellular biology of angiogenesis and inflammation in moyamoya angiopathy and related vascular diseases.Frontiers in neurology · 2023Review
- Systemic Profile of Cytokines in Arteriovenous Fistula Patients and Their Associations with Maturation Failure.Kidney360 · 2022Article
- Novel Multifaceted Roles for RNF213 Protein.International journal of molecular sciences · 2022Review
- Experimental Animal Models for Moyamoya Disease: A Species-Oriented Scoping Review.Frontiers in surgery · 2022Article
- RNF213 and GUCY1A3 in Moyamoya Disease: Key Regulators of Metabolism, Inflammation, and Vascular Stability.Frontiers in neurology · 2021Review
- Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases.The application of clinical genetics · 2021Review
- Vascular Remodeling in Moyamoya Angiopathy: From Peripheral Blood Mononuclear Cells to Endothelial Cells.International journal of molecular sciences · 2020Article
- A bioassay system of autologous human endothelial, smooth muscle cells, and leukocytes for use in drug discovery, phenotyping, and tissue engineering.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Circulating endothelial progenitor cells and endothelial cells in moyamoya disease.Brain and behavior · 2018Article
- Alcohol consumption promotes colorectal carcinoma metastasis via a CCL5-induced and AMPK-pathway-mediated activation of autophagy.Scientific reports · 2018Article
- Pro-angiogenic effect of RANTES-loaded polysaccharide-based microparticles for a mouse ischemia therapy.Scientific reports · 2017Article
- Endothelial Progenitor Cells in Moyamoya Disease: Current Situation and Controversial Issues.Cell transplantationReview
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology and pathogenesis of moyamoya disease (MMD) are still obscure. Previous studies indicated that angiogenic chemokines may play an important role in the pathogenesis of the disease. Recently, it was discovered that peripheral blood-derived endothelial colony-forming cells (ECFCs) and smooth muscle progenitor cells (SPCs) have defective functions in MMD patients. Therefore, the interaction of ECFCs and SPCs, the precursors of two crucial cellular components of vascular walls, with some paracrine molecules is an intriguing subject. In this study, co-culture of ECFCs and SPCs from MMD patients and healthy normal subjects revealed that MMD ECFCs, not SPCs, are responsible for the defective functions of both ECFCs and SPCs. Enhanced migration of SPCs toward MMD ECFCs supported the role for some chemokines secreted by MMD ECFCs. Expression arrays of MMD and normal ECFCs suggested that several candidate cytokines differentially produced by MMD ECFCs. We selected chemokine (C-X-C motif) ligand 6 (CXCR6), interleukin-8 (IL8), chemokine (C-C motif) ligand 2 (CCL2), and CCL5 for study, based on the relatively higher expression of these ligands in MMD ECFCs and their cognate receptors in MMD SPCs. Migration assays showed that only CCL5 significantly augmented the migration activities of SPCs toward ECFCs. Treatment with siRNA for the CCL5 receptor (CCR5) abrogated the effect, confirming that CCL5 is responsible for the interaction of MMD ECFCs and SPCs. These data indicate that ECFCs, not SPCs, are the major players in MMD pathogenesis and that the chemokine CCL5 mediates the interactions. It can be hypothesized that in MMD patients, defective ECFCs direct aberrant SPC recruitment to critical vascular locations through the action of CCL5.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.