| Estradiol accelerates endothelial healing through the retrograde commitment of uninjured endothelium. | |
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MedLine Citation:
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PMID: 18441207 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although the accelerative effect of 17beta-estradiol (E2) on endothelial regrowth has been clearly demonstrated, the local cellular events accounting for this beneficial vascular action are still uncertain. In the present work, we compared the kinetics of endothelial healing of mouse carotid arteries after endovascular and perivascular injury. Both basal reendothelialization as well as the accelerative effect of E2 were similar in the two models. Three days after endothelial denudation, a regenerative area was observed in both models, characterized by similar changes in gene expression after injury, visualized by en face confocal microscopy (EFCM). A precise definition of the injury limits was only possible with the perivascular model, since it causes a complete and lasting decellularization of the media. Using this model, we demonstrated that the migration of uninjured endothelial cells precedes proliferation (bromodeoxyuridine incorporation) and that these events occur at earlier time points with E2 treatment. We have also identified an uninjured retrograde zone as an intimate component of the endothelial regeneration process. Thus, in the perivascular model, the regenerative area can be subdivided into a retrograde zone and a reendothelialized area. Importantly, both areas are significantly enlarged by E2. In conclusion, the combination of the electric perivascular injury model and EFCM is well adapted to the visualization of the endothelial monolayer and to investigate cellular events involved in reendothelialization. This process is accelerated by E2 as a consequence of the retrograde commitment of an uninjured endothelial zone to migrate and proliferate, contributing to an enlargement of the regenerative area. |
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Authors:
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Cédric Filipe; Laetitia Lam Shang Leen; Laurent Brouchet; Audrey Billon; Vincent Benouaich; Vincent Fontaine; Pierre Gourdy; Françoise Lenfant; Jean-François Arnal; Alain-Pierre Gadeau; Henrik Laurell |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2008-04-25 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 294 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-06-09 Completed Date: 2008-08-15 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H2822-30 Citation Subset: IM |
Affiliation:
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Institut National de la Santé et de la Recherche Médicale (INSERM) U858, I2MR, Equipe 9, Université de Toulouse III Paul Sabatier and Centre Hospitalier Universitaire de Toulouse-Rangueil, Toulouse, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bone Marrow Transplantation Carotid Artery Injuries / metabolism*, pathology, physiopathology Cell Movement Cell Proliferation Disease Models, Animal Drug Implants Endothelium, Vascular / metabolism*, pathology, physiopathology Estradiol / administration & dosage, metabolism* Female Green Fluorescent Proteins / genetics, metabolism Immunohistochemistry Kinetics Mice Mice, Inbred C57BL Mice, Transgenic Microscopy, Confocal / methods Muscle, Smooth, Vascular / metabolism, physiopathology Ovariectomy Recombinant Fusion Proteins / metabolism Wound Healing* |
| Chemical | |
Reg. No./Substance:
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0/Drug Implants; 0/Recombinant Fusion Proteins; 0/enhanced green fluorescent protein; 147336-22-9/Green Fluorescent Proteins; 50-28-2/Estradiol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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