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Titel: Inhibition of Cyclooxygenase-2 Suppresses the Recruitment of Endothelial Progenitor Cells in the Microvasculature of Endometriotic Lesions
VerfasserIn: Rudzitis-Auth, Jeannette
Nickels, Ruth M.
Menger, Michael D.
Laschke, Matthias W.
Sprache: Englisch
Titel: The American Journal of Pathology
Bandnummer: 188 (2018)
Heft: 2
Seiten: 450-460
Verlag/Plattform: Elsevier
Erscheinungsjahr: 2017
DDC-Sachgruppe: 610 Medizin, Gesundheit
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: The incorporation of endothelial progenitor cells (EPCs) into newly developing blood vessels contributes to the vascularization of endometriotic lesions. We analyzed whether cyclooxygenase (COX)-2 signaling regulates this vasculogenic process. Endometriotic lesions were surgically induced in irradiated FVB/N mice, which were reconstituted with bone marrow from FVB/N-TgN [Tie2/green fluorescent protein (GFP)] 287 Sato mice. The animals received b-estradiol 17-valerate once a week and were treated daily with the selective COX-2 inhibitor parecoxib (25 mg/kg) or vehicle (control) for 7 and 28 days. Analyses involved the determination of lesion growth, cyst formation, homing of GFPþ/Tie2þ EPCs, numbers of circulating EPCs, vascularization, cell proliferation, apoptosis, and immune cell infiltration by means of highresolution ultrasonography, caliper measurements, flow cytometry, histologic analysis, and immunohistochemical analysis. In parecoxib-treated mice, blood circulating EPCs were higher, but numbers of recruited EPCs in endometriotic lesions were significantly lower when compared with controls. This finding was associated with an impaired early vascularization and stromal tissue growth as well as reduced glandular secretory activity of the lesions. Parecoxib-treated lesions further contained less proliferating and more apoptotic cells and exhibited lower numbers of infiltrating macrophages and neutrophilic granulocytes. These findings demonstrate that the inhibition of COX-2 suppresses vasculogenesis in endometriotic lesions, which may contribute to an impaired lesion vascularization and growth.
DOI der Erstveröffentlichung: 10.1016/j.ajpath.2017.10.013
URL der Erstveröffentlichung: https://doi.org/10.1016/j.ajpath.2017.10.013
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-442176
hdl:20.500.11880/39524
http://dx.doi.org/10.22028/D291-44217
ISSN: 0002-9440
Datum des Eintrags: 29-Jan-2025
Fakultät: M - Medizinische Fakultät
Fachrichtung: M - Chirurgie
Professur: M - Prof. Dr. Michael D. Menger
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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