A potential role for colony-stimulating factor 1 in the genesis of the early endometriotic lesion  

Oleh:

Jensen, Jani R. ; Witz, Craig A. ; Schenken, Robert S. ; Tekmal, Rajeshwar R.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 93 no. 01 (Jan. 2010), page 251-256.
Topik: Endometriosis; animal model; colony-stimulating factor 1; CSF-1; imatinib

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2010.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To investigate the role(s) of colony-stimulating factor 1 (CSF-1) on the development of early endometriosis in a murine model by comparing rate of lesion formation in mice [1] homozygous for a CSF-1 mutation versus syngeneic controls and [2] after treatment with imatinib, a commercially available tyrosine kinase inhibitor that alters interaction(s) between CSF-1 and its receptor, c-fms. Design Prospective, placebo-controlled animal study. Setting Academic medical center. Animals Six- to 8-week old female FVB, wild-type C57BL/6, and CSF-1 op/op mice. Intervention(s) Endometrial tissue from donor mice was used to induce endometriosis in murine recipients. In some experiments, mice homozygous for a CSF-1 mutation (CSF-1 op/op) were donors or recipients. In other experiments, donor and/or recipient mice received imatinib. Main Outcome Measure(s) Histologic confirmation of endometriosis, rate of lesion formation. Result(s) By 40 hours, recipient mice developed a mean of 7.2 ± 0.9 endometriotic lesions that had invaded host surfaces, and mesothelial cells had proliferated over the entire surface of the implants. The CSF-1 op/op mice developed significantly fewer (mean 0.9 ± 0.3) endometriotic lesions versus syngeneic controls. Imatinib treatment resulted in significantly fewer lesions when compared with sham-treated controls. Conclusion(s) Colony-stimulating factor 1 has a role in establishing early endometriotic lesions. Agents targeting CSF-1 or its actions have therapeutic potential for treating endometriosis.

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