ArticleExperimental neurology2015
Progesterone protects endothelial cells after cerebrovascular occlusion by decreasing MCP-1- and CXCL1-mediated macrophage infiltration.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Macrophage immunometabolism in stroke: a view from single-cell and nano technologies.Journal of translational medicine · 2026Review
- The Clinical Implications of Progesterone in Preeclampsia.Biomolecules · 2025Review
- Sex-Specific Effects of Estradiol and Progesterone in Ischemic Kidney Injury.International journal of molecular sciences · 2024Article
- Stem Cell- and Cell-Based Therapies for Ischemic Stroke.Bioengineering (Basel, Switzerland) · 2022Review
- The Role of CCL2/CCR2 Axis in Cerebral Ischemia-Reperfusion Injury and Treatment: From Animal Experiments to Clinical Trials.International journal of molecular sciences · 2022Review
- Identification of the key genes and immune infiltrating cells determined by sex differences in ischaemic stroke through co-expression network module.IET systems biology · 2022Article
- Crosstalk between high-density lipoproteins and endothelial cells in health and disease: Insights into sex-dependent modulation.Frontiers in cardiovascular medicine · 2022Review
- Serum progesterone and retinopathy in male patients with type 2 diabetes: A cross-sectional study.Journal of diabetes investigation · 2021Article
- Activation of Yes-Associated Protein/PDZ-Binding Motif Pathway Contributes to Endothelial Dysfunction and Vascular Inflammation in AngiotensinII Hypertension.Frontiers in physiology · 2021Article
- Blockage of C-X-C Motif Chemokine Receptor 2 (CXCR2) Suppressed Uric Acid (UA)-Induced Cardiac Remodeling.Frontiers in physiology · 2021Article
- Neural stem cell therapy for stroke: A multimechanistic approach to restoring neurological function.Brain and behavior · 2019Review
- Parity History Determines a Systemic Inflammatory Response to Spread of Ovarian Cancer in Naturally Aged Mice.Aging and disease · 2017Article
- CTLA4 blockade reduces immature myeloid cells in head and neck squamous cell carcinoma.Oncoimmunology · 2016Article
- Sex-specific differences in basilar artery vasospasm after subarachnoid hemorrhage: evidence from a rabbit model.Frontiers in neurologyArticle
- LAG-3 confers poor prognosis and its blockade reshapes antitumor response in head and neck squamous cell carcinoma.OncoimmunologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The neuroprotective effects of progesterone after ischemic stroke have been established, but the role of progesterone in promoting cerebrovascular repair remains under-explored. Male Sprague-Dawley rats underwent transient middle cerebral artery occlusion (tMCAO) for 90 min followed by reperfusion for 3 days. Progesterone (8 mg/kg/day) was administered intraperitoneally at 1h after initial occlusion followed by subcutaneous injections at 6, 24 and 48 h post-occlusion. Rats were euthanized after 72 h and brain endothelial cell density and macrophage infiltration were evaluated within the cerebral cortex. We also assessed progesterone's ability to induce macrophage migration toward hypoxic/reoxygenated cultured endothelial cells. We found that progesterone treatment post-tMCAO protects ischemic endothelial cells from macrophage infiltration. We further demonstrate that infiltration of monocytes/macrophages can be induced by potent chemotactic factors such as monocyte chemoattractant protein-1 (MCP-1) and the chemokine ligand 1 (CXCL1), secreted by hypoxic/reoxygenated endothelial cells. Progesterone blunts secretion of MCP-1 and CXCL1 from endothelial cells after hypoxia/reoxygenation injury and decreases leukocyte infiltration. The treatment protects ischemic endothelial cells from macrophage infiltration and thus preserves vascularization after ischemic injury.
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Registered trials
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