ArticleAngiogenesis2025
Genetic deletion of microRNA-15a/16-1 in pericytes stimulates cerebral angiogenesis and promotes functional recovery after ischemic stroke.
Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Endothelial miR-15a/16-1 Regulation of SYNE1 Mediates Structural and Functional Recovery after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- DHCR24 in cholesterol metabolism and diseases of the nervous system.Lipids in health and disease · 2026Review
- Spatiotemporal dynamics of brain pericytes in ischemic stroke.Journal of neuroinflammation · 2026Review
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- The stem cell within the vessel wall: multipotent pericytes modulating β-cell function and diabetic complications.Stem cell research & therapy · 2025Review
- A review of the link between the lactate-GPR81 axis and mitochondrial angiopathy in MELAS based on imaging characteristics.Journal of neurology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Stroke is a leading cause of mortality and disability globally. Despite advancements in acute stroke therapies, patient outcomes with ischemic stroke remain suboptimal. Understanding its molecular mechanisms is crucial for developing effective treatments. Angiogenesis actively contributes to post-stroke functional recovery and improves long-term survival in stroke patients. Pericytes are essential for maintaining vascular stability and promoting angiogenesis. We hypothesized that microRNA-15a/16-1 in pericytes significantly modulates post-stroke angiogenesis and neurological recovery. Using a pericyte-specific miR-15a/16-1 conditional knockout (cKO) mouse model, we found that genetic deletion of miR-15a/16-1 in pericytes enhances angiogenesis, promotes cerebral blood flow recovery, and improves sensorimotor and cognitive outcomes following ischemic stroke. Mechanistically, RNA sequencing identified several novel targets of miR-15a/16-1, including Pappa2, Fgf9, Islr, and Ccr2. Interestingly, Pappa2, Fgf9, and Islr function as secreted proteins. Luciferase reporter assays demonstrated that miR-15a/16-1 directly binds and suppresses Pappa2, Fgf9, Islr, and Ccr2 activity in cultured pericytes. In vivo and in vitro assays further confirmed that miR-15a/16-1 silencing in pericytes significantly elevates the protein levels of Pappa2, Fgf9, Islr, and Ccr2 and enhances endothelial cell proliferation, migration, and tube formation under ischemic conditions. These findings suggest that targeting miR-15a/16-1 in pericytes offers a promising therapeutic strategy for enhancing stroke recovery by promoting neurovascular repair and reducing brain damage.
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Registered trials
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