ArticleBiochemical and biophysical research communications2021
Adropin decreases endothelial monolayer permeability after cell-free hemoglobin exposure and reduces MCP-1-induced macrophage transmigration.
Article in Biochemical and biophysical research communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 27 citations in OpenAlex.
- Exosome-Transferred STAT3 from Cancer-Associated Fibroblasts Expedites Thymic Carcinoma Malignant Progression and M2 Macrophage Polarization Through Transcriptionally Activating KLHL5.Applied biochemistry and biotechnology · 2026Article
- KAT3B Protects Against Septic Lung Injury by Regulating TSLP Succinylation and Macrophage Polarization.Applied biochemistry and biotechnology · 2025Article
- Exploring endothelial dysfunction in major rheumatic diseases: current trends and future directions.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Adropin: a key player in immune cell homeostasis and regulation of inflammation in several diseases.Frontiers in immunology · 2025Review
- Role of the Unique Secreted Peptide Adropin in Various Physiological and Disease States.Biomolecules · 2024Review
- Adropin: A crucial regulator of cardiovascular health and metabolic balance.Metabolism open · 2024Review
- IBR1, a novel endogenous IFIH1-binding dsRNA, governs IFIH1 activation and M1 macrophage polarisation in ARDS.Clinical and translational medicine · 2024Article
- Subarachnoid hemorrhage-associated brain injury and neurobehavioral deficits are reversed with synthetic adropin treatment through sustained Ser1179 phosphorylation of endothelial nitric oxide synthase.Frontiers in stroke · 2024Article
- Low circulating adropin levels in late-middle aged African Americans with poor cognitive performance.npj aging · 2023Article
- Emerging Evidence Linking the Liver to the Cardiovascular System: Liver-derived Secretory Factors.Journal of clinical and translational hepatology · 2023Review
- Clinical Potential of Immunotherapies in Subarachnoid Hemorrhage Treatment: Mechanistic Dissection of Innate and Adaptive Immune Responses.Aging and disease · 2023Review
- Adropin attenuates pancreatitis‑associated lung injury through PPARγ phosphorylation‑related macrophage polarization.International journal of molecular medicine · 2023Article
- Blood-spinal cord barrier disruption in degenerative cervical myelopathy.Fluids and barriers of the CNS · 2023Review
- Adropin Predicts Chronic Kidney Disease in Type 2 Diabetes Mellitus Patients with Chronic Heart Failure.Journal of clinical medicine · 2023Article
- Adropin's Role in Energy Homeostasis and Metabolic Disorders.International journal of molecular sciences · 2022Review
- Neutrophil Extracellular Traps and Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage.Critical care explorations · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCell-free heme-containing proteins mediate endothelial injury in a variety of disease states including subarachnoid hemorrhage and sepsis by increasing endothelial permeability. Inflammatory cells are also attracted to sites of vascular injury by monocyte chemotactic protein 1 (MCP-1) and other chemokines. We have identified a novel peptide hormone, adropin, that protects against hemoglobin-induced endothelial permeability and MCP-1-induced macrophage migration.
methodsHuman microvascular endothelial cells were exposed to cell-free hemoglobin (CFH) with and without adropin treatment before measuring monolayer permeability using a FITC-dextran tracer assay. mRNA and culture media were collected for molecular studies. We also assessed the effect of adropin on macrophage movement across the endothelial monolayer using an MCP-1-induced migration assay.
resultsCFH exposure decreases adropin expression and increases paracellular permeability of human endothelial cells. Treating cells with synthetic adropin protects against the increased permeability observed during the natural injury progression. Cell viability was similar in all groups and Hmox1 expression was not affected by adropin treatment. MCP-1 potently induced macrophage migration across the endothelial monolayer and adropin treatment effectively reduced this phenomenon.
conclusionsEndothelial injury is a hallmark of many disease states. Our results suggest that adropin treatment could be a valuable strategy in preventing heme-mediated endothelial injury and macrophage infiltration. Further investigation of adropin therapy in animal models and human tissue specimens is needed.
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