Increased expression of macrophage colony–stimulating factor and its receptor in patients with endometriosis  

Oleh:

Budrys, Nicole M. ; Nair, Hareesh B. ; Liu, Ya-guang ; Kirma, Nameer B.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 97 no. 05 (May 2012), page 1129-1135.
Topik: ENDOMETRIOSIS; Endometriosis; colony-stimulating factor 1; C-FMS; early lesion development; macrophage; cell culture; peritoneal fluid

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2012.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Objective To investigate the expression and regulation of colony-stimulating factor 1 (CSF-1) and its receptor, C-FMS, in endometriosis. Design In vivo and vitro study. Setting University-based academic medical center. Patient(s) Reproductive-age women undergoing surgery for benign conditions. Intervention(s) Peritoneal and endometrial tissue samples were obtained. Main Outcome Measure(s) CSF-1 and C-FMS expression. Result(s) Significantly higher CSF-1 levels were found in peritoneal fluid of patients with endometriosis compared with control subjects. Ectopic endometriotic tissue had 3.5-fold and 1.7-fold increases in CSF-1 and C-FMS expression, respectively, compared with eutopic tissue. Coculture of endometrial cells from either established cell lines or patient samples with peritoneal mesothelial cells (PMCs) led to increased expression of CSF-1 and C-FMS. A higher but nonsignificant increase in levels of C-FMS and CSF-1 was found in cocultures of endometrial epithelial cells from patients with endometriosis compared with those without endometriosis. Conclusion(s) Increased CSF-1 levels may contribute to endometriosis lesion formation and progression. Elevation in CSF-1 after coculture of endometrial cells with PMCs suggests that endometrial tissue may be a source of peritoneal CSF-1. Increased C-FMS expression in endometrial cells from women with endometriosis cocultured with PMCs suggests that endometrial tissue involved in lesion formation is highly responsive to CSF-1 signaling.

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