Identification and analysis of induced endometriotic lesions.

Cássia G. T. Silveira (492705), Dominique Finas (492706), Peter Hunold (492707), Frank Köster (492708), Katharina Stroschein (492709), Geraldine O. Canny (492710), Gerhard Moldenhauer (135129), Peter Altevogt (223601), Achim Rody (190314), Daniela Hornung (332203)
2015 · doi:10.1371/journal.pone.0082512.g002 · W6885592699
other OA: green CC0
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The study utilized murine models to identify and analyze induced endometriotic lesions following treatment with a monoclonal antibody targeting the L1 Cell Adhesion Molecule. Researchers excised endometrial implants from B6C3F1 and CD-1 nude mice four weeks post-treatment, observing associated adhesions involving the liver and gut in immunocompetent hosts. Histological evaluation via hematoxylin-eosin staining and immunohistochemistry confirmed the presence of L1CAM within these autologous and heterologous endometriotic implants. This paper is centrally about endometriosis — specifically the identification and molecular characterization of induced endometriotic lesions in mouse models.

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Abstract

(A) Four weeks after treatment, B6C3F1 (I, II) and CD-1 nude (III, IV) mice were sacrificed; endometrial implants were identified (black arrows) and excised for further analysis. Adhesions were also observed at implant sites in the B6C3F1 (II) and CD-1 (IV) mice and involved the liver (L) and gut (G). (B) Hematoxylin-eosin staining of the endometriotic tissues derived from both mouse groups was performed for histological evaluation (magnification: x100). (C) The presence of L1CAM was observed in the endometriotic implants derived from autologous (I) and heterologous (II) models by immunohistochemistry. Negative (III) and positive (colon, squamous epithelium) (IV) controls are shown (magnification: x200).
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L1 Cell Adhesion Molecule as a Potential Therapeutic Target in Murine Models of Endometriosis Using a Monoclonal Antibody Approach Figure 2 Identification and analysis of induced endometriotic lesions. (A) Four weeks after treatment, B6C3F1 (I, II) and CD-1 nude (III, IV) mice were sacrificed; endometrial implants were identified (black arrows) and excised for further analysis. Adhesions were also observed at implant sites in the B6C3F1 (II) and CD-1 (IV) mice and involved the liver (L) and gut (G). (B) Hematoxylin-eosin staining of the endometriotic tissues derived from both mouse groups was performed for histological evaluation (magnification: x100). (C) The presence of L1CAM was observed in the endometriotic implants derived from autologous (I) and heterologous (II) models by immunohistochemistry. Negative (III) and positive (colon, squamous epithelium) (IV) controls are shown (magnification: x200).

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